@article{barron_defrancesco_chou_bonagura_tropf_murphy_mcmanamey_yuan_mochel_ward_2023, title={Echocardiographic caudal vena cava measurements in healthy cats and in cats with congestive heart failure and non-cardiac causes of cavitary effusions}, volume={48}, ISSN={["1875-0834"]}, url={https://doi.org/10.1016/j.jvc.2023.05.004}, DOI={10.1016/j.jvc.2023.05.004}, abstractNote={Echocardiographic indices of the inferior vena cava have been associated with elevated right atrial pressures in humans.Describe caudal vena caval (CVC) sonographic dimensions in healthy cats compared to cats with cardiogenic cavitary effusion (CCE), cardiogenic pulmonary edema (CPE), or non-cardiac causes of cavitary effusion (NCE).30 healthy control cats and 52 client-owned cats with CCE, CPE, or NCE examined at two university hospitals.Sagittal 2-dimensional (2D) and M-mode CVC dimensions were acquired from the subxiphoid view. Caudal vena cava collapsibility index (CVC-CI) was calculated. Variables were compared between study groups using Kruskal-Wallis and Dunn's Bonferroni testing. Receiver operating characteristic curves were used to assess sensitivity and specificity for diagnostic categories.Healthy cats had sagittal 2D and M-mode (median, interquartile range) CVC maximal dimensions of 2.4 mm (1.3-4.0) and 3.4 mm (1.5-4.9) and CVC-CI of 52% (45.2-61.8) and 55% (47.8-61.3), respectively. The CVC maximal dimensions in healthy controls were smaller than in cats with cavitary effusions or pulmonary edema (all P<0.05). CVC-CI was different between CCE and NCE (P<0.0001) with cutoffs of CVC-CI ≤38% (2D) or ≤29% (M-mode) being 90.5% and 85.7% sensitive, and 94.4% and 100% specific for diagnosis of CCE, respectively.Caudal vena cava measurements are larger in cats with cavitary effusions and cats with CPE than healthy cats. In cats with cavitary effusion, decreased CVC-CI, ≤38% (2D) or ≤29% (M-mode), was helpful in distinguishing between cardiogenic and noncardiogenic etiology.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Barron, L. Z. and DeFrancesco, T. C. and Chou, Y. -y. and Bonagura, J. D. and Tropf, M. A. and Murphy, S. D. and McManamey, A. K. and Yuan, L. and Mochel, J. P. and Ward, J. L.}, year={2023}, month={Aug}, pages={7–18} }
 @article{mcgrath_dixon_hirst_bode_defrancesco_fries_gordon_hogan_pereira_mederska_et al._2023, title={Pacemaker-lead-associated thrombosis in dogs: a multicenter retrospective study}, url={https://doi.org/10.1016/j.jvc.2023.06.004}, DOI={10.1016/j.jvc.2023.06.004}, abstractNote={Pacemaker implantation is the treatment of choice for clinically relevant bradyarrhythmias. Pacemaker-lead-associated thrombosis (PLAT) occurs in 23.0-45.0% of people with permanent transvenous pacemakers. Serious thromboembolic complications are reported in 0.6-3.5%. The incidence of PLAT in dogs is unknown.multicenter retrospective study of seven centers with 606 client-owned dogs undergoing permanent pacemaker implantation between 2012 and 2019. 260 dogs with a transvenous pacemaker with echocardiographic follow-up, 268 dogs with a transvenous pacemaker without echocardiographic follow-up and 78 dogs with an epicardial pacemaker.10.4% (27/260) of dogs with transvenous pacemakers and echocardiographic follow-up had PLAT identified. The median time to diagnosis was 175 days (6-1853 days). Pacemaker-lead-associated thrombosis was an incidental finding in 15/27 (55.6%) dogs. Of dogs with a urine protein:creatinine ratio measured at pacemaker implantation, dogs with PLAT were more likely to have proteinuria at pacemaker implantation vs. dogs without PLAT (6/6 (100.0%) vs. 21/52 (40.4%), P=0.007). Urine protein:creatinine ratio was measured in 12/27 (44.4%) dogs at PLAT diagnosis, with proteinuria identified in 10/12 (83.3%) dogs. Anti-thrombotic drugs were used following the identification of PLAT in 22/27 (81.5%) dogs. The thrombus resolved in 9/15 (60.0%) dogs in which follow-up echocardiography was performed. Dogs with PLAT had shorter survival times from implantation compared to those without PLAT (677 days [9-1988 days] vs. 1105 days [1-2661 days], P=0.003).Pacemaker-lead-associated thrombosis is identified in 10.4% (27/260) of dogs following transvenous pacing, is associated with proteinuria, can cause significant morbidity, and is associated with reduced survival times.}, journal={Journal of Veterinary Cardiology}, author={McGrath, C. and Dixon, A. and Hirst, C. and Bode, E.F. and DeFrancesco, T. and Fries, R. and Gordon, S. and Hogan, D. and Pereira, Y. Martinez and Mederska, E. and et al.}, year={2023}, month={Oct} }
 @article{walker_defrancesco_bonagura_keene_meurs_tou_kurtz_aona_barron_mcmanamey_et al._2022, title={Association of diet with clinical outcomes in dogs with dilated cardiomyopathy and congestive heart failure*}, volume={40}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2021.02.001}, abstractNote={Dilated cardiomyopathy (DCM) in dogs has been associated with feeding of grain-free (GF), legume-rich diets. Some dogs with presumed diet-associated DCM have shown improved myocardial function and clinical outcomes following a change in diet and standard medical therapy. Prior GF (pGF) diet influences reverse cardiac remodeling and clinical outcomes in dogs with DCM and congestive heart failure (CHF). A retrospective study was performed with 67 dogs with DCM and CHF for which diet history was known. Dogs were grouped by diet into pGF and grain-inclusive (GI) groups. Dogs in the pGF group were included if diet change was a component of therapy. Survival was analyzed using Kaplan–Meier curves and the Cox proportional-hazards model. The median survival time was 344 days for pGF dogs vs. 253 days for GI dogs (P = 0.074). Statistically significant differences in median survival were identified when the analysis was limited to dogs surviving longer than one week (P = 0.033). Prior GF dogs had a significantly worse outcome the longer a GF diet was fed prior to diagnosis (P = 0.004) or if they were diagnosed at a younger age (P = 0.017). Prior GF dogs showed significantly greater improvement in normalized left ventricular internal diastolic diameter (P = 0.038) and E-point septal separation (P = 0.031) measurements and significant decreases in their furosemide (P = 0.009) and pimobendan (P < 0.005) dosages over time compared to GI dogs. Prior GF dogs that survived at least one week after diagnosis of DCM, treatment of CHF, and diet change had better clinical outcomes and showed reverse ventricular remodeling compared to GI dogs.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Walker, A. L. and DeFrancesco, T. C. and Bonagura, J. D. and Keene, B. W. and Meurs, K. M. and Tou, S. P. and Kurtz, K. and Aona, B. and Barron, L. and McManamey, A. and et al.}, year={2022}, month={Apr}, pages={99–109} }
 @article{guillaumin_defrancesco_scansen_quinn_whelan_hanel_goy-thollot_bublot_robertson_bonagura_2022, title={Bilateral lysis of aortic saddle thrombus with early tissue plasminogen activator (BLASTT): a prospective, randomized, placebo-controlled study in feline acute aortic thromboembolism}, volume={11}, ISSN={["1532-2750"]}, DOI={10.1177/1098612X221135105}, abstractNote={Objectives The aim of this study was to investigate the impact of tissue plasminogen activator (TPA) on the treatment of feline aortic thromboembolism (FATE). Methods Cats diagnosed with FATE involving ⩾2 limbs were enrolled in a prospective, multicenter, double-blinded, randomized, placebo-controlled study within 6 h of an event. Diagnosis was made by clinical findings and one confirmatory criterion. Cats received placebo or TPA (1 mg/kg/h with the first 10% by bolus). All cats received pain control and thromboprophylaxis. The primary outcome was a change from baseline in a published limb score at 48 h. Secondary outcomes included 48 h survival, survival to discharge and complication proportions. Statistical analyses included pattern-mixture models, logistic regression and Fisher’s exact, Student’s t- and Mann–Whitney–Wilcoxon tests. Results Based on a power analysis, 40 cats were enrolled; however, only 20 survived to 48 h (TPA, n = 12; placebo, n = 8 [ P = 0.34]). There was a statistically significant improvement in limb scores compared with baseline for both groups ( P <0.001). Limb score at 48 h was 1 point lower (better) in the TPA group ( P = 0.19). Thrombolysis had no statistically significant effect on 48 h survival ( P = 0.22). Lower affected limb lactate was associated with better 48 h survival (odds ratio 1.53, 95% confidence interval 1.08–2.17; P = 0.02). The survival to discharge rates were 45% (TPA) and 30% (placebo; P = 0.51). Complications in the TPA and placebo groups included acute kidney injury (22% and 19%, respectively; P = 1.00) and/or reperfusion injuries (33% and 19%, respectively; P = 0.45). Conclusions and relevance Survival and complication rates of acute FATE were not different with or without thrombolysis. High in-hospital mortality decreased the statistical power to detect a statistically significant difference between treatments with regard to our primary outcome.}, journal={JOURNAL OF FELINE MEDICINE AND SURGERY}, author={Guillaumin, Julien and DeFrancesco, Teresa C. and Scansen, Brian A. and Quinn, Rebecca and Whelan, Megan and Hanel, Rita and Goy-Thollot, Isabelle and Bublot, Isabelle and Robertson, James B. and Bonagura, John D.}, year={2022}, month={Nov} }
 @article{karp_freeman_rush_arsenault_cunningham_defrancesco_karlin_laste_lefbom_plante_et al._2022, title={Dilated cardiomyopathy in cats: survey of veterinary cardiologists and retrospective evaluation of a possible association with diet}, volume={39}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2021.11.002}, abstractNote={The objectives were to conduct a survey of cardiologists on their recent experiences with cats that have dilated cardiomyopathy (DCM) and to retrospectively review individual cases of feline DCM.Part one: A survey was distributed to cardiologists with questions regarding caseload and clinical management of cats with DCM diagnosed over the past two years. Part two: Cardiologists completing the survey were invited to submit data from cats recently diagnosed with DCM. Data on signalment, clinical signs, diet, echocardiographic measurements and outcome were recorded.Part one: From 52 completed surveys, many cardiologists responded that measuring and supplementing taurine and recommending a diet change in cats with DCM are common practices. Few (15%) cardiologists reported an increase in the number of feline DCM cases over the past two years, although some had cases that improved even if taurine deficiency was not present. Part two: Twenty of 37 (54%) cats ate low pea/lentil (low PL) diets, and 14/37 (38%) ate high PL diets at the time of diagnosis; three had incomplete diet information. Two of 13 cats (15%) in which taurine was measured had levels below the reference range. After adjusting for other variables, cats eating high PL diets that changed diets after diagnosis had a significantly longer survival time than that of cats eating high PL diets that did not change diets after diagnosis (P = 0.025).Additional research is warranted to determine whether there could be a possible association between diet and DCM in cats.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Karp, S. and Freeman, L. M. and Rush, J. E. and Arsenault, W. G. and Cunningham, S. M. and DeFrancesco, T. C. and Karlin, E. T. and Laste, N. J. and Lefbom, B. K. and Plante, C. and et al.}, year={2022}, month={Feb}, pages={22–34} }
 @article{meurs_williams_deprospero_friedenberg_malarkey_ezzell_keene_adin_defrancesco_tou_2021, title={A deleterious mutation in the ALMS1 gene in a naturally occurring model of hypertrophic cardiomyopathy in the Sphynx cat}, volume={16}, ISSN={["1750-1172"]}, DOI={10.1186/s13023-021-01740-5}, abstractNote={Familial hypertrophic cardiomyopathy is a common inherited cardiovascular disorder in people. Many causal mutations have been identified, but about 40% of cases do not have a known causative mutation. Mutations in the ALMS1 gene are associated with the development of Alstrom syndrome, a multisystem familial disease that can include cardiomyopathy (dilated, restrictive). Hypertrophic cardiomyopathy has not been described. The ALMS1 gene is a large gene that encodes for a ubiquitously expressed protein. The function of the protein is not well understood although it is believed to be associated with energy metabolism and homeostasis, cell differentiation and cell cycle control. The ALMS1 protein has also been shown to be involved in the regulation of cell cycle proliferation in perinatal cardiomyocytes. Although cardiomyocyte cell division and replication in mammals generally declines soon after birth, inhibition of ALMS1 expression in mice lead to increased cardiomyocyte proliferation, and deficiency of Alstrom protein has been suggested to impair post-natal cardiomyocyte cell cycle arrest. Here we describe the association of familial hypertrophic cardiomyopathy in Sphynx cats with a novel ALMS1 mutation.A G/C variant was identified in exon 12 (human exon 13) of the ALMS1 gene in affected cats and was positively associated with the presence of hypertrophic cardiomyopathy in the feline population (p < 0.0001). The variant was predicted to change a highly conserved nonpolar Glycine to a positively charged Arginine. This was predicted to be a deleterious change by three in silico programs. Protein prediction programs indicated that the variant changed the protein structure in this region from a coil to a helix. Light microscopy findings included myofiber disarray with interstitial fibrosis with significantly more nuclear proliferative activity in the affected cats than controls (p < 0.0001).This study demonstrates a novel form of cardiomyopathy associated with ALMS1 in the cat. Familial hypertrophic cardiomyopathy is a disease of genetic heterogeneity; many of the known causative genes encoding for sarcomeric proteins. Our findings suggest that variants in genes involved with cardiac development and cell regulation, like the ALMS1 gene, may deserve further consideration for association with familial hypertrophic cardiomyopathy.}, number={1}, journal={ORPHANET JOURNAL OF RARE DISEASES}, author={Meurs, Kathryn M. and Williams, Brian G. and DeProspero, Dylan and Friedenberg, Steven G. and Malarkey, David E. and Ezzell, J. Ashley and Keene, Bruce W. and Adin, Darcy B. and DeFrancesco, Teresa C. and Tou, Sandra}, year={2021}, month={Feb} }
 @article{k. o'donnell_adin_atkins_defrancesco_keene_tou_meurs_2021, title={Absence of known feline MYH7 and MYBPC3 variants in a diverse cohort of cats with hypertrophic cardiomyopathy}, volume={52}, ISSN={["1365-2052"]}, DOI={10.1111/age.13074}, abstractNote={Hypertrophic cardiomyopathy (HCM) is the most common cause of heart disease in the domestic cat with a genetic predisposition in a few breeds. In the Maine Coon and Ragdoll breeds, two variants associated with the HCM phenotype have been identified in the cardiac myosin binding protein C gene (MYBPC3; p.Ala31Pro and p.Arg820Trp respectively), and a single variant has been identified in the myosin heavy chain gene (MYH7; p.Glu1883Lys) in one domestic cat with HCM. It is not known if these variants influence the development of HCM in other cohorts of the feline population. The objective of this study was to evaluate the presence of the known MYBPC3 and MYH7 variants in a population of cats with HCM. DNA was isolated from samples collected from non-Ragdoll and non-Maine Coon domestic cats diagnosed with HCM through the North Carolina State University College of Veterinary Medicine and genotyped for the three variants. One-hundred and three DNA samples from cats with HCM were evaluated from domestic shorthair, domestic longhair and purebred cats. All samples were wt for the MYBPC3 and MYH7 variants. Although this study was limited by its inclusion of cats from one tertiary hospital, the lack of these MYBPC3 and MYH7 variants in this feline HCM population indicates that the clinical utility of genetic testing for these variants may be isolated to the two cat breeds in which these variants have been identified. Further studies to identify the causative variants for the feline HCM population are warranted.}, number={4}, journal={ANIMAL GENETICS}, author={K. O'Donnell and Adin, D. and Atkins, C. E. and DeFrancesco, T. and Keene, B. W. and Tou, S. and Meurs, K. M.}, year={2021}, month={Aug}, pages={542–544} }
 @article{defrancesco_ward_2021, title={Focused Canine Cardiac Ultrasound}, volume={51}, ISSN={["1878-1306"]}, DOI={10.1016/j.cvsm.2021.07.005}, abstractNote={Focused cardiac ultrasound (FCU) is a useful point-of-care imaging tool to assess cardiovascular status in symptomatic dogs in the acute care setting. Unlike complete echocardiography, FCU is a time-sensitive examination involving a subset of targeted ultrasound views to identify severe cardiac abnormalities and is performed as part of an integrated thoracic ultrasound including interrogation of the pleural space and lungs. When integrated with other clinical information, FCU can be helpful in the diagnosis of left-sided and right-sided congestive heart failure, pericardial effusion and tamponade, and severe pulmonary hypertension, and can provide estimates of fluid responsiveness in hypotensive dogs.}, number={6}, journal={VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE}, author={DeFrancesco, Teresa C. and Ward, Jessica L.}, year={2021}, month={Nov}, pages={1203–1216} }
 @article{chou_ward_barron_murphy_tropf_lisciandro_yuan_mochel_defrancesco_2021, title={Focused ultrasound of the caudal vena cava in dogs with cavitary effusions or congestive heart failure: A prospective, observational study}, volume={16}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0252544}, abstractNote={Ultrasonographic indices of the inferior vena cava are useful for predicting right heart filling pressures in people.To determine whether ultrasonographic indices of caudal vena cava (CVC) differ between dogs with right-sided CHF (R-CHF), left-sided CHF (L-CHF), and noncardiac causes of cavitary effusion (NC).113 dogs diagnosed with R-CHF (n = 51), L-CHF (30), or NC effusion (32) were enrolled. Seventeen of the R-CHF dogs had pericardial effusion and tamponade. Focused ultrasound was performed prospectively to obtain 2-dimensional and M-mode subxiphoid measures of CVC maximal and minimal size (CVCmax and CVCmin), CVCmax indexed to aortic dimension (CVC:Ao), and CVC collapsibility index (CVC-CI). Variables were compared between study groups using Kruskal-Wallis and Dunn's-Bonferroni testing, and receiver operating characteristics curves were used to assess sensitivity and specificity.All sonographic CVC indices were significantly different between R-CHF and NC dogs (P < 0.001). Variables demonstrating the highest diagnostic accuracy for discriminating R-CHF versus NC were CVC-CI <33% in 2D (91% sensitive and 96% specific) and presence of hepatic venous distension (84% sensitive and 90% specific). L-CHF dogs had higher CVC:Ao and lower CVC-CI compared to NC dogs (P = 0.016 and P = 0.043 in 2D, respectively) but increased CVC-CI compared to the R-CHF group (P < 0.001).Ultrasonographic indices of CVC size and collapsibility differed between dogs with R-CHF compared to NC causes of cavitary effusions. Dogs with L-CHF have CVC measurements intermediate between R-CHF and NC dogs.}, number={5}, journal={PLOS ONE}, author={Chou, Yen-Yu and Ward, Jessica L. and Barron, Lara Z. and Murphy, Shane D. and Tropf, Melissa A. and Lisciandro, Gregory R. and Yuan, Lingnan and Mochel, Jonathan P. and DeFrancesco, Teresa C.}, year={2021}, month={May} }
 @misc{atkins_keene_defrancesco_tou_chetboul_cote_ettinger_fox_hamlin_mochel_et al._2021, title={Letter to the editor regarding "Efficacy of adding ramipril (VAsotop) to the combination of furosemide (Lasix) and pimobendan (VEtmedin) in dogs with mitral valve degeneration: The VALVE trial"}, volume={35}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16035}, abstractNote={The manuscript entitled Efficacy of adding ramipril (VAsotop) to the combination of furosemide (Lasix) and pimobendan (VEtmedin) in dogs with mitral valve degeneration: The VALVE trial1 reports a study which sought to answer the question “could pimobendan be all that is needed beyond loop diuretics to manage congestive heart failure (CHF) in myxomatous mitral valve disease (MMVD)?” This was done by prospectively comparing the efficacy of pimobendan + ramipril + furosemide (triple treatment) to pimobendan + furosemide (double treatment) to treat new-onset CHF caused by MMVD. While agreeing with the authors that this question has merit, we share several comments and questions regarding applicability of their study results to current practice. During the VALVE trial, worsening signs of CHF were primarily managed with progressively larger diuretic dosages, as opposed to other potential pharmacological interventions such as greater renin-angiotensin-aldosterone system (RAAS) suppression, alternative diuretic use, higher pimobendan dosing, and arterial vasodilator treatment. While the angiotensin-converting enzyme inhibitor (ACEI) ramipril (VASOTOP) was begun at a once daily dosage according to label recommendation, the initial furosemide dosage (median, 8 mg/kg/d), high by current clinical standards, was increased to as much as 15 mg/kg/d, before predefined treatment failure was reached; ramipril dosage was increased (doubled) in only 3 dogs. Spironolactone dosing was left to the clinicians' discretion (added to baseline treatment in only 13 dogs, 8 in the triple treatment group, and 5 dogs in the double treatment group). The VALVE trial did not assess the efficacy of RAAS suppression using biomarkers. Therefore, the question of whether ramipril adequately or optimally suppressed RAAS, while failing to improve survival in the face of these diuretic dosages, remains unanswered. We are also concerned that dogs in both treatment groups received ACEI for an average of 9 months before entering the study (44% of triple treatment group vs 26% of double treatment group; P = .02), indicating that over one-quarter of the double treatment group (the no ACEI group) previously had received an ACEI—and for a duration longer than the median 7.6 months that these dogs remained in the study. This is important because it is known that RAAS suppression before the onset of CHF has favorable effects on cardiac remodeling.2 Although unknowable by the authors at the time of the VALVE trial design, other studies completed during the 10-year duration of the VALVE trial have demonstrated significant benefit from greater, longer, and more broad-spectrum RAAS suppression (eg, higher or q12h ACEI dosing and mineralocorticoid antagonist [MRA] inclusion) in treating proteinuria and CHF.3-5 Because the VALVE trial was performed under Good Clinical Practice guidelines, owner adherence to the trial protocol was quantified. It would be useful to know whether those measurements identified “adherence parity” between the 2 treatment groups, thus eliminating 1 potential source of unintentional bias. Ramipril, a narrow-spectrum RAAS suppressant (ie, it causes no direct MRA effect), was tested as an “add-on” to drugs providing symptomatic relief (pimobendan and furosemide). Although the absence of an MRA as part of the test article is understandable because of the timing of the VALVE study design, its absence impairs our understanding of the potential role that true RAAS suppression (ie, more RAAS suppression than ACE inhibition alone) might play in managing CHF caused by MMVD. It is now known that incomplete RAAS suppression (aldosterone breakthrough) is common with either ACEI or angiotensin II receptor blockers (ARB) in normal dogs challenged with furosemide or amlodipine5, 6; with ACEI in natural MMVD before CHF (without furosemide)5, 7; and in MMVD with CHF in dogs receiving ACEI and furosemide.5, 7 Furthermore, inclusion of MRAs in therapeutic protocols has improved survival in CHF caused by MMVD.3, 5 Although it has not been directly investigated, it is likely that the high doses of furosemide used in the VALVE Trial, with greater RAAS stimulatory potential, enhanced the propensity for aldosterone breakthrough.8 In dogs treated with ACEI and ARBs, there is an estimated 30% to 40% incidence of aldosterone breakthrough at conventional furosemide dosages, and a proportional clinical benefit is seen with broad-spectrum RAAS suppression.3, 5-7, 9 For this reason, it would be important to know the average maximum furosemide dosage received, as well as the number of dogs that experienced renal compromise, were euthanized, or exited the study for polyuria and polydipsia or worsening renal dysfunction. It would also be relevant to know the number of cases accrued from each institution, as well as the average furosemide dosage, number of dogs receiving spironolactone or doubled ramipril dosage, and how these potential institutional differences were accounted for during data analysis. A large number of cases from a single center may diminish the benefits of a multicenter study design or raise the possibility of unintentional institutional acquisition bias. Although the VALVE results are surprising and interesting, a conclusion that they obviate the need for ACEI treatment in the management of CHF from MMVD is not justified. We believe this study to be hypothesis generating, rather than pivotal. A larger study, employing methodology that provides evidence of more complete RAAS inhibition with contemporary adjunctive heart failure treatment is needed to provide pivotal data upon which to guide practice. Programmatic or institutional grant support, consultant/speaker for pharmaceutical companies marketing veterinary cardiovascular drugs are as follows: Clarke Atkins: Boehringer-Ingelheim, CEVA Sant Animalé, Vetoquinol, Virbac; Bruce Keene: Boehringer-Ingelheim, CEVA Santa Animalé; Teresa C. DeFrancesco: Boehringer-Ingelheim, CEVA Santé Animale; Sandra Tou: Boehringer-Ingelheim, CEVA Santé Animale; Valérie Chetboul: Boehringer-Ingelheim, CEVA Santé Animale, Vetoquinol; Étienne Côté, Boehringer-Ingelheim, CEVA Santé Animale; Stephen Ettinger: Purina-Nestle; Philip R. Fox: Boehringer-Ingelheim; Robert L. Hamlin: none; Jonathan P. Mochel: Boehringer-Ingelheim, Ceva Santé Animale, Ethos, LEAH Labs, 3D Health Solutions; Jean-Louis Pouchelon: Boehringer-Ingelheim, CEVA Santé Animale, Vetoquinol; Rebecca L. Stepien: Boehringer-Ingelheim, CEVA Santé Animale.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Atkins, Clarke and Keene, Bruce and DeFrancesco, Teresa C. and Tou, Sandra and Chetboul, Valerie and Cote, Etienne and Ettinger, Stephen and Fox, Philip R. and Hamlin, Robert L. and Mochel, Jonathan P. and et al.}, year={2021}, month={Mar}, pages={698–699} }
 @article{deprospero_kerry a. o'donnell_defrancesco_keene_tou_adin_atkins_meurs_2021, title={Myxomatous mitral valve disease in Miniature Schnauzers and Yorkshire Terriers: 134 cases (2007-2016)}, volume={259}, ISSN={["1943-569X"]}, DOI={10.2460/javma.20.05.0291}, abstractNote={To characterize features of myxomatous mitral valve disease (MMVD) in Miniature Schnauzers and Yorkshire Terriers.69 Miniature Schnauzers and 65 Yorkshire Terriers, each with MMVD.Medical record data for each dog were collected; the study period was January 2007 through December 2016. If available, radiographic data were evaluated, and a vertebral heart scale score was assigned for each dog. Statistical analysis was performed with Student t and Fisher exact tests.Compared with Yorkshire Terriers, the prevalence of MMVD was significantly higher in Miniature Schnauzers and affected dogs were significantly younger at the time of diagnosis. Miniature Schnauzers were significantly more likely to have mitral valve prolapse and syncope, compared with Yorkshire Terriers. Yorkshire Terriers were significantly more likely to have coughing and have had previous or current treatment with cardiac medications, compared with Miniature Schnauzers. There was no statistical difference between breeds with regard to abnormally high vertebral heart scale scores or radiographic evidence of congestive heart failure.With regard to MMVD, features of the disease among Miniature Schnauzers and Yorkshire Terriers were similar, but there were also a few discernable differences between these 2 breeds and from historical findings for dogs with MMVD of other breeds. Clinical signs at the time of diagnosis differed between the 2 breeds, which may have reflected concurrent breed-specific conditions (sick sinus syndrome or airway disease [eg, tracheal collapse]). Future work should include prospective studies to provide additional information regarding the natural progression of MMVD in these dog breeds.}, number={12}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={DeProspero, Dylan J. and Kerry A. O'Donnell and DeFrancesco, Teresa C. and Keene, Bruce W. and Tou, Sandra P. and Adin, Darcy B. and Atkins, Clarke E. and Meurs, Kathryn M.}, year={2021}, month={Dec}, pages={1428–1432} }
 @article{williams_friedenberg_keene_tou_defrancesco_meurs_2021, title={Use of whole genome analysis to identify shared genomic variants across breeds in canine mitral valve disease}, volume={6}, ISSN={["1432-1203"]}, DOI={10.1007/s00439-021-02297-w}, journal={HUMAN GENETICS}, author={Williams, Brian and Friedenberg, Steven G. and Keene, Bruce W. and Tou, Sandy P. and DeFrancesco, Teresa C. and Meurs, Kathryn M.}, year={2021}, month={Jun} }
 @article{murphy_ward_viall_tropf_walton_fowler_ware_defrancesco_2021, title={Utility of point-of-care lung ultrasound for monitoring cardiogenic pulmonary edema in dogs}, volume={35}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.15990}, DOI={10.1111/jvim.15990}, abstractNote={Point-of-care lung ultrasound (LUS) is an effective tool to diagnose left-sided congestive heart failure (L-CHF) in dogs via detection of ultrasound artifacts (B-lines) caused by increased lung water.To determine whether LUS can be used to monitor resolution of cardiogenic pulmonary edema in dogs, and to compare LUS to other indicators of L-CHF control.Twenty-five client-owned dogs hospitalized for treatment of first-onset L-CHF.Protocolized LUS, thoracic radiographs (TXR), and plasma N-terminal pro-B-type natriuretic peptide were performed at hospital admission, hospital discharge, and recheck examinations. Lung ultrasound findings were compared between timepoints and to other clinical measures of L-CHF.From time of hospital admission to discharge (mean 19.6 hours), median number of LUS sites strongly positive for B-lines (>3 B-lines per site) decreased from 5 (range, 1-8) to 1 (range, 0-5; P < .001), and median total B-line score decreased from 37 (range, 6-74) to 5 (range, 0-32; P = .002). Lung ultrasound indices remained improved at first recheck (P < .001). Number of strong positive sites correlated positively with respiratory rate (r = 0.52, P = .008) and TXR edema score (r = 0.51, P = .009) at hospital admission. Patterns of edema resolution differed between LUS and TXR, with cranial quadrants showing more significant reduction in B-lines compared to TXR edema score (80% vs 29% reduction, respectively; P = .003).Lung ultrasound could be a useful tool for monitoring resolution of pulmonary edema in dogs with L-CHF.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Murphy, Shane D. and Ward, Jessica L. and Viall, Austin K. and Tropf, Melissa A. and Walton, Rebecca L. and Fowler, Jennifer L. and Ware, Wendy A. and DeFrancesco, Teresa C.}, year={2021}, month={Jan}, pages={68–77} }
 @article{coleman_defrancesco_griffiths_lascelles_kleisch_atkins_keene_2020, title={Atenolol in cats with subclinical hypertrophic cardiomyopathy: a double-blind, placebo-controlled, randomized clinical trial of effect on quality of life, activity, and cardiac biomarkers}, volume={30}, ISSN={["1875-0834"]}, url={https://doi.org/10.1016/j.jvc.2020.06.002}, DOI={10.1016/j.jvc.2020.06.002}, abstractNote={Abstract Objective To compare quality of life (QOL) and activity measures between healthy control cats and cats with subclinical hypertrophic cardiomyopathy (HCM), and to evaluate the effect of oral atenolol therapy on QOL, activity, and circulating biomarkers in cats with subclinical HCM. Animals Thirty-two client-owned cats with subclinical HCM and 27 healthy control cats. Methods Owner responses to a QOL questionnaire, circulating cardiac biomarker concentrations, and accelerometer-based activity measures were compared prospectively in cats with and without HCM, and in cats with HCM before and after treatment with oral atenolol (6.25 mg/cat q 12 h) for 6 months. Results Owner-assessed activity of daily living score was lower in cats with HCM than in cats in controls (p=0.0420). No differences were identified between control cats and cats with HCM for any activity variable. Compared with placebo, treatment with atenolol was associated with a lower baseline-adjusted mean ± SD heart rate (157 ± 30 vs. 195 ± 20 bpm; p=0.0001) and rate-pressure product (22,446 ± 6,237 vs. 26,615 ± 4,623 mmHg/min; p=0.0146). A treatment effect of atenolol on QOL or activity was not demonstrated. Conclusions This study failed to identify an effect of subclinical HCM on owner-assessed QOL or activity or a treatment effect of atenolol on these variables at the dosage evaluated. These findings do not support a treatment benefit of atenolol for the goal of symptom reduction in cats with subclinical HCM.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Coleman, A. E. and DeFrancesco, T. C. and Griffiths, E. H. and Lascelles, B. D. X. and Kleisch, D. J. and Atkins, C. E. and Keene, B. W.}, year={2020}, month={Aug}, pages={77–91} }
 @article{adin_atkins_domenig_defrancesco_keene_tou_stern_meurs_2020, title={Renin-angiotensin aldosterone profile before and after angiotensin-converting enzyme-inhibitor administration in dogs with angiotensin-converting enzyme gene polymorphism}, volume={34}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.15746}, DOI={10.1111/jvim.15746}, abstractNote={Background An angiotensin-converting enzyme (ACE) gene polymorphism occurs in dogs; however, functional importance is not well studied. Hypothesis We hypothesized that dogs with the polymorphism would show alternative renin-angiotensin aldosterone system (RAAS) pathway activation and classical RAAS pathway suppression before and after ACE-inhibitor administration, as compared to dogs without the polymorphism that would show this pattern only after ACE-inhibitor administration. Animals Twenty-one dogs with mitral valve disease that were genotyped for the ACE gene polymorphism. Methods This retrospective study utilized stored samples from 8 ACE gene polymorphism-negative (PN) dogs and 13 ACE gene polymorphism-positive (PP) dogs before and after enalapril administration. Equilibrium analysis was performed to evaluate serum RAAS metabolites and enzyme activities. Results were compared before and after enalapril, and between groups. Results The classical RAAS pathway was suppressed and the alternative RAAS pathway was enhanced for both genotypes after administration of enalapril, with no differences before enalapril administration. Aldosterone breakthrough occurred in both PN (38%) and PP (54%) dogs despite angiotensin II suppression. Aldosterone was significantly higher (P = .02) in ACE gene PP dogs (median, 92.17 pM; IQR, 21.85-184.70) compared to ACE gene PN dogs (median, 15.91 pM; IQR, <15.00-33.92) after enalapril. Conclusions and Clinical Importance The ACE gene polymorphism did not alter baseline RAAS activity. Aldosterone breatkthrough in some dogs suggests nonangiotensin mediated aldosterone production that might be negatively influenced by genotype. These results support the use of aldosterone receptor antagonists with ACE-inhibitors when RAAS inhibition is indicated for dogs, especially those positive for the ACE gene polymorphism.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Adin, Darcy and Atkins, Clarke and Domenig, Oliver and DeFrancesco, Teresa and Keene, Bruce and Tou, Sandra and Stern, Joshua A. and Meurs, Kathryn M.}, year={2020}, month={Mar}, pages={600–606} }
 @article{ward_kussin_tropf_tou_defrancesco_keene_2020, title={Retrospective evaluation of the safety and tolerability of pimobendan in cats with obstructive vs nonobstructive cardiomyopathy}, volume={34}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.15920}, DOI={10.1111/jvim.15920}, abstractNote={Abstract Background Pimobendan is frequently used off‐label for treatments of cats with congestive heart failure (CHF). Concern exists regarding the safety of pimobendan in cats with outflow tract obstruction (OTO). Objectives In cats treated with pimobendan, incidence of adverse effects will not differ between cats with OTO vs cats with nonobstructive cardiomyopathy. Animals Two‐hundred sixty cats with CHF (57 with OTO, 203 with nonobstructive disease). Methods Retrospective medical record review. Groups were compared using 2‐sample t ‐tests, Wilcoxon rank‐sum tests, and Fisher exact tests. Results Compared to cats with nonobstructive cardiomyopathy, cats with OTO were younger (8.9 [interquartile range (IQR) 6.6] vs 10.8 [6.3] years, P = .0036), more likely to have a heart murmur (51/57 [90%] vs 76/203 [37.8%] cats, P < .0001), more likely to manifest CHF as pulmonary edema (53/57 [83%] vs 144/203 [70.9%] cats, P = .0004), and less likely to have pleural effusion (19/57 [33%] vs 122/203 [60.1%] cats, P = .0005). Adverse effects suspected to be related to pimobendan administration occurred in 12/260 cats (4.6%), including 11/203 cats (5.4%) with nonobstructive cardiomyopathy and 1/57 cat (2%) with OTO ( P = .7). Pimobendan was discontinued due to adverse effects in 4/260 cats (1.5%), 3 with nonobstructive disease and 1 with OTO ( P = 1.0). Acute adverse hemodynamic effects after pimobendan administration were not detected in any cats. Conclusions and Clinical Importance Pimobendan is well tolerated in cats with cardiomyopathy and CHF, regardless of the presence of OTO.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ward, Jessica L. and Kussin, Efrem Z. and Tropf, Melissa A. and Tou, Sandra P. and DeFrancesco, Teresa C. and Keene, Bruce W.}, year={2020}, month={Nov}, pages={2211–2222} }
 @article{meurs_friedenberg_kolb_saripalli_tonino_woodruff_olby_keene_adin_yost_et al._2019, title={A missense variant in the titin gene in Doberman pinscher dogs with familial dilated cardiomyopathy and sudden cardiac death}, volume={138}, ISSN={0340-6717 1432-1203}, url={http://dx.doi.org/10.1007/s00439-019-01973-2}, DOI={10.1007/s00439-019-01973-2}, number={5}, journal={Human Genetics}, publisher={Springer Science and Business Media LLC}, author={Meurs, Kathryn M. and Friedenberg, Steven G. and Kolb, Justin and Saripalli, Chandra and Tonino, Paola and Woodruff, Kathleen and Olby, Natasha J. and Keene, Bruce W. and Adin, Darcy B. and Yost, Oriana L. and et al.}, year={2019}, month={Feb}, pages={515–524} }
 @article{adin_defrancesco_keene_tou_meurs_atkins_aona_kurtz_barron_saker_et al._2019, title={Echocardiographic phenotype of canine dilated cardiomyopathy differs based on diet type}, volume={21}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2018.11.002}, abstractNote={Canine dilated cardiomyopathy (DCM) can result from numerous etiologies including genetic mutations, infections, toxins, and nutritional imbalances. This study sought to characterize differences in echocardiographic findings between dogs with DCM fed grain-free (GF) diets and grain-based (GB) diets.Forty-eight dogs with DCM and known diet history.This was a retrospective analysis of dogs with DCM from January 1, 2015 to May 1, 2018 with a known diet history. Dogs were grouped by diet (GF and GB), and the GF group was further divided into dogs eating the most common grain-free diet (GF-1) and other grain-free diets (GF-o). Demographics, diet history, echocardiographic parameters, taurine concentrations, and vertebral heart scale were compared between GB, all GF, GF-1, and GF-o groups at diagnosis and recheck.Dogs eating GF-1 weighed less than GB and GF-o dogs, but age and sex were not different between groups. Left ventricular size in diastole and systole was greater, and sphericity index was less for GF-1 compared with GB dogs. Diastolic left ventricular size was greater for all GF compared with that of GB dogs. Fractional shortening, left atrial size, and vertebral heart scale were not different between groups. Taurine deficiency was not identified in GF dogs, and presence of congestive heart failure was not different between groups. Seven dogs that were reevaluated after diet change (6 received taurine supplementation) had clinical and echocardiographic improvement.Dietary-associated DCM occurs with some GF diets and can improve with nutritional management, including diet change. The role of taurine supplementation, even without deficiency, is uncertain.}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Adin, Darcy and DeFrancesco, Teresa and Keene, Bruce and Tou, Sandra and Meurs, Kathryn and Atkins, Clarke and Aona, Brent and Kurtz, Kari and Barron, Lara and Saker, Korinn and et al.}, year={2019}, month={Feb}, pages={1–9} }
 @article{ward_lisciandro_ware_miles_viall_defrancesco_2019, title={Lung ultrasonographic findings in dogs with various underlying causes of cough}, volume={255}, DOI={10.2460/javma.255.5.574}, abstractNote={To characterize lung ultrasonography (LUS) findings in dogs with a primary clinical complaint of cough.100 client-owned coughing dogs.A standardized LUS examination was performed for all dogs to quantify the number of B lines and identify subpleural abnormalities at 4 sites on each hemithorax. The final clinical diagnosis (reference standard) was determined by medical record review, and sensitivity and specificity of LUS for the diagnosis of selected causes of cough was determined.Common underlying causes of cough included dynamic airway collapse (n = 37), cardiogenic pulmonary edema (CPE; 12), and bronchitis (10). Compared with dogs with other causes of cough, dogs with bacterial pneumonia (n = 7) were more likely to have subpleural shred signs, whereas dogs with pulmonary neoplasia (4) were more likely to have subpleural nodule signs. Dogs with CPE had higher total B-line scores and higher numbers of LUS sites strongly positive for B lines (> 3 B lines/site) than other dogs. The LUS criteria of total B-line score ≥ 10 and presence of ≥ 2 sites strongly positive for B lines were each 92% sensitive and 94% specific for CPE diagnosis. Notably, 18% (16/88) of dogs with noncardiac causes of cough had been treated previously with diuretics because of prior CPE misdiagnosis.LUS profiles in dogs with cough differed by the underlying cause. In dogs with a clinical history of cough, this imaging modality could be diagnostically useful, particularly to help exclude the possibility of underlying CPE.}, number={5}, journal={Journal of the American Veterinary Medical Association}, author={Ward, J.L. and Lisciandro, G.R. and Ware, W.A. and Miles, K.G. and Viall, A.K. and DeFrancesco, T.C.}, year={2019}, month={Sep}, pages={574–583} }
 @article{meurs_adin_k. o'donnell_keene_atkins_defrancesco_tou_2019, title={Myxomatous mitral valve disease in the miniature poodle: A retrospective study}, volume={244}, ISSN={["1532-2971"]}, DOI={10.1016/j.tvjl.2018.12.019}, abstractNote={Myxomatous mitral valve disease (MMVD) is the most common cardiovascular disease in the dog. The natural history of the disease is wide ranging and includes patients without clinical signs as well as those with significant clinical consequences from cardiac arrhythmias, pulmonary hypertension and/or congestive heart failure. The factors that determine which dogs remain asymptomatic and which develop clinical disease are not known. Disease characteristics could be breed or family related; some breeds of dogs, particularly the Cavalier King Charles spaniels, develop MMVD at an early age. The purpose of this study was to retrospectively characterize MMVD in the miniature poodle, a commonly affected breed in which MMVD has not been well characterized. Thirty-two miniature poodles met the inclusion criteria. Mean age was 11±three years. Clinical signs included exercise intolerance, syncope and coughing. Eighteen dogs were classified as ACVIM Stage B1, 12 as stage B2, and two as stage C. Mean vertebral heart scale (VHS) was 10.2 (±standard deviation of 0.9); 15 of 28 dogs had a VHS <10.3. One dog had radiographic evidence of congestive heart failure. Mean diastolic left ventricle dimension normalized to body weight was 1.6 (±0.4) and mean systolic was 0.8 (±0.3). Mitral valve prolapse was subjectively classified as mild or moderate in 19 dogs and severe in two. In the miniature poodles reported here, MMVD appears to be a fairly late onset disease and often is a mild phenotype.}, journal={VETERINARY JOURNAL}, author={Meurs, K. M. and Adin, D. and K. O'Donnell and Keene, B. W. and Atkins, C. E. and DeFrancesco, T. and Tou, S.}, year={2019}, month={Feb}, pages={94–97} }
 @article{defrancesco_royal_2018, title={A survey of point-of-care ultrasound use in veterinary general practice}, volume={1}, ISSN={2590-1761}, url={http://dx.doi.org/10.4103/ehp.ehp_21_18}, DOI={10.4103/ehp.ehp_21_18}, abstractNote={Background: The use of ultrasound (US) continues to expand in veterinary and human medicine. The purpose of this study was to assess the current practices and potential barriers to the use of US in veterinary small animal general practices. Methods: An electronic survey was administered to approximately 1000 veterinary practitioners in the Southeastern United States. A total of 296 veterinarians completed the survey. Results: Among respondents, 53% reported having an US unit in their practice and 45% reported performing USs more than five times weekly. The most common reasons for not having an US unit were prohibitive cost (27%) and lack of training (27%). In addition, 74% responded that US training for a new graduate was extremely or very important. Conclusions: This study is the first to document the common use of US in small animal general practices and highlights the need for instruction of basic US skills for veterinary students and small animal practitioners.}, number={2}, journal={Education in the Health Professions}, publisher={Medknow}, author={DeFrancesco, Teresa and Royal, Kenneth}, year={2018}, pages={50} }
 @article{meurs_olsen_reimann_keene_atkins_adin_aona_condit_defrancesco_reina-doreste_et al._2018, title={Angiotensin-converting enzyme activity in Cavalier King Charles Spaniels with an ACE gene polymorphism and myxomatous mitral valve disease}, volume={28}, DOI={10.1097/FPC.0000000000000322}, abstractNote={Objectives Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog. It is particularly common in the Cavalier King Charles Spaniel (CKCS) breed and affected dogs are frequently managed with angiotensin-converting enzyme inhibitors (ACE-I). We have previously identified a canine ACE gene polymorphism associated with a decrease in angiotensin-converting enzyme (ACE) activity. The aim of this study was to evaluate for the prevalence of the ACE polymorphism in CKCS with mitral valve disease and to determine whether the presence of the polymorphism is associated with alterations in ACE activity at different stages of cardiac disease. Methods Seventy-three dogs with a diagnosis of mitral valve disease were evaluated and a blood sample was drawn for ACE polymorphism genotyping and ACE activity measurement. Results Forty-three dogs were homozygous for the ACE polymorphism; five were heterozygous and 25 were homozygous wild type. The mean age and the median severity of disease were not different for dogs with the polymorphism and dogs with the wild-type sequence. The median baseline ACE activity was significantly lower for the ACE polymorphism (27.0 U/l) than the wild-type sequence dogs (31.0 U/l) (P=0.02). Dogs with more severe disease and the ACE polymorphism had significantly lower levels of ACE activity than dogs with the wild-type sequence (P=0.03). Conclusion The CKCS appears to have a high prevalence of the ACE variant. Dogs with the ACE variant had lower levels of ACE activity even in more advanced mitral valve disease than dogs without the variant. The clinical significance of this finding and its impact on the need for ACE-I in dogs with the polymorphism and heart disease deserves further study.}, number={2}, journal={Pharmacogenetics and Genomics}, author={Meurs, K.M. and Olsen, L.H. and Reimann, M.J. and Keene, B.W. and Atkins, C.E. and Adin, D. and Aona, B. and Condit, J. and DeFrancesco, T. and Reina-Doreste, Y. and et al.}, year={2018}, pages={37–40} }
 @article{ward_lisciandro_defrancesco_2018, title={Distribution of alveolar-interstitial syndrome in dogs and cats with respiratory distress as assessed by lung ultrasound versus thoracic radiographs}, volume={28}, ISSN={["1476-4431"]}, DOI={10.1111/vec.12750}, abstractNote={To assess distribution of alveolar-interstitial syndrome (AIS) detected by lung ultrasound (LUS) compared to thoracic radiographs (TXR).Prospective study.University teaching hospital.Seventy-six dogs and 24 cats with acute respiratory distress or tachypnea.Patients underwent LUS and TXR within 6 hours. Lung ultrasound images were scored for presence and quantity of B-lines in 4 lung quadrants (right cranial, right caudal, left cranial, left caudal). An individual LUS quadrant was scored positive if > 3 B-lines were observed within a single intercostal space. Dorsoventral TXR were scored for presence of AIS in the same 4 quadrants. An individual TXR quadrant was scored positive if infiltrate was present in ≥ 25% of the quadrant. Medical records were evaluated for final diagnosis.Quadrant-by-quadrant spatial agreement in assigning AIS using LUS versus TXR was fair (K = 0.24 - 0.56). Lung ultrasound scored a higher number of quadrants positive per patient (2.65 ± 1.59 vs. 2.13 ± 1.48; P = 0.012). Patterns of distribution of AIS differed significantly based on final diagnosis. Patients with left-sided congestive heart failure were more likely to have diffuse AIS on LUS (P < 0.001) or bilateral caudal AIS on TXR (P = 0.04) while patients with noncardiac disease were more likely to have absence of AIS in all quadrants using either modality (P < 0.001). Differences in spatial distribution of AIS were also noted among disease subcategories.Lung ultrasound and TXR were both useful to detect and categorize distribution of alveolar or interstitial pulmonary pathology. Spatial agreement between modalities was only fair. Overall, LUS detected a higher incidence of AIS compared to TXR. Both modalities detected differences in distribution of AIS based on final diagnosis, suggesting that a regional pattern-based approach to thoracic imaging may prove diagnostically useful.}, number={5}, journal={JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE}, author={Ward, Jessica L. and Lisciandro, Gregory R. and DeFrancesco, Teresa C.}, year={2018}, pages={415–428} }
 @article{meurs_friedenberg_williams_keene_atkins_adin_aona_defrancesco_tou_mackay_et al._2018, title={Evaluation of genes associated with human myxomatous mitral valve disease in dogs with familial myxomatous mitral valve degeneration}, volume={232}, ISSN={["1532-2971"]}, DOI={10.1016/j.tvjl.2017.12.002}, abstractNote={Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog. It is believed to be heritable in Cavalier King Charles spaniels (CKCS) and Dachshunds. Myxomatous mitral valve disease is a familial disease in human beings as well and genetic mutations have been associated with its development. We hypothesized that a genetic mutation associated with the development of the human form of MMVD was associated with the development of canine MMVD. DNA was isolated from blood samples from 10 CKCS and 10 Dachshunds diagnosed with MMVD, and whole genome sequences from each animal were obtained. Variant calling from whole genome sequencing data was performed using a standardized bioinformatics pipeline for all samples. After filtering, the canine genes orthologous to the human genes known to be associated with MMVD were identified and variants were assessed for likely pathogenic implications. No variant was found in any of the genes evaluated that was present in least eight of 10 affected CKCS or Dachshunds. Although mitral valve disease in the CKCS and Dachshund is a familial disease, we did not identify genetic cause in the genes responsible for the human disease in the dogs studied here.}, journal={VETERINARY JOURNAL}, author={Meurs, Kathryn and Friedenberg, S. G. and Williams, B. and Keene, B. W. and Atkins, C. E. and Adin, D. and Aona, B. and DeFrancesco, Teresa and Tou, S. and Mackay, T. and et al.}, year={2018}, month={Feb}, pages={16–19} }
 @article{ward_lisciandro_ware_viall_aona_kurtz_reina-doreste_defrancesco_2018, title={Evaluation of point-of-care thoracic ultrasound and NT-proBNP for the diagnosis of congestive heart failure in cats with respiratory distress}, volume={32}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.15246}, DOI={10.1111/jvim.15246}, abstractNote={Background The diagnosis of congestive heart failure (CHF) in cats is challenging. Point-of-care (POC) thoracic ultrasound and NT-proBNP testing are emerging tools that may aid in diagnosis. Hypothesis/Objectives To assess the diagnostic accuracy of POC lung ultrasound (LUS), focused cardiac ultrasound (FCU), and NT-proBNP in predicting a final diagnosis of CHF. Animals Fifty-one cats in respiratory distress. Methods Blood NT-proBNP, LUS, and FCU evaluating left atrial (LA) size and presence of pericardial effusion (PCEFF) were performed in all cats. Lung ultrasound findings including pleural effusion (PLEFF), number of B-lines, and sub-pleural abnormalities were noted. Medical records were evaluated for final diagnosis. Results Thirty-three of 51 (65%) cats were diagnosed with CHF. Lung ultrasound and blood NT-proBNP were significant predictors of CHF in a multivariate model. The LUS criterion that maximized accuracy for CHF diagnosis was presence of >1 site strongly positive for B-lines (>3 B-lines per site), resulting in sensitivity of 78.8%, specificity of 83.3%, and area under the curve (AUC) of 0.833. Subjective LA enlargement was 97.0% sensitive and 100% specific for CHF (AUC 0.985). Presence of PCEFF also was 100% specific, but only 60.6% sensitive, for CHF (AUC 0.803). A positive blood NT-proBNP test was 93.9% sensitive and 72.2% specific for the diagnosis of CHF (AUC 0.831). Conclusions and Clinical Importance Point-of-care diagnostic techniques of LUS, FCU, and NT-proBNP are useful to diagnose CHF in cats with respiratory distress.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ward, Jessica L. and Lisciandro, Gregory R. and Ware, Wendy A. and Viall, Austin K. and Aona, Brent D. and Kurtz, Kari A. and Reina-Doreste, Yamir and DeFrancesco, Teresa C.}, year={2018}, pages={1530–1540} }
 @article{ward_lisciandro_keene_tou_defrancesco_2017, title={Accuracy of point-of-care lung ultrasonography for the diagnosis of cardiogenic pulmonary edema in dogs and cats with acute dyspnea}, volume={250}, ISSN={["1943-569X"]}, DOI={10.2460/javma.250.6.666}, abstractNote={Abstract OBJECTIVE To determine the accuracy of a point-of-care lung ultrasonography (LUS) protocol designed to diagnose cardiogenic pulmonary edema (CPE) in dyspneic dogs and cats. DESIGN Diagnostic test evaluation. ANIMALS 76 dogs and 24 cats evaluated for dyspnea. PROCEDURES Dogs and cats were evaluated by LUS; B lines were counted at 4 anatomic sites on each hemithorax. A site was scored as positive when > 3 B lines were identified. Animals with ≥ 2 positive sites identified on each hemithorax were considered positive for CPE. Medical records were evaluated to obtain a final diagnosis (reference standard) for calculation of the sensitivity and specificity of LUS and thoracic radiography for the diagnosis of CPE. RESULTS Dogs and cats with a final diagnosis of CPE had a higher number of positive LUS sites than did those with noncardiac causes of dyspnea. Overall sensitivity and specificity of LUS for the diagnosis of CPE were 84% and 74%, respectively, and these values were similar to those of thoracic radiography (85% and 87%, respectively). Use of LUS generally led to the misdiagnosis of CPE (ie, a false-positive result) in animals with diffuse interstitial or alveolar disease. Interobserver agreement on LUS results was high (κ > 0.85). CONCLUSIONS AND CLINICAL RELEVANCE LUS was useful for predicting CPE as the cause of dyspnea in dogs and cats, although this technique could not be used to differentiate CPE from other causes of diffuse interstitial or alveolar disease. Point-of-care LUS has promise as a diagnostic tool for dyspneic dogs and cats.}, number={6}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Ward, Jessica L. and Lisciandro, Gregory R. and Keene, Bruce W. and Tou, Sandra P. and DeFrancesco, Teresa C.}, year={2017}, month={Mar}, pages={666–675} }
 @article{meurs_stern_atkins_adin_aona_condit_defrancesco_reina-doreste_keene_tou_et al._2017, title={Angiotensin-converting enzyme activity and inhibition in dogs with cardiac disease and an angiotensin-converting enzyme polymorphism}, volume={18}, ISSN={["1752-8976"]}, DOI={10.1177/1470320317737184}, abstractNote={The objective of this study was to evaluate angiotensin-converting enzyme (ACE) activity in dogs and with and without an ACE polymorphism in the canine ACE gene, before and after treatment with an ACE inhibitor.Thirty-one dogs (20 wild-type, 11 ACE polymorphism) with heart disease were evaluated with ACE activity measurement and systolic blood pressure before and after administration of an ACE inhibitor (enalapril).Median pre-treatment ACE activity was significantly lower for ACE polymorphism dogs than for dogs with the wild-type sequence ( P=0.007). After two weeks of an ACE inhibitor, ACE activity was significantly reduced for both genotypes (wild-type, P<0.0001; ACE polymorphism P=0.03); mean post-therapy ACE activity was no different between the groups.An ACE polymorphism is associated with lower levels of ACE activity. Dogs with the polymorphism still experience suppression of ACE activity in response to an ACE inhibitor. It is possible that the genetic status and ACE activity of dogs may impact the response of dogs with this variant to an ACE inhibitor.}, number={4}, journal={JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM}, author={Meurs, Kathryn M. and Stern, Joshua A. and Atkins, Clarke E. and Adin, Darcy and Aona, Brent and Condit, Julia and DeFrancesco, Teresa and Reina-Doreste, Yamir and Keene, Bruce W. and Tou, Sandy and et al.}, year={2017}, month={Oct} }
 @article{adin_atkins_papich_defrancesco_griffiths_penteado_kurtz_klein_2017, title={Furosemide continuous rate infusion diluted with 5% dextrose in water or hypertonic saline in normal adult dogs: a pilot study}, volume={19}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2016.09.004}, abstractNote={The goal of this study was to investigate the short-term safety and diuretic efficacy of furosemide constant rate infusion (CRI) diluted with 5% dextrose in water (D5W) compared to dilution with 2.4% hypertonic saline in healthy dogs. Six healthy dogs. Dogs were studied in a randomized, blinded, crossover manner. Furosemide 3.3mg/kg was diluted to 2.2mg/mL with either 1.5mL/kg D5W for the DEX method or with 1.0mL/kg D5W and 0.5mL/kg of 7.2% hypertonic saline for the H-SAL method. After a 0.66mg/kg furosemide IV bolus, the infusion rate was 0.3 mL/kg/hr for 5 h such that both methods delivered 0.66 mg/kg/hr (total 3.3mg/kg) furosemide in equal volume for the study duration. Urine output, water intake, central venous pressure (CVP), physical parameters, furosemide concentrations, blood and urine electrolytes, and urine aldosterone to creatinine ratio (UAldo:C) were evaluated. Measured variables were not different between methods but showed changes over time consistent with diuresis. Mean CVP decreased over time similarly for both methods. Plasma furosemide and urine concentrations were stable and not different between methods. Both furosemide CRI methods showed an increase in the UAldo:C, however, the rise was greater for DEX than for H-SAL. Diuresis was similar for both furosemide CRI methods; however, the H-SAL method induced less renin-angiotensin-aldosterone system activation than the DEX method. The absence of intravascular volume expansion based on CVP suggests that dilution of a furosemide CRI with 2.4% hypertonic saline may be well tolerated in heart failure.}, number={1}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Adin, D. and Atkins, C. and Papich, M. and DeFrancesco, T. and Griffiths, E. and Penteado, M. and Kurtz, K. and Klein, A.}, year={2017}, month={Feb}, pages={44–56} }
 @article{hensley_tang_woodruff_defrancesco_tou_williams_breen_meurs_keene_cheng_et al._2017, title={Intracoronary allogeneic cardiosphere-derived stem cells are safe for use in dogs with dilated cardiomyopathy}, volume={21}, ISSN={1582-1838}, url={http://dx.doi.org/10.1111/jcmm.13077}, DOI={10.1111/jcmm.13077}, abstractNote={Cardiosphere-derived cells (CDCs) have been shown to reduce scar size and increase viable myocardium in human patients with mild/moderate myocardial infarction. Studies in rodent models suggest that CDC therapy may confer therapeutic benefits in patients with non-ischaemic dilated cardiomyopathy (DCM). We sought to determine the safety and efficacy of allogeneic CDC in a large animal (canine) model of spontaneous DCM. Canine CDCs (cCDCs) were grown from a donor dog heart. Similar to human CDCs, cCDCs express CD105 and are slightly positive for c-kit and CD90. Thirty million of allogeneic cCDCs was infused into the coronary vessels of Doberman pinscher dogs with spontaneous DCM. Adverse events were closely monitored, and cardiac functions were measured by echocardiography. No adverse events occurred during and after cell infusion. Histology on dog hearts (after natural death) revealed no sign of immune rejection from the transplanted cells.}, number={8}, journal={Journal of Cellular and Molecular Medicine}, publisher={Wiley}, author={Hensley, Michael Taylor and Tang, Junnan and Woodruff, Kathleen and DeFrancesco, Teresa and Tou, Sandra and Williams, Christina M. and Breen, Mathew and Meurs, Kathryn and Keene, Bruce and Cheng, Ke and et al.}, year={2017}, month={Mar}, pages={1503–1512} }
 @article{nolan_arkans_lavine_defrancesco_myers_griffith_posner_keene_tou_gieger_et al._2017, title={Pilot study to determine the feasibility of radiation therapy for dogs with right atrial masses and hemorrhagic pericardial effusion}, volume={19}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2016.12.001}, DOI={10.1016/j.jvc.2016.12.001}, abstractNote={To determine the short-term safety and biologic activity of radiation therapy (RT) for presumptive cardiac hemangiosarcoma in pet dogs. Six dogs with echocardiographic evidence of a right atrial/auricular mass, and hemorrhagic pericardial effusion, were enrolled in a prospective, single-arm clinical trial. A single fraction of 12 Gy was delivered using conformal external beam irradiation. Serum cardiac troponin I and plasma concentrations of vascular endothelial growth factor were quantified before, 4 and 24 h after RT. The frequency of required pericardiocenteses (quantified as the number of pericardiocenteses per week) before RT was compared to that after treatment. Overall survival time was determined. No treatment-related complications were observed. Pericardiocentesis was performed an average of 0.91 times per week before RT, and an average of 0.21 times per week after RT; this difference was statistically significant (p=0.03, as compared using a Wilcoxon signed-rank test of paired data). Pre- and post-treatment plasma vascular endothelial growth factor concentrations were not significantly different at any time point; there was a statistically significant (p=0.04; Friedman's test for non-parametric repeated measures) increase in cardiac troponin concentrations 4 h after irradiation. Median overall survival time was 79 days. In this population of dogs, RT was delivered without complication, and appears to have reduced the frequency of periacardial tamponade that necessitated pericardiocentesis. Serum cardiac troponin levels are altered after RT. RT alone, or in combination with chemotherapy, may provide clinical benefit to dogs with presumptive diagnoses of cardiac hemangiosarcoma.}, number={2}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Nolan, M.W. and Arkans, M.M. and LaVine, D. and DeFrancesco, Teresa and Myers, J.A. and Griffith, E.H. and Posner, L.P. and Keene, B.W. and Tou, S.P. and Gieger, Tracy and et al.}, year={2017}, month={Apr}, pages={132–143} }
 @article{ward_defrancesco_tou_atkins_griffith_keene_2016, title={Outcome and survival in canine sick sinus syndrome and sinus node dysfunction: 93 cases (2002-2014)}, volume={18}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2016.04.004}, abstractNote={To evaluate the clinical presentation, diagnosis, treatment, and outcomes of a group of dogs with sinoatrial node abnormalities. Ninety-three client-owned dogs at a referral institution. Medical records were reviewed for clinical history, diagnostic testing, and medical or permanent artificial pacemaker (PAP) treatment. Owners or veterinarians were contacted for long-term follow-up. Sixty-one dogs were symptomatic for their bradyarrhythmia and were diagnosed with sick sinus syndrome (SSS). Thirty-two dogs were asymptomatic for their bradyarrhythmia and were diagnosed with sinus node dysfunction (SND). Miniature Schnauzers, West Highland White terriers, Cocker spaniels, and female dogs were overrepresented. Medical management with positive chronotropic drugs successfully controlled syncope long-term in 54% of SSS dogs, and acted as a bridge to PAP in 20%. Positive atropine response predicted medical treatment success. Forty-six percent of SSS dogs eventually underwent PAP implantation. Median survival time was approximately 18 months in SND and SSS dogs regardless of treatment strategy. Congestive heart failure (CHF) associated with progressive valvular heart disease occurred commonly in all groups, particularly in dogs with bradycardia–tachycardia syndrome. Sinus node dysfunction and SSS represent a spectrum of sinoatrial node disease, which for some dogs may also involve a component of autonomic dysfunction. Dogs with SND do not require treatment. Dogs with SSS often require treatment to reduce the frequency of syncope; medical management is often useful, particularly in atropine responsive dogs. Prognosis of SSS with treatment is good, though development of CHF does not appear to be mitigated by treatment.}, number={3}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Ward, J. L. and DeFrancesco, T. C. and Tou, S. P. and Atkins, C. E. and Griffith, E. H. and Keene, B. W.}, year={2016}, month={Sep}, pages={199–212} }
 @article{lantis_ames_atkins_defrancesco_keene_werre_2015, title={Aldosterone breakthrough with benazepril in furosemide-activated renin-angiotensin-aldosterone system in normal dogs}, volume={38}, ISSN={["1365-2885"]}, DOI={10.1111/jvp.12154}, abstractNote={Pilot studies in our laboratory revealed that furosemide-induced renin-angiotensin-aldosterone system (RAAS) activation was not attenuated by the subsequent co-administration of benazepril. This study was designed to evaluate the effect of benazepril on angiotensin-converting enzyme (ACE) activity and furosemide-induced circulating RAAS activation. Our hypothesis was that benazepril suppression of ACE activity would not suppress furosemide-induced circulating RAAS activation, indicated by urinary aldosterone concentration. Ten healthy hound dogs were used in this study. The effect of furosemide (2 mg/kg p.o., q12h; Group F; n = 5) and furosemide plus benazepril (1 mg/kg p.o., q24h; Group FB; n = 5) on circulating RAAS was determined by plasma ACE activity, 4–6 h posttreatment, and urinary aldosterone to creatinine ratio (UAldo:C) on days −1, −2, 1, 3, and 7. There was a significant increase in the average UAldo:C (μg/g) after the administration of furosemide (Group F baseline [average of days −1 and −2] UAldo:C = 0.41, SD 0.15; day 1 UAldo:C = 1.1, SD 0.56; day 3 UAldo:C = 0.85, SD 0.50; day 7 UAldo:C = 1.1, SD 0.80, P < 0.05). Benazepril suppressed ACE activity (U/L) in Group FB (Group FB baseline ACE = 16.4, SD 4.2; day 1 ACE = 3.5, SD 1.4; day 3 ACE = 1.6, SD 1.3; day 7 ACE = 1.4, SD 1.4, P < 0.05) but did not significantly reduce aldosterone excretion (Group FB baseline UAldo:C = 0.35, SD 0.16; day 1 UAldo:C = 0.79, SD 0.39; day 3 UAldo:C 0.92, SD 0.48, day 7 UAldo:C = 0.99, SD 0.48, P < 0.05). Benazepril decreased plasma ACE activity but did not prevent furosemide-induced RAAS activation, indicating aldosterone breakthrough (escape). This is particularly noteworthy in that breakthrough is observed at the time of initiation of RAAS suppression, as opposed to developing after months of therapy.}, number={1}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Lantis, A. C. and Ames, M. K. and Atkins, C. E. and Defrancesco, T. C. and Keene, B. W. and Werre, S. R.}, year={2015}, month={Feb}, pages={65–73} }
 @article{ward_defrancesco_tou_atkins_griffith_keene_2015, title={Complication Rates Associated with Transvenous Pacemaker Implantation in Dogs with High-Grade Atrioventricular Block Performed During versus After Normal Business Hours}, volume={29}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.12512}, abstractNote={Background Transvenous pacemaker implantation in dogs is associated with a relatively high complication rate. At our institution, pacemaker implantation in dogs with high-grade atrioventricular block (HG-AVB) frequently is performed as an after-hours emergency. Hypothesis Among dogs with HG-AVB, the rate of major complications is higher when pacemakers are implanted after hours (AH) compared to during business hours (BH). Animals Client-owned dogs with HG-AVB that underwent transvenous pacemaker implantation between January 2002 and December 2012 at the North Carolina State University Veterinary Teaching Hospital. Methods Retrospective medical record review. Two-year follow-up was required for complications analysis. Results Major complications occurred in 14/79 dogs (18%) and included lead dislodgement, lead or generator infection, lead or generator migration, and pacing failure. Incidence of major complications was significantly higher AH (10/36, 28%) compared to BH (4/43, 9%; P = .041), and all infectious complications occurred AH. Median survival time for all dogs was 27 months and did not differ between AH and BH groups for either all-cause (P = .70) or cardiac (P = .40) mortality. AH dogs were younger than BH dogs (P = .010), but there were no other clinically relevant differences between BH and AH groups in terms of demographic, clinical, or procedural variables. Conclusions and Clinical Importance At our institution, AH transvenous pacemaker placement is associated with a higher rate of major complications (especially infections) compared to BH placement. This difference may be because of a variety of human factor differences AH versus BH.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ward, J. L. and DeFrancesco, T. C. and Tou, S. P. and Atkins, C. E. and Griffith, E. H. and Keene, B. W.}, year={2015}, pages={157–163} }
 @article{ferasin_defrancesco_2015, title={Management of acute heart failure in cats}, volume={17}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2015.09.007}, DOI={10.1016/j.jvc.2015.09.007}, abstractNote={Acute heart failure in cats represents a complex clinical situation in feline practice and this review has been designed to focus on the description of acute heart failure in cats, the diagnostic approach and clinical management of acutely decompensated feline cardiac patients. The authors acknowledge the lack of scientific evidence regarding many treatments used for heart disease in cats, and hence their approach may differ from recommendations given by other cardiologists. Every individual cardiac cat is also different, and it is important that all treatments are carefully tailored to the individual. Therefore this review provides generic advice based on the authors' personal experience but should not provide prescriptive guidelines on when to use particular drugs and doses and readers are encouraged to seek the latest information when managing these challenging cases.}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Ferasin, L. and DeFrancesco, T.}, year={2015}, month={Dec}, pages={S173–S189} }
 @article{defrancesco_2015, place={Tulsa, OK}, title={Mitral valve disease in a dog}, url={https://www.cliniciansbrief.com/article/mitral-valve-disease-dog}, journal={Plumb's Therapeutics Brief}, publisher={Brief Media}, author={DeFrancesco, T.C.}, year={2015}, month={May} }
 @inbook{defrancesco_2015, place={St. Louis, MO}, edition={3rd}, title={Myocarditis}, booktitle={Clinical Veterinary Advisor: Dogs and Cats}, publisher={Elsevier (Mosby)}, author={DeFrancesco, T.C.}, editor={Cote, E.Editor}, year={2015}, pages={685–686} }
 @inbook{defrancesco_2015, place={St. Louis, MO}, edition={3rd}, title={Pacemaker: Transthoracic Cardiac Pacing}, booktitle={Clinical Veterinary Advisor: Dogs and Cats}, publisher={Elsevier (Mosby)}, author={DeFrancesco, T.C.}, editor={Cote, E.Editor}, year={2015} }
 @article{fox_oyama_hezzell_rush_nguyenba_defrancesco_lehmkuhl_kellihan_bulmer_gordon_et al._2015, title={Relationship of Plasma N- terminal Pro- brain Natriuretic Peptide Concentrations to Heart Failure Classification and Cause of Respiratory Distress in Dogs Using a 2nd Generation ELISA Assay}, volume={29}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.12472}, abstractNote={Cardiac biomarkers provide objective data that augments clinical assessment of heart disease (HD).Determine the utility of plasma N-terminal pro-brain natriuretic peptide concentration [NT-proBNP] measured by a 2nd generation canine ELISA assay to discriminate cardiac from noncardiac respiratory distress and evaluate HD severity.Client-owned dogs (n = 291).Multicenter, cross-sectional, prospective investigation. Medical history, physical examination, echocardiography, and thoracic radiography classified 113 asymptomatic dogs (group 1, n = 39 without HD; group 2, n = 74 with HD), and 178 with respiratory distress (group 3, n = 104 respiratory disease, either with or without concurrent HD; group 4, n = 74 with congestive heart failure [CHF]). HD severity was graded using International Small Animal Cardiac Health Council (ISACHC) and ACVIM Consensus (ACVIM-HD) schemes without knowledge of [NT-proBNP] results. Receiver-operating characteristic curve analysis assessed the capacity of [NT-proBNP] to discriminate between dogs with cardiac and noncardiac respiratory distress. Multivariate general linear models containing key clinical variables tested associations between [NT-proBNP] and HD severity.Plasma [NT-proBNP] (median; IQR) was higher in CHF dogs (5,110; 2,769-8,466 pmol/L) compared to those with noncardiac respiratory distress (1,287; 672-2,704 pmol/L; P < .0001). A cut-off >2,447 pmol/L discriminated CHF from noncardiac respiratory distress (81.1% sensitivity; 73.1% specificity; area under curve, 0.84). A multivariate model comprising left atrial to aortic ratio, heart rate, left ventricular diameter, end-systole, and ACVIM-HD scheme most accurately associated average plasma [NT-proBNP] with HD severity.Plasma [NT-proBNP] was useful for discriminating CHF from noncardiac respiratory distress. Average plasma [NT-BNP] increased significantly as a function of HD severity using the ACVIM-HD classification scheme.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Fox, P. R. and Oyama, M. A. and Hezzell, M. J. and Rush, J. E. and Nguyenba, T. P. and DeFrancesco, T. C. and Lehmkuhl, L. B. and Kellihan, H. B. and Bulmer, B. and Gordon, S. G. and et al.}, year={2015}, pages={171–179} }
 @inbook{defrancesco_2015, title={Temporary Cardiac Pacing}, ISBN={9781455703067}, url={http://dx.doi.org/10.1016/b978-1-4557-0306-7.00203-8}, DOI={10.1016/b978-1-4557-0306-7.00203-8}, booktitle={Small Animal Critical Care Medicine}, publisher={Elsevier}, author={DeFrancesco, Teresa}, year={2015}, pages={1049–1054} }
 @article{reina-doreste_stern_keene_tou_atkins_defrancesco_ames_hodge_meurs_2014, title={Case-control study of the effects of pimobendan on survival time in cats with hypertrophic cardiomyopathy and congestive heart failure}, volume={245}, ISSN={["1943-569X"]}, DOI={10.2460/javma.245.5.534}, abstractNote={Abstract Objective —To assess survival time and adverse events related to the administration of pimobendan to cats with congestive heart failure (CHF) secondary to hypertrophic cardiomyopathy (HCM) or hypertrophic obstructive cardiomyopathy (HOCM). Design —Retrospective case-control study. Animals —27 cats receiving treatment with pimobendan and 27 cats receiving treatment without pimobendan. Procedures —Medical records between 2003 and 2013 were reviewed. All cats with HCM or HOCM treated with a regimen that included pimobendan (case cats) were identified. Control cats (cats with CHF treated during the same period with a regimen that did not include pimobendan) were selected by matching to case cats on the basis of age, sex, body weight, type of cardiomyopathy, and manifestation of CHF. Data collected included signalment, physical examination findings, echocardiographic data, serum biochemical values, and survival time from initial diagnosis of CHF. Kaplan-Meier survival curves were constructed and compared by means of a log rank test. Results —Cats receiving pimobendan had a significant benefit in survival time. Median survival time of case cats receiving pimobendan was 626 days, whereas median survival time for control cats not receiving pimobendan was 103 days. No significant differences were detected for any other variable. Conclusions and Clinical Relevance —The addition of pimobendan to traditional treatment for CHF may provide a substantial clinical benefit in survival time for HCM-affected cats with CHF and possibly HOCM-affected cats with CHF.}, number={5}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Reina-Doreste, Yamir and Stern, Joshua A. and Keene, Bruce W. and Tou, Sandra P. and Atkins, Clarke E. and DeFrancesco, Teresa C. and Ames, Marisa K. and Hodge, Timothy E. and Meurs, Kathryn M.}, year={2014}, month={Sep}, pages={534–539} }
 @inbook{defrancesco_2014, place={Ames, IA}, edition={1st}, title={Focused or COAST3 : echo (heart)}, booktitle={Focused Ultrasound Techniques for the Small Animal Practitioner}, publisher={Wiley & Sons, Inc}, author={DeFrancesco, T.C.}, editor={Liscandro, G.Editor}, year={2014}, pages={189–205} }
 @article{edwards_coleman_brainard_defrancesco_hansen_keene_koenig_2014, title={Outcome of positive-pressure ventilation in dogs and cats with congestive heart failure: 16 cases (1992-2012)}, volume={24}, ISSN={["1476-4431"]}, DOI={10.1111/vec.12230}, abstractNote={Objective To describe the indications, duration of ventilation, underlying cardiac diseases, and outcome of dogs and cats undergoing positive-pressure ventilation (PPV) for treatment of congestive heart failure (CHF). Design Two-site retrospective study (1992–2012). Setting Two university small animal teaching hospitals. Animals Six cats and 10 dogs undergoing PPV for CHF. Interventions None. Measurements and Main Results Medical records were searched to identify patients requiring PPV for treatment of pulmonary edema secondary to CHF. Sixteen animals fulfilled these criteria. Patient signalment, duration of PPV, underlying cardiac disease, arterial or venous blood gas values, pharmacologic therapy before, during, and after PPV, anesthetic drugs, complications, and outcome were recorded. Overall survival to discharge was 62.5% (10/16). Mean (±SD) duration of PPV was 30.8 ± 21.3 hours and average time from presentation for CHF to initiation of PPV was 5.9 ± 6.4 hours. Azotemia at the time of initiation of ventilation, development of anuria or oliguria, and use of pentobarbital for anesthesia were negatively associated with survival (P = 0.011, P = 0.036, and P = 0.036, respectively). Survival-to-discharge rate was 77% (10/13) for patients treated after 2005 and those not receiving pentobarbital. There was no significant effect attributed to age, sex, weight, species, nature of heart disease, furosemide dose, length of ventilation, use of vasopressors, first-time CHF events, or plasma lactate concentration on survival to discharge. Conclusions Dogs and cats requiring PPV for CHF have a good overall prognosis for hospital discharge and require PPV for a relatively short duration. Azotemia, oliguria or anuria, and the use of pentobarbital are negatively associated with outcome.}, number={5}, journal={JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE}, author={Edwards, Thomas H. and Coleman, Amanda Erickson and Brainard, Benjamin M. and DeFrancesco, Teresa C. and Hansen, Bernard D. and Keene, Bruce W. and Koenig, Amie}, year={2014}, pages={586–593} }
 @article{meurs_stern_sisson_kittleson_cunningham_ames_atkins_defrancesco_hodge_keene_et al._2013, title={Association of Dilated Cardiomyopathy with the Striatin Mutation Genotype in Boxer Dogs}, volume={27}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.12163}, abstractNote={Background Myocardial disease in the Boxer dog is characterized by 1 of 2 clinical presentations, dilated cardiomyopathy (DCM) characterized by ventricular systolic dysfunction, dilatation and tachyarrhythmias, and arrhythmogenic right ventricular cardiomyopathy (ARVC) characterized by ventricular tachyarrhythmias, syncope, and sudden death. Boxer ARVC has been associated with a deletion in the striatin gene in some families. Hypothesis/Objectives We hypothesized that both presentations represent a single disease, and the development of DCM in the Boxer is associated with the striatin deletion. Animals Thirty-three adult Boxer dogs with DCM, 29 adult Boxer dogs with the striatin deletion and ARVC, and 16 Boxers without cardiac disease. Methods DNA samples were evaluated for the striatin deletion. Association of the deletion with the DCM phenotype was tested by a Fisher's exact test. T-tests were used to evaluate potential differences between the positive heterozygous and positive homozygous groups with DCM with regard to age, LVIDD, LVIDS, and FS%. Results Thirty of 33 dogs with DCM were positive for the striatin deletion. The striatin mutation and the homozygous genotype were strongly associated with the DCM phenotype (P < .001 and P = .005). There was no statistical difference between the heterozygous and homozygous groups with regard to age and echocardiographic measurements. Conclusions and Clinical Importance This study demonstrates an association between DCM in the Boxer dog and the striatin mutation, particularly with the homozygous genotype. The observation that 3/33 dogs developed DCM and lacked the striatin mutation suggests that there is at least 1 other cause of DCM in the Boxer dog.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Meurs, K. M. and Stern, J. A. and Sisson, D. D. and Kittleson, M. D. and Cunningham, S. M. and Ames, M. K. and Atkins, C. E. and DeFrancesco, T. and Hodge, T. E. and Keene, B. W. and et al.}, year={2013}, month={Nov}, pages={1437–1440} }
 @article{kane_defrancesco_boyle_malarkey_ritchey_atkins_cullen_kornegay_keene_2013, title={Cardiac structure and function in female carrier's of a canine model of Duchenne muscular dystrophy}, volume={94}, ISSN={["1532-2661"]}, DOI={10.1016/j.rvsc.2012.09.027}, abstractNote={This investigation tested the hypothesis that carriers of golden retriever muscular dystrophy (GRMD), a genetically homologous condition of Duchenne muscular dystrophy (DMD), have quantifiable abnormalities in myocardial function, structure, or cardiac rhythm. Eleven GRMD carriers and four matched controls had cardiac evaluations and postmortem examinations. 24-h ECG Holter monitoring disclosed ventricular ectopy in 10 of 11 carriers and 2 of 4 controls. Conventional echocardiography failed to demonstrate significant differences between carriers and controls in systolic function. All carriers had multifocal, minimal to marked myofiber necrosis, fibrosis, mineralization, inflammation, and/or fatty change in their hearts. Immunohistochemistry revealed a mosaic dystrophin deficiency in scattered cardiac myofibers in all carriers. No controls had cardiac histologic lesions; all had uniform dystrophin staining. Despite cardiac mosaic dystrophin expression and degenerative cardiac lesions, GRMD carriers at up to 3 years of age could not be distinguished statistically from normal controls by echocardiography or 24-h Holter monitoring.}, number={3}, journal={RESEARCH IN VETERINARY SCIENCE}, author={Kane, A. M. and DeFrancesco, T. C. and Boyle, M. C. and Malarkey, D. E. and Ritchey, J. W. and Atkins, C. E. and Cullen, J. M. and Kornegay, J. N. and Keene, B. W.}, year={2013}, month={Jun}, pages={610–617} }
 @article{defrancesco_2013, title={Management of Cardiac Emergencies in Small Animals}, volume={43}, ISSN={["1878-1306"]}, DOI={10.1016/j.cvsm.2013.03.012}, abstractNote={Cardiac emergencies are life-threatening conditions that must be diagnosed quickly to avoid delays in therapy. A timely and accurate diagnosis leads to early relief of symptoms and improved survival. This article provides both a comprehensive review and updated management recommendations for common cardiac emergencies in dogs and cats. Specifically, the article confers updates for the efficient clinical recognition of decompensated cardiac patients, including focused echocardiography, cardiac biomarkers, and electrocardiogram interpretation. This article also reviews the latest recommendations for the treatment of heart failure (including the use of pimobendan) and the management of arrhythmias, pericardial effusion, and aortic thromboembolism.}, number={4}, journal={VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE}, author={DeFrancesco, Teresa C.}, year={2013}, month={Jul}, pages={817-+} }
 @article{leblanc_defrancesco_adams_atkins_tou_fudge_keene_2012, title={Cutting balloon catheterization for interventional treatment of cor triatriatum dexter: 2 Cases}, volume={14}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2012.04.006}, DOI={10.1016/j.jvc.2012.04.006}, abstractNote={Cutting balloon dilatation was performed successfully in two dogs with cor triatriatum dexter and clinical signs of ascites. The cutting balloon catheter uses incisional microtomes embedded in a balloon catheter. During balloon expansion, these microtomes incise the adjacent tissue, decreasing circumferential wall stress. This theoretically reduces both the likelihood of fracturing the adjacent tissues in an uncontrolled manner and the potential neoproliferative response to standard balloon dilatation and the subsequent incidence of re-stenosis. In both cases described, clinical signs resolved completely following cutting balloon dilatation of the anomalous membrane. Based on the outcome of these 2 cases, cutting balloon dilatation appears to be a viable treatment option for dogs affected with cor triatriatum dexter.}, number={4}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={LeBlanc, Nicole and DeFrancesco, Teresa C. and Adams, Allison K. and Atkins, Clark E. and Tou, Sandra P. and Fudge, James Curt and Keene, Bruce W.}, year={2012}, month={Dec}, pages={525–530} }
 @article{defrancesco_2012, title={Electrocardiographic review – 5 cases}, url={www.cliniciansbrief.com}, journal={Clinician's Brief}, author={DeFrancesco, T.C.}, year={2012}, month={May} }
 @article{coleman_defrancesco_chanoit_2012, title={Pacemaker malfunction due to mechanical failure of the lead–header interface}, volume={14}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2012.07.003}, DOI={10.1016/j.jvc.2012.07.003}, abstractNote={An 8 year old female spayed Boxer dog, diagnosed with concurrent vasovagal syncope and arrhythmogenic right ventricular cardiomyopathy, presented for routine evaluation approximately three months following epicardial pacemaker implantation. Routine device interrogation revealed intermittent loss of ventricular capture and intermittent failure to appropriately sense. Following evaluation of chronic impedance data, failure of the pacemaker lead-header interface or lead conductor fracture was suspected. Radiographic and pacemaker interrogator findings suggested incomplete lead insertion into the device header with intermittent loss of ventricular capture and variable pacemaker sensing. We hypothesize that either the presence of a loose or cross-threaded set screw or operator error at the time of device implantation may have caused this complication. This report details the diagnosis of mechanical failure of the lead-header interface, a complication not previously reported in a veterinary patient.}, number={4}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Coleman, Amanda E. and DeFrancesco, Teresa C. and Chanoit, Guillaume}, year={2012}, month={Dec}, pages={519–523} }
 @article{defrancesco_2011, title={Cardiac biomarkers}, journal={NAVC Clinicians’ Brief}, author={DeFrancesco, T.C.}, year={2011}, month={Feb} }
 @article{olby_sharp_nghiem_keene_defrancesco_sidley_kornegay_schatzberg_2011, title={Clinical progression of X-linked muscular dystrophy in two German Shorthaired Pointers}, volume={238}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.238.2.207}, DOI={10.2460/javma.238.2.207}, abstractNote={Abstract Case Description —2 full-sibling male German Shorthaired Pointer (GSHP) puppies (dogs 1 and 2) with X-linked muscular dystrophy and deletion of the dystrophin gene (gene symbol, DMD ) each had poor growth, skeletal muscle atrophy, pelvic limb weakness, episodic collapse, and episodes of coughing. Clinical Findings —Initial examination revealed stunted growth, brachygnathism, trismus, and diffuse neuromuscular signs in each puppy; clinical signs were more severe in dog 2 than in dog 1. Immunohistochemical analysis revealed a lack of dystrophin protein in both dogs. During the next 3 years, each dog developed hyperinflation of the lungs, hypertrophy of the cervical musculature, and hypertrophy of the lateral head of the triceps brachii muscle. Treatment and Outcome —Monitoring and supportive care were provided at follow-up visits during an approximately 7-year period. No other specific treatment was provided. Neuromuscular signs in both dogs remained stable after 3 years of age, with dog 2 consistently more severely affected than dog 1. The dogs had multiple episodes of aspiration pneumonia; dogs 1 and 2 were euthanatized at 84 and 93 months of age, respectively. Clinical Relevance —The clinical course of disease in these dogs was monitored for a longer period than has been monitored in previous reports of dystrophin-deficient dogs. The clinical progression of muscular dystrophy in the 2 GSHPs was compared with that for other breeds and species with dystrophin-deficient conditions, and the potential basis for the phenotypic variation observed between these littermates, along with potential therapeutic ramifications for dogs and humans, was evaluated.}, number={2}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Olby, Natasha J. and Sharp, Nick J. H. and Nghiem, Peter E and Keene, Bruce W. and DeFrancesco, Teresa C. and Sidley, Jennifer A. and Kornegay, Joe N. and Schatzberg, Scott J.}, year={2011}, month={Jan}, pages={207–212} }
 @article{meurs_heaney_atkins_defrancesco_fox_keene_kellihan_miller_oyama_oaks_et al._2011, title={Comparison of Polymerase Chain Reaction with Bacterial 16s Primers to Blood Culture to Identify Bacteremia in Dogs with Suspected Bacterial Endocarditis}, volume={25}, ISSN={0891-6640}, url={http://dx.doi.org/10.1111/j.1939-1676.2011.0742.x}, DOI={10.1111/j.1939-1676.2011.0742.x}, abstractNote={Identification of the bacterial organism in dogs with endocarditis is challenging. Human studies have reported the utility of the polymerase chain reaction (PCR) to amplify and identify bacterial nucleic acid from infected valvular tissue and blood.We hypothesized that PCR using primers designed to amplify the bacterial 16s gene would identify circulating bacteria in dogs with suspected bacterial endocarditis more consistently than standard blood culture techniques.Eighteen dogs with suspected bacterial endocarditis based upon clinical and echocardiographic findings. Fifteen clinically normal dogs served as negative controls.Prospective study of dogs evaluated for suspect endocarditis at 6 veterinary hospitals. A blood sample was drawn from all dogs and evaluated with both a single-sample PCR and standard 3-sample blood culture techniques.Blood culture identified noncontaminant bacteria in 6/18 study animals (33%) and 1 control dog; PCR identified noncontaminant bacteria in 7/18 study animals (39%). There were no study animals in which the 2 tests identified different bacteria (κ = 1.0). However, bacteria were identified by both techniques in only 2/18 study animals. When results from both PCR and blood culture were considered together, a noncontaminant bacterial organism was identified in 11/18 study animals (61%).The results of this study suggest that although single sample PCR with 16s primers was not more sensitive than blood culture for detection of bacteremia in dogs with suspect endocarditis, performing both techniques simultaneously did increase the likelihood of identification of bacteria in blood.}, number={4}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Meurs, K.M. and Heaney, A.M. and Atkins, C.E. and DeFrancesco, T.C. and Fox, P.R. and Keene, B.W. and Kellihan, H.B. and Miller, M.W. and Oyama, M.A. and Oaks, J.L. and et al.}, year={2011}, month={Jun}, pages={959–962} }
 @article{hofer_defrancesco_williams_2011, title={Detection of tumour necrosis factor-alpha in dogs with lymphoma}, volume={9}, ISSN={["1476-5810"]}, DOI={10.1111/j.1476-5829.2011.00267.x}, abstractNote={Tumour necrosis factor-alpha (TNF-α) production by malignant lymphoblasts has been identified in vitro and in vivo in mice and humans, respectively. The goals of this study were (1) to evaluate a novel single-sample TNF-α assay and (2) to determine whether TNF-α is increased in dogs with lymphoma prior to and following treatment. Canine TNF-α was analysed concurrently using the novel Siemens Immulite® single-sample automated ELISA and the previously validated Quantikine® standard ELISA. Serum from dogs with lymphoma and from breed-, age- and gender-matched control dogs was evaluated at two time points. Three of 25 (12%) dogs with lymphoma had detectable TNF-α at diagnosis, whereas none had detectable TNF-α following complete or partial remission. TNF-α was not detectable in control dogs. Despite 91% homology between human and canine TNF-α, the Immulite® automated ELISA failed to detect canine TNF-α. Serum TNF-α appears to have limited value as a tumour marker in dogs with lymphoma.}, number={4}, journal={VETERINARY AND COMPARATIVE ONCOLOGY}, author={Hofer, J. and DeFrancesco, T. C. and Williams, L. E.}, year={2011}, month={Dec}, pages={290–295} }
 @article{tou_defrancesco_keene_2011, title={ECG of the Month}, volume={239}, ISSN={["1943-569X"]}, DOI={10.2460/javma.239.1.55}, number={1}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Tou, Sandra P. and DeFrancesco, Teresa C. and Keene, Bruce W.}, year={2011}, month={Jul}, pages={55–57} }
 @article{lantis_atkins_defrancesco_keene_werre_2011, title={Effects of furosemide and the combination of furosemide and the labeled dosage of pimobendan on the circulating renin-angiotensin-aldosterone system in clinically normal dogs}, volume={72}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.72.12.1646}, DOI={10.2460/ajvr.72.12.1646}, abstractNote={Abstract Objective —To evaluate the effect of administration of the labeled dosage of pimobendan to dogs with furosemide-induced activation of the renin-angiotensin-aldosterone system (RAAS). Animals —12 healthy hound-type dogs. Procedures —Dogs were allocated into 2 groups (6 dogs/group). One group received furosemide (2 mg/kg, PO, q 12 h) for 10 days (days 1 to 10). The second group received a combination of furosemide (2 mg/kg, PO, q 12 h) and pimobendan (0.25 mg/kg, PO, q 12 h) for 10 days (days 1 to 10). To determine the effect of the medications on the RAAS, 2 urine samples/d were obtained for determination of the urinary aldosterone-to-creatinine ratio (A:C) on days 0 (baseline), 5, and 10. Results —Mean ± SD urinary A:C increased significantly after administration of furosemide (baseline, 0.37 ± 0.14 μg/g; day 5, 0.89 ± 0.23 μg/g) or the combination of furosemide and pimobendan (baseline, 0.36 ± 0.22 μg/g; day 5, 0.88 ± 0.55 μg/g). Mean urinary A:C on day 10 was 0.95 ± 0.63 μg/g for furosemide alone and 0.85 ± 0.21 μg/g for the combination of furosemide and pimobendan. Conclusions and Clinical Relevance —Furosemide-induced RAAS activation appeared to plateau by day 5. Administration of pimobendan at a standard dosage did not enhance or suppress furosemide-induced RAAS activation. These results in clinically normal dogs suggested that furosemide, administered with or without pimobendan, should be accompanied by RAAS-suppressive treatment.}, number={12}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Lantis, Andrea C. and Atkins, Clarke E. and DeFrancesco, Teresa C. and Keene, Bruce W. and Werre, Stephen R.}, year={2011}, month={Dec}, pages={1646–1651} }
 @article{fox_rush_reynolds_defrancesco_keene_atkins_gordon_schober_bonagura_stepien_et al._2011, title={Multicenter Evaluation of Plasma N-Terminal Probrain Natriuretic Peptide (NT-pro BNP) as a Biochemical Screening Test for Asymptomatic (occult) Cardiomyopathy in Cats}, volume={25}, number={5}, journal={Journal of Veterinary Internal Medicine}, author={Fox, P. R. and Rush, J. E. and Reynolds, C. A. and DeFrancesco, T. C. and Keene, B. W. and Atkins, C. E. and Gordon, S. G. and Schober, K. E. and Bonagura, J. D. and Stepien, R. L. and et al.}, year={2011}, pages={1010–1016} }
 @inbook{defrancesco_2011, place={St. Louis, MO}, edition={2nd}, title={Myocarditis}, booktitle={Clinical Veterinary Advisor: Dogs and Cats}, publisher={Mosby}, author={DeFrancesco, T.C.}, editor={Cote, E.Editor}, year={2011}, pages={743–744} }
 @inbook{defrancesco_2011, place={St. Louis, MO}, edition={2nd}, title={Pacemaker: Transthoracic Cardiac Pacing}, booktitle={Clinical Veterinary Advisor: Dogs and Cats}, publisher={Mosby}, author={DeFrancesco, T.C.}, editor={Cote, E.Editor}, year={2011}, pages={1320–1321} }
 @inbook{defrancesco_2010, place={Ames, Iowa}, edition={1st}, title={Aortic Thromboembolism}, booktitle={Blackwell's five-minute veterinary consult clinical companion: Small animal emergency and critical care}, publisher={Blackwell Publishing}, author={DeFrancesco, T.C.}, editor={Mazzaferro, E.Editor}, year={2010}, pages={55–65} }
 @article{sayer_atkins_fujii_adams_defrancesco_keene_2009, title={Acute Effect of Pimobendan and Furosemide on the Circulating Renin-Angiotensin-Aldosterone System in Healthy Dogs}, volume={23}, ISSN={["1939-1676"]}, DOI={10.1111/j.1939-1676.2009.0367.x}, abstractNote={Background: The renin-angiotensin-aldosterone system (RAAS) is activated in states of decreased cardiac output and by certain cardiovascular therapeutic agents, such as loop diuretics and vasodilators. Hypothesis: Short-term treatment with the inodilator, pimobendan, will not activate the circulating RAAS because its vasodilatory action will be offset by its positive inotropic property, thereby ameliorating RAAS stimulation at the juxtaglomerular apparatus. Furthermore, pimobendan will suppress RAAS activation produced by furosemide. Animals: Nine healthy laboratory dogs were used in this study. Methods: Experimental, cross-over study. Dogs were administered pimobendan (0.5 mg/kg q12h) for 4 days followed by furosemide (2 mg/kg q12h) and then, after a wash-out period, a combination of the drugs. Aldosterone : creatinine (A : Cr) was measured at the end of each treatment cycle. Results: There was no significant increase in the average urinary A : Cr with the administration of pimobendan (control urinary A : Cr = 0.46, standard deviation (SD) 0.33; pimobendan A : Cr = 0.48, SD 0.28). There was a significant increase in the average urinary A : Cr after administration of furosemide (urinary A : Cr = 1.3, SD 0.70) and with the combination of furosemide and pimobendan (urinary A : Cr = 2.9, SD 1.6). Conclusions and Clinical Relevance: Short-term administration of high-dose pimobendan, does not activate the RAAS in healthy dogs. Pimobendan did not prevent RAAS activation associated with furosemide therapy. These results in healthy dogs suggest that furosemide therapy, with or without pimobendan, should be accompanied by RAAS suppressive therapy.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Sayer, M. B. and Atkins, C. E. and Fujii, Y. and Adams, A. K. and DeFrancesco, T. C. and Keene, B. W.}, year={2009}, pages={1003–1006} }
 @article{scott_hansen_defrancesco_2009, title={Coagulation effects of low molecular weight heparin compared with heparin in dogs considered to be at risk for clinically significant venous thrombosis}, volume={19}, ISSN={["1476-4431"]}, DOI={10.1111/j.1476-4431.2008.00339.x}, abstractNote={Objective – Compare the effects of 3 anticoagulation protocols on anti-factor Xa activity (AXa). Design – Prospective, randomized, double-blind study. Setting – University veterinary teaching hospital. Animals – Eighteen dogs considered to be at risk for venous thrombosis. Interventions – Each dog was randomly assigned to 1 of the following 3 groups (n=6/group) and was treated for 24 hours: low-dose heparin (LDH), high-dose heparin (HDH), and dalteparin (DP). Dogs in the LDH group received a constant rate infusion (CRI) of unfractionated heparin (UFH) at 300 U/kg/d, the HDH group received a bolus of 100 U/kg of UFH IV, then a CRI of 900 U/kg/day, and the DP group received 100 U/kg DP SC at 0, 12, and 24 hours. Measurements and Main Results – A total of 54 samples for activated partial thromboplastin time (aPTT) and AXa assays were collected at 0, 4, and 28 hours. Six samples had an AXa >0.1 U/mL, 5 of those were from the HDH group at hour 4. Two samples from the HDH group at hour 4 had a prolonged aPTT (93 and 200 seconds) and the highest AXa (0.6 and 1.0 U/mL, respectively). Four additional dogs in the HDH group did not complete the study due to hemorrhage; none of the dogs completing the study showed signs of hemorrhage. Conclusions: Neither DP nor LDH increased AXa to values considered therapeutic in humans (0.5–1 and 0.35–0.75 U/mL, respectively), and both protocols appear to be inadequate to increase AXa in dogs with clinical illness. HDH increased AXa to this range in 2 of 6 dogs, but had unpredictable effects on aPTT and resulted in hemorrhage in some dogs.}, number={1}, journal={JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE}, author={Scott, Kielyn C. and Hansen, Bernie D. and DeFrancesco, Teresa C.}, year={2009}, month={Feb}, pages={74–80} }
 @article{holowaychuk_hansen_defrancesco_marks_2009, series={Contributed cases and assisted in data collection and interpretation of findings}, title={Ionized Hypocalcemia in Critically Ill Dogs}, volume={23}, ISSN={["1939-1676"]}, DOI={10.1111/j.1939-1676.2009.0280.x}, abstractNote={Background: Ionized hypocalcemia (iHCa) is a common electrolyte disturbance in critically ill people, especially those with sepsis. The cause of the iHCa is not entirely understood and is likely multifactorial. Critically ill people with iHCa have longer hospital stays and higher mortality rates compared to people with normocalcemia. There are no published clinical studies evaluating the incidence and impact of iHCa in critically ill dogs. Hypothesis: iHCa occurs in critically ill dogs, is more prevalent in dogs with systemic inflammatory response syndrome (SIRS) or sepsis, and is associated with longer hospital stays and higher mortality. Animals: One hundred and forty-one client-owned dogs admitted to a companion animal intensive care unit (ICU) in a veterinary teaching hospital. Methods: Prospective observational study of sequentially enrolled dogs. Blood was collected and analyzed within an hour of admission from all dogs presented to the ICU that met study inclusion criteria. Results: The incidence of iHCa (iCa < 1.11 mmol/L) was 16%. The presence of iHCa was associated with longer ICU (P= .038) and hospital (P= .012) stays but not with decreased survival (P= .60). Dogs with sepsis as defined by ≥3 SIRS criteria and a positive culture were more likely to have iHCa (P= .050). Conclusions and Clinical Relevance: In dogs not previously treated with fluids or blood products intravenously, the finding of iHCa upon admission to the ICU predicted a longer duration of ICU and hospital stay. Septic dogs with positive cultures were more likely to have iHCa.}, number={3}, journal={Journal of Veterinary Internal Medicine}, author={Holowaychuk, M.K. and Hansen, B.D. and DeFrancesco, T.C. and Marks, S.L.}, year={2009}, pages={509–513}, collection={Contributed cases and assisted in data collection and interpretation of findings} }
 @article{cherry_diniz_maggi_hummel_hardie_behrend_rozanski_defrancesco_cadenas_breitschwerdt_et al._2009, title={Isolation or Molecular Detection of Bartonella  henselae and Bartonella vinsonii subsp. berkhoffii from Dogs with Idiopathic Cavitary Effusions}, volume={23}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2008.0246.x}, DOI={10.1111/j.1939-1676.2008.0246.x}, abstractNote={There are a substantial number of pathophysiologic causes for effusions in dogs.1 Previously, using an insect cell culture medium (Bartonella alpha-proteobacteria growth medium—BAPGM), our laboratory isolated Mycobacterium kansasii from a dog with therapeutically intractable pleural effusion.2 Recently, we developed a combined assay incorporating BAPGM pre-enrichment culture, so as to increase Bartonella bacterial numbers, followed by PCR amplification of organism-specific DNA sequences.3 The combined assay has substantially increased the sensitivity of molecular detection of Bartonella infection.3-5 This pre-enrichment culture medium has also isolated numerous other bacterial species of undetermined pathogenicity from human patients in our laboratory.4 In the past decade, several Bartonella species, including B. henselae, B. vinsonii subsp. berkhoffii, B. clarridgeiae, B. elizabethae, B. washoensis, and B. quintana, have been found to infect dogs.6 Currently, case-based evidence suggests that occult infection with these bacteria may contribute to a wide range of disease manifestations in dogs, humans, and potentially other animals.6B. henselae and B. vinsonii subsp. berkhoffii have been reported in association with granulomatous lymphadenitis, hepatic disease,7 and endocarditis in dogs.8 Between July 2004 and December 2007, blood and effusion samples from 20 dogs of varying breeds and ages, were submitted for BAPGM culture by veterinarians at Auburn University, North Carolina State University and Tufts University's Veterinary Teaching Hospitals, of which 5 were found to be infected with a Bartonella spp. Using a previously described approach, DNA was extracted directly from EDTA-anticoagulated blood or thoracic and abdominal effusion samples, from BAPGM pre-enrichment liquid blood and effusion cultures, and from pooled bacterial subculture isolates.3-5, 9 Extracted DNA was screened by PCR with Bartonella genus primers, targeting the 16S-23S intergenic spacer region (ITS), which has a detection limit of 2–3 genomic copies per reaction.9 ITS amplicons were sequenced to confirm the Bartonella species and strain.5, 9 This study provides the first molecular and microbiologic evidence to support infection with B. henselae and B. vinsonii subsp. berkhoffii in dogs with idiopathic cavitary effusions or constrictive pericarditis. An 8-year-old-female spayed Labrador mix was referred to Tufts for evaluation of recurrent pleural effusion. Thoracic fluid cytology was consistent with a transudate with a specific gravity of 1.019, total protein of 2.6 g/dL and 255 cells/μL. No bacterial growth or neoplastic cells were documented. A CBC, serum biochemical profile, coagulation profile, and urinalysis were unremarkable except for mild hyperbilirubinemia and hematuria. A torsed lung lobe was surgically removed. Postoperatively despite administration of azathioprine, prednisone, and spironolactone, thoracocentesis was required for 10 consecutive months. When immunosuppressive therapy was tapered, pleural effusion rapidly recurred. Antibiotics, including doxycycline, azithromycin, or enrofloxacin, did not decrease the rate of fluid accumulation, which had become a modified transudate. The dog underwent an exploratory thoracotomy and died postoperatively. B. henselae strain Houston-I was isolated and sequenced from the thoracic fluid and B. henselae strain Houston-I and B. vinsonii subsp. berkhoffii genotype II were isolated from a BAPGM blood culture. Bartonella serology was not requested. A 3-year-old-female spayed Leonberger was referred to Auburn for evaluation of lethargy, anorexia, weight loss (11 kg), and cervical pain. The only central nervous system abnormality was mild pain on cervical flexion. A possible abdominal mass was noted. There were no hematologic abnormalities. Serum biochemical abnormalities included increased alkaline phosphatase (130 U/L; reference range, 4–95) and alanine amino transferase activities (385 U/L; reference range, 26–200), increased serum creatinine concentration (1.5 mg/dL; reference range, 0.68–1.45), and hypoglobulinemia (2.1 g/dL; reference range, 2.6–5.0). Urinalysis was within normal limits and urine culture failed to grow bacteria. Thoracic radiographs indicated moderate pleural effusion. Ultrasonographic abnormalities included a thickened, stiff stomach wall, abdominal effusion, and irregular kidney margins. An echocardiogram identified no cardiac abnormalities. Pleural fluid analysis was consistent with a modified transudate with a specific gravity of 1.026, total protein of 3.9 g/dL, and 670 total cells/μL. Serum antibodies were not detected to Neospora caninum, Ehrlichia canis, Rickettsia rickettsii, Toxoplasma gondii, canine distemper virus, and Pythium insidiosum. Abdominal exploratory surgery identified a large volume of grossly pink peritoneal fluid. No histologic lesions were found in stomach, liver, omentum, duodenum, mesenteric, and pyloric lymph nodes, kidney, pancreas, and jejunum. B. henselae and B. vinsonii subsp. berkhoffii antibodies were not detected, but B. vinsonii subsp. berkhoffii genotype II was sequenced from the BAPGM pre-enrichment blood culture and the subculture isolate. Azithromycin 250 mg daily and doxycycline 100 mg PO q12 h were administered for 14 days. Nine days after beginning treatment, the dog was eating and drinking normally but pleural effusion failed to resolve. Antibiotics were continued for 2 more weeks. During the next year, the cervical pain continued. The dog was euthanized because of severe peripheral edema with spontaneous fluid extravasation 2 years later. An insulin-dependent diabetic 12-year-old-male castrated Vizsla was evaluated for coughing, gagging, and lethargy. Idiopathic chylothorax initially was diagnosed by the referring veterinarian based on cytological evaluation, which was confirmed by pleural fluid analysis at NCSU-VTH as chylous with a specific gravity of 1.023, total protein of 3.3 g/dL, and 1,940 total cells/μL. A CBC was normal. Biochemical abnormalities included hyperglycemia (serum glucose concentration 258 g/dL; reference range, 73–116), and increased SAP (270 U/L; reference range, 15–156), and ALT activities (100 U/L; reference range, 16–73). Abdominal and thoracic ultrasonography, an echocardiogram, and a helical computed tomography (CT) scan of the thorax and anterior abdomen with lymphangiography were unremarkable, except for pleural effusion. Thoracic duct ligation and partial pericardectomy were performed. The dog recovered uneventfully but continued to accumulate lesser quantities of thoracic fluid, consistently characterized as a modified transudate. Two months postsurgery, the dog developed lethargy, inability to rise, and edema involving the neck, sternum, and right front leg. Urine and pleural fluid cultures failed to grow bacteria. Pleural fluid again was classified as a modified transudate, containing atypical mesothelial cells. A seroma, accompanied by spontaneous leakage of fluid, formed in the ventral neck region. The owner elected euthanasia before availability of the BAPGM culture results. B. henselae DNA was amplified and sequenced directly from the pleural fluid and from the BAPGM enrichment culture. After subculture, an Arthrobacter spp. was isolated, as defined by sequencing the 16S rRNA gene. Serology was not requested. At necropsy, no cause was identified for the severe emaciation, pleural effusion, and subcutaneous edema. A 5-year-old-female spayed Pomeranian was referred to the NCSU-VTH for diagnostic evaluation of panhypoproteinemia. The owners reported infrequent bouts of diarrhea and poorly localized abdominal pain. Serum total protein concentration (2.6 g/dL; reference range, 5.1–7.4), albumin (1.3 g/dL; reference range, 2.8–4.0), and globulin concentrations (1.3 g/dL; reference range, 2.0–4.1) were low. Hematologic abnormalities included lymphopenia (283 lymphocytes/μL; reference range, 480–3,762) and neutrophilia (13,745 neutrophils/μL; reference range, 2,529–12,876). With the exception of bilirubinuria, urinalysis was unremarkable, urine protein/creatinine ratio was normal, and urine culture was negative. Radiographs confirmed thoracic and abdominal effusion. Ultrasonography identified bicavitary anechoic effusion, consistent with a transudate, a collapsed right lung lobe, and portal vein thrombosis. The liver was hypoechoic, abdominal lymph nodes slightly enlarged, and the intestinal lumen was distended with fluid. Echocardiography did not identify pericardial effusion or support a diagnosis of right-sided heart failure. By abdominocentesis, a clear transudative fluid with a specific gravity of 1.005 was obtained. Aerobic and anaerobic culture of the abdominal fluid failed to grow bacteria. Endoscopic gastric biopsies were unremarkable, whereas the duodenum was moderately infiltrated with lymphocytes and plasma cells, accompanied by multifocal lymphangiectasia. A heartworm antigen test was negative. Antibodies to B. henselae and B. vinsonii subsp. berkhoffii, R. rickettsii, E. canis, and Babesia canis were not detected by IFA testing. B. vinsonii subsp. berkhoffii genotype II was isolated from pleural fluid and B. henselae from the blood. Protein-losing enteropathy, accompanied by a portal vein thrombosis, was diagnosed. Treatment consisted of a high protein, low residue diet and metronidazole 10.5 mg/kg PO q8h for 4 weeks. Within 2 weeks, the portal vein thrombosis was no longer visible by ultrasonography. Serum protein concentrations increased progressively and were within reference ranges (total protein, 5.8 g/dL; albumin, 3.6 g/dL; globulin, 2.2 g/dL) by 3 months after initial evaluation. Effusion resolved and did not recur during a 3-year follow-up period. A 6-year-old-female spayed Labrador Retriever was referred for diagnostic evaluation of abdominal effusion. Historically, the dog had remained alert and active. Six liters of serosanguineous, modified transudate with a specific gravity of 1.026, total protein of 4 g/dL and 770 total cells/μL was aspirated from the abdomen. There were no hematologic or coagulation abnormalities, except hypocholesterolemia (134 mg/dL; reference range, 138–317). Central venous pressure was slightly increased (8–9 mmHg). Abdominal and thoracic CT scans identified distention of the hepatic veins and the cranial and caudal vena cava, indicative of right-sided heart failure. By echocardiography, minimal pericardial effusion and hypokinetic left ventricle free wall were documented. Catheterization of the right side of the heart detected a cranial vena cava pressure of 16.1 mmHg, right atrial pressure of 17.4 mmHg, right ventricle pressure at the end of the diastole of 15.6 mmHg and wedge pressure of 17.4 mmHg. The tracing of the right atrial pressure, with prominent x and y descents, was consistent with constrictive pericarditis. Subtotal pericardectomy was performed. On histopathology, the pericardium was variably thickened (up to 0.5 cm) with densely packed collagen fibers, containing few blood vessels and rare hemosiderin-laden macrophages. No etiologic agents were seen, no fungal species were isolated and aerobic and anaerobic blood cultures were negative. On day 8 postpericardectomy, the dog became febrile (T 104°F), vomited, and had diarrhea. A CBC was unremarkable. Two liters of serosanguineous fluid, removed by thoracocentesis, was classified cytologically as an inflammatory sterile effusion containing neutrophils, some phagocytosed by macrophages, and large, atypical mesothelial cells. Anaerobic and aerobic cultures again were negative, potentially because amoxicillin-clavulanate was started by the referring veterinarian 36 hours before sample collection. The treatment regimen was changed to ciprofloxacin, azithromycin, and metoclopramide. Pleural fluid, cultured in BAPGM, resulted in the isolation of Bartonella spp., which was not successfully sequenced. Serum was not available for Bartonella IFA testing. Once culture results became available, treatment with azithromycin (7.8 mg/kg PO q2h) was begun for 5 weeks. At reevaluation 1 month later, the dog was eating normally, active, and alert, and there was no radiographic evidence of thoracic or abdominal effusion. Nine months postpericardectomy, the dog remained healthy with normal exercise tolerance when running and swimming. In this study, we detected infection with B. henselae, B. vinsonii subsp. berkhoffii or both organisms in 5 dogs ranging in age from 3 to 12 years that were diagnosed with pleural, pericardial (constrictive pericarditis), or abdominal effusion. Clinical signs generally were nonspecific and included lethargy, fever, vomiting, diarrhea, abdominal distention, lameness, and cervical pain. DNA was not amplified directly from 3 of 3 blood samples or from 2 of 3 effusion samples, but was amplified from pre-enrichment BAPGM blood and effusion cultures and from subculture isolates, a finding that further supports the utility of the enrichment process before PCR for more optimal detection of infection with a Bartonella spp.3, 5, 9 In humans, thoracic effusions have been reported as infrequent sequelae of Cat Scratch Disease, caused by B. henselae and due to infection with B. quintana.10 Unfortunately, BAPGM cultures often were established after administration of antibiotics. If blood and effusion samples had been cultured earlier in the course of illness and before antibiotic therapy, enhanced detection of Bartonella or other fastidious bacteria may have been achieved in other cases. As extravascular accumulation of fluid is always caused by a pathologic process and as dogs can be chronically infected with B. vinsonii subsp. berkhoffii for at least a year,11 microbiologic and molecular documentation of infection with this genus of bacteria may reflect an opportunistic role, a cofactor in disease expression or a primary pathogenic role in various patients with cavitary effusion. Exudates are the expected inflammatory response induced by bacterial infection, but this paradigm may not apply to Bartonella spp. Recently, the lipopolysaccharide of B. quintana was shown to have anti-inflammatory rather than proinflammatory properties.12 In addition, previous experimental infection studies in dogs suggest that B. vinsonii subsp. berkhoffii is associated with organism-induced immunosuppression.11 These and other unknown factors potentially could contribute to the development of an effusion in the absence of a strong host inflammatory response. Recent experimental studies using rodent models emphasize the ability of Bartonella spp. to invade vascular endothelial cells.13 In immunocompromised people, endothelial infection with B. henselae induces single or multiple vasoproliferative lesions (peliosis hepatis and bacillary angiomatosis).14, 15 Therefore, it is plausible that vascular endothelial infection contributes to increased vascular permeability and aberrant fluid accumulation. Despite isolation or molecular detection of B. henselae and B. vinsonii subsp. berkhoffii in these dogs, no direct cause and effect association can be implicated. However, our results may be clinically relevant because most idiopathic effusions obtained from dogs generally are considered aseptic based on conventional microbiological culture approaches. Two dogs in this study, for which serum was available for testing, were not seroreactive to B. henselae and B. vinsonii subsp. berkhoffii antigens by IFA testing, as described previously.9 Antigenic variability among B. henselae test strains previously has resulted in false negative B. henselae IFA results in human patients with suspected cat scratch disease,16 and a similar occurrence may explain discrepant serology and PCR results. The concept that bacterial infection in transudates or modified transudates obtained from dogs is an infrequent occurrence should be reassessed in the context of Bartonella infection. This research was supported by the State of North Carolina and in part through graduate student stipend support provided to NA Cherry by Novartis Animal Health, and salary support provided by IDEXX Laboratories and Bayer Corporation. We thank Mrs Tonya Lee for editorial assistance.}, number={1}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Cherry, N. A. and Diniz, P. P. V. P. and Maggi, Ricardo and Hummel, J. B. and Hardie, E. M. and Behrend, E. N. and Rozanski, E. and DeFrancesco, Teresa and Cadenas, M. B. and Breitschwerdt, Edward and et al.}, year={2009}, month={Jan}, pages={186–189} }
 @inbook{defrancesco_2009, place={St. Louis, MO}, title={Temporary Transvenous Pacing}, booktitle={Critical Care Medicine for Dogs and Cats}, publisher={Saunders Elsevier}, author={DeFrancesco, T.C.}, editor={Silverstein, D and Hopper, KEditors}, year={2009}, pages={214–216} }
 @inbook{defrancesco_2009, place={St. Louis, MO}, title={Transcutaneous Pacing}, booktitle={Small Animal Critical Care Medicine}, publisher={Saunders Elsevier}, author={DeFrancesco, T.C.}, editor={Silverstein, D. and Hopper, K.Editors}, year={2009}, pages={217–219} }
 @article{fox_oyama_reynolds_rush_defrancesco_keene_atkins_macdonald_schober_bonagura_et al._2009, title={Utility of plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) to distinguish between congestive heart failure and non-cardiac causes of acute dyspnea in cats}, volume={11}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2008.12.001}, DOI={10.1016/j.jvc.2008.12.001}, abstractNote={Circulating plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) concentration facilitates emergency diagnosis of congestive heart failure (CHF) in people. Its utility to discriminate between dyspneic cats with CHF vs. primary respiratory disease requires further assessment. Our objectives were to determine if NT-proBNP (1) differentiates dyspneic cats with CHF vs. primary respiratory disease; (2) increases with renal insufficiency; (3) correlates with left atrial dimension, radiographic cardiomegaly, and estimated left ventricular filling pressure (E/E(a)).NT-proBNP was measured in 167 dyspneic cats (66 primary respiratory disease, 101 CHF) to evaluate (1) relationship with clinical parameters; (2) ability to distinguish CHF from primary respiratory disease; (3) optimal cut-off values using receiver operating characteristic (ROC) curve analysis.NT-proBNP (1) was higher (median and inter-quartile [25th-75th] percentile) in CHF (754 pmol/L; 437, 1035 pmol/L) vs. primary respiratory disease (76.5 pmol/L; 24, 180 pmol/L) cohorts (P<0.001); (2) positively correlated in CHF cats with increased inter-ventricular septal end-diastolic thickness (rho=0.266; P=0.007) and LV free wall thickness (rho=0.218; P=0.027), but not with radiographic heart size, left atrial size, left ventricular dimensions, E/E(a) ratio, BUN, creatinine, or thyroxine; (3) distinguished dyspneic CHF cats from primary respiratory disease at 265 pmol/L cut-off value with 90.2% sensitivity, 87.9% specificity, 92% positive predictive value, and 85.3% negative predictive value (area under ROC curve, 0.94).NT-proBNP accurately discriminated CHF from respiratory disease causes of dyspnea.}, number={Supplement 1}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Fox, Philip R. and Oyama, Mark A. and Reynolds, Caryn and Rush, John E. and DeFrancesco, Terri C. and Keene, Bruce W. and Atkins, Clark E. and MacDonald, Kristin A. and Schober, Karsten E. and Bonagura, John D. and et al.}, year={2009}, month={May}, pages={S51–S61} }
 @article{cruse_booth_defrancesco_2008, title={ECG of the month}, volume={232}, ISSN={["1943-569X"]}, DOI={10.2460/javma.232.4.510}, number={4}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Cruse, Ashley M. and Booth, Margaret A. and DeFrancesco, Teresa C.}, year={2008}, month={Feb}, pages={510–512} }
 @article{defrancesco_2008, title={Maintaining fluid and electrolyte balance in heart failure}, volume={38}, ISSN={["0195-5616"]}, DOI={10.1016/j.cvsm.2008.02.005}, abstractNote={Advanced heart failure and its treatment are often associated with a variety of hemodynamic, fluid, and electrolyte derangements. This article gives the practitioner an overview of the pathophysiology of common fluid and electrolyte alterations present in animals with heart failure, highlighting specific clinical correlates. Additionally, specific therapeutic interventions are discussed to manage these fluid and electrolyte abnormalities.}, number={3}, journal={VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE}, author={DeFrancesco, Teresa C.}, year={2008}, month={May}, pages={727-+} }
 @article{finster_defrancesco_atkins_hansen_keene_2008, title={Supraventricular tachycardia in dogs: 65 cases (1990-2007)}, volume={18}, ISSN={["1476-4431"]}, DOI={10.1111/j.1476-4431.2008.00346.x}, abstractNote={Objective – To characterize the signalment, clinical findings, and prognosis of dogs with supraventricular tachycardia (SVT). Design – Retrospective study. Setting – North Carolina State University Veterinary Teaching Hospital. Animals, Intervention, and Measurements – Case selection included all patients at the veterinary teaching hospital with SVT during years 1990–2007. Medical records from dogs with at least 1 recorded episode of SVT were extracted. The signalment, history, electrocardiographic, radiographic, and echocardiographic findings, therapy, and response to therapy were reviewed and summarized. Follow-up was conducted to determine the date and cause of death. Kaplan-Meier survival curves were constructed and analyzed. The relationships between patient characteristics and responses to therapy and prognosis were evaluated. Main Results – Sixty-five records documented a diagnosis of SVT. Sixty-two percent were males. Labrador Retrievers and Boxers were overrepresented compared with the general hospital population. Median age at presentation was 9 years (range 0.5–15.5 y). The median heart rate during SVT was 270/minute (range 187–375/min). The most common presenting complaint was syncope (30%), 23% were asymptomatic at the time of diagnosis. Most dogs had structural heart disease (65%). Median survival was 472 days (<1–2007 d). Identification of sustained SVT (>30 s) did not affect survival (P=0.50), nor did the presence of congestive heart failure (P=0.70). Conclusions – The majority of dogs with SVT had structural heart disease or a severe concurrent illness at the time of SVT diagnosis. SVT, though often a persistent and occasionally sustained arrhythmia, does not appear to be a primary factor in mortality.}, number={5}, journal={JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE}, author={Finster, Sharon T. and DeFrancesco, Teresa C. and Atkins, Clarke E. and Hansen, Bernie D. and Keene, Bruce W.}, year={2008}, month={Oct}, pages={503–510} }
 @inbook{defrancesco_2007, place={Ames, Iowa}, edition={4th}, title={Aortic Thromboembolism}, booktitle={Blackwell’s Five-Minute Veterinary Consult: Canine and Feline}, publisher={Blackwell Publishing Professional}, author={DeFrancesco, T.C.}, editor={Tilley, LP and Smith, FWKEditors}, year={2007}, pages={98–99} }
 @inbook{defrancesco_2007, place={Ames, Iowa}, edition={4th}, title={Dilated Cardiomyopathy - Cats}, booktitle={Blackwell’s Five-Minute Veterinary Consult: Canine and Feline}, publisher={Blackwell Publishing Professional}, author={DeFrancesco, T.C.}, editor={Tilley, LP and Smith, FWKEditors}, year={2007}, pages={208–209} }
 @article{gardner_atkins_rausch_defrancesco_chandler_keene_2007, title={Estimation of 24-h aldosterone secretion in the dog using the urine aldosterone:Creatinine ratio}, volume={9}, ISSN={1760-2734}, url={http://dx.doi.org/10.1016/j.jvc.2006.11.001}, DOI={10.1016/j.jvc.2006.11.001}, abstractNote={One potential method of evaluating renin–angiotensin–aldosterone system (RAAS) activation involves the quantification of urinary aldosterone excretion. While blood concentrations of aldosterone are easily obtained, results may be misleading because of minute-to-minute variation in aldosterone secretion and subsequent blood concentrations. Urinary aldosterone concentration measurement represents a more consistent “pooled” index of aldosterone secretion, but obtaining 24-h urine samples is time-consuming, difficult, and fraught with potential error. We postulated that the urinary aldosterone:creatinine ratio, measured from spot urine samples, would correlate well with 24-h urinary aldosterone excretion, and would provide a simple index of aldosterone excretion that would eliminate the need for 24-h urine collection. After validating an assay for aldosterone in canine urine, 24-h urinary aldosterone excretion was determined by radioimmunoassay from 8 normal, male beagle dogs under control conditions, after RAAS stimulation with amlodipine administration, and after RAAS attenuation with the addition of enalapril to amlodipine administration. Spot urine samples, each obtained at the same time of day, were used to determine the aldosterone:creatinine ratio during control conditions, RAAS stimulation, and RAAS attenuation. The aldosterone:creatinine ratio from spot-checked urine samples correlated well with 24-h urinary aldosterone excretion (r = 0.77, P < 0.0001). A spot urinary aldosterone:creatinine ratio might be substituted for 24-h urinary aldosterone determination.}, number={1}, journal={Journal of Veterinary Cardiology}, publisher={Elsevier BV}, author={Gardner, Sarah Y. and Atkins, Clarke E. and Rausch, William P. and DeFrancesco, Teresa C. and Chandler, Donald Walt and Keene, Bruce W.}, year={2007}, month={May}, pages={1–7} }
 @article{defrancesco_rush_rozanski_hansen_keene_moore_atkins_2007, title={Prospective clinical evaluation of an ELISA B-type natriuretic peptide assay in the diagnosis of congestive heart failure in dogs presenting with cough or dyspnea}, volume={21}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2007)21[243:PCEOAE]2.0.CO;2}, abstractNote={B-type natriuretic peptide (BNP) is increased in dogs with congestive heart failure (CHF).The purpose of this study was to evaluate the clinical utility of a novel canine-specific enzyme-linked immunosorbent assay of BNP for the diagnosis of CHF in dogs presenting with either cough or dyspnea.Three hundred and thirty dogs from 2 large university teaching hospitals.We prospectively measured plasma BNP concentrations in 3 groups of dogs: (1) normal adult dogs (n = 75), (2) dogs with asymptomatic heart disease (n = 76), and (3) dogs with cough or dyspnea (n = 179). The final diagnosis of dogs with cough or dyspnea and the severity of CHF (International Small Animal Cardiac Health Council Heart Failure Classification [ISACHC]) were determined by medical record review by a study cardiologist who was blinded to the results of the BNP assay.Dogs with CHF had a higher median BNP concentration (24.6 pg/mL) than dogs with noncardiac causes of cough or dyspnea (2.6 pg/mL) (P < .0001). The area under the curve was 0.91 for the receiver operating curve analysis of the diagnostic accuracy of the BNP measurement to differentiate CHF from other causes of cough or dyspnea. The median BNP concentrations in dogs were 3.0 pg/mL with ISACHC I, 17.8 pg/mL with ISACHC II, and 30.5 pg/mL with ISACHC III. (P < .0001)Measurement of BNP is useful in establishing or in excluding the diagnosis of CHF in dogs with cough or dyspnea. B-type natriuretic peptide concentrations rose significantly as a function of severity of CHF.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={DeFrancesco, Teresa C. and Rush, John E. and Rozanski, Elizabeth A. and Hansen, Bernard D. and Keene, Bruce W. and Moore, Dominic T. and Atkins, Clarke E.}, year={2007}, pages={243–250} }
 @article{atkins_keene_brown_coats_crawford_defrancesco_edwards_fox_lehmkuhl_luethy_et al._2007, title={Results of the veterinary enalapril trial to prove reduction in onset of heart failure in dogs chronically treated with enalapril alone for compensated, naturally occurring mitral valve insufficiency}, volume={231}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.231.7.1061}, DOI={10.2460/javma.231.7.1061}, abstractNote={Abstract Objective —To determine the efficacy of long-term enalapril administration in delaying the onset of congestive heart failure (CHF). Design —Placebo-controlled, double-blind, multicenter, randomized trial. Animals —124 dogs with compensated mitral valve regurgitation (MR). Procedures —Dogs randomly assigned to receive enalapril or placebo were monitored for the primary endpoint of onset of CHF for ≤ 58 months. Secondary endpoints included time from study entry to the combined endpoint of CHF-all-cause death; number of dogs free of CHF at 500, 1,000, and 1,500 days; and mean number of CHF-free days. Results —Kaplan-Meier estimates of the effect of enalapril on the primary endpoint did not reveal a significant treatment benefit. Chronic enalapril administration did have a significant benefit on the combined endpoint of CHF-all-cause death (benefit was 317 days [10.6 months]). Dogs receiving enalapril remained free of CHF for a significantly longer time than those receiving placebo and were significantly more likely to be free of CHF at day 500 and at study end. Conclusions and Clinical Relevance —Chronic enalapril treatment of dogs with naturally occurring, moderate to severe MR significantly delayed onset of CHF, compared with placebo, on the basis of number of CHF-free days, number of dogs free of CHF at days 500 and study end, and increased time to a combined secondary endpoint of CHF-all-cause death. Improvement in the primary endpoint, CHF-free survival, was not significant. Results suggest that enalapril modestly delays the onset of CHF in dogs with moderate to severe MR.}, number={7}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Atkins, Clarke E. and Keene, Bruce W. and Brown, William A. and Coats, Julie R. and Crawford, Mary Ann and DeFrancesco, Teresa C. and Edwards, N. Joel and Fox, Phillip R. and Lehmkuhl, Linda B. and Luethy, Michael W. and et al.}, year={2007}, month={Oct}, pages={1061–1069} }
 @article{atkins_rausch_gardner_defrancesco_keene_levine_2007, title={The effect of amlodipine and the combination of amlodipine and enalapril on the renin-angiotensin-aldosterone system in the dog}, volume={30}, ISSN={0140-7783 1365-2885}, url={http://dx.doi.org/10.1111/j.1365-2885.2007.00894.x}, DOI={10.1111/j.1365-2885.2007.00894.x}, abstractNote={Excessive aldosterone secretion is detrimental to the heart, vessels and kidneys, contributing to hypertension and the signs and progression of heart failure. Aldosterone secretion, abnormally elevated in heart failure and hypertension, can be blunted with angiotensin-converting enzyme inhibitors. Amlodipine, used to treat hypertension and heart failure, was hypothesized to activate the renin-angiotensin-aldosterone system (RAAS). A study was conducted with six normal adult male beagle dogs. Each dog received amlodipine (0.57 mg/kg b.i.d.) for 6 days, followed by amlodipine (0.57 mg/kg b.i.d.) and enalapril (0.57 mg/kg b.i.d.) for 4 days. Blood pressure, heart rate, serum chemistries and urinary aldosterone excretion, as a measure of RAAS activation, were compared with baseline values. Blood pressure fell by approximately 7% with amlodipine (P = 0.05) and a further 7% with the combination of amlodipine and enalapril (P < 0.01). Blood urea nitrogen increased with the combination (P < 0.05) but only one dog became mildly azotemic. Renin-angiotensin-aldosterone system activation, based on 24 h urinary aldosterone excretion and by aldosterone:creatinine ratio was increased by approximately threefold (P < 0.05) with amlodipine administration. This effect was blunted by enalapril, such that aldosterone excretion was no longer different from that observed under control conditions, although values for 24-h aldosterone excretion did not return to pretreament levels.}, number={5}, journal={Journal of Veterinary Pharmacology and Therapeutics}, publisher={Wiley}, author={Atkins, C. E. and Rausch, W. P. and Gardner, S. Y. and Defrancesco, T. C. and Keene, B. W. and Levine, J. F.}, year={2007}, month={Oct}, pages={394–400} }
 @article{fujii_keene_mathews_atkins_defrancesco_hardie_wakao_2006, title={Coil occlusion of residual shunts after surgical closure of patent ductus arteriosus}, volume={35}, ISSN={["0161-3499"]}, DOI={10.1111/j.1532-950X.2006.00222.x}, abstractNote={Objective— To describe use of coil embolization to occlude residual flow through a patent ductus arteriosus (PDA) after incomplete surgical ligation. Study Design— Clinical study. Animals— Dogs (n=4) with continuous murmur after surgical ligation of PDA. Methods— After PDA ligation, residual ductal flow through the PDA was visible on color-flow Doppler examination and left ventricular end-diastolic diameter remained increased. Coil embolization by an arterial approach was performed to achieve complete occlusion of the PDA. Results— Embolization coils were delivered without complications and hemodynamically successful occlusion was achieved. Doppler-visible flow resolved in 2 dogs within 3 months after embolization. Left ventricular end-diastolic diameter indexed to body weight decreased in all dogs. Conclusions— Transcatheter coil embolization appears to be a safe and minimally invasive procedure for complete occlusion of residual PDA flow after incomplete surgical ligation. Clinical Relevance— Transcatheter coil embolization should be considered for correction of hemodynamically significant residual shunts in dogs that have incomplete PDA occlusion after open surgical ligation.}, number={8}, journal={VETERINARY SURGERY}, author={Fujii, Yoko and Keene, Bruce W. and Mathews, Kyle G. and Atkins, Clarke E. and Defrancesco, Teresa C. and Hardie, Elizabeth M. and Wakao, Yoshito}, year={2006}, month={Dec}, pages={781–785} }
 @article{buur_baynes_yeatts_davidson_defrancesco_2005, title={Analysis of diltiazem in Lipoderm (R) transdermal gel using reversed-phase high-performance liquid chromatography applied to homogenization and stability studies}, volume={38}, ISSN={["0731-7085"]}, DOI={10.1016/j.jpba.2004.11.053}, abstractNote={A simple and novel method for the extraction and quantification of diltiazem hydrochloride was developed and applied to homogenization and stability studies. The method used solid phase extraction coupled with reversed-phase high-performance liquid chromatography (HPLC) with ultraviolet (UV) detection. Validation showed inter-day recoveries ranging from 84.00 to 96.52% with relative standard deviations ranging from 12.01 to 15.94%. Intra-day recoveries ranged from 67.95 to 106.1% with relative standard deviations less than 5%. The method showed excellent linearity from 50 to 250 mg/ml in undiluted gel (R2 = 0.996). The homogenization study showed good homogenization using both 50 and 100 depression techniques. Diltiazem was stable at a concentration of 246 mg/ml for 30 days and at a concentration of 99.6 mg/ml for 60 days no matter the storage conditions explored in this study.}, number={1}, journal={JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS}, author={Buur, JL and Baynes, RE and Yeatts, JL and Davidson, G and DeFrancesco, TC}, year={2005}, month={Jun}, pages={60–65} }
 @article{baumwart_meurs_atkins_bonagura_defrancesco_keene_koplitz_fuentes_miller_rausch_et al._2005, title={Clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003)}, volume={226}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2005.226.1102}, DOI={10.2460/javma.2005.226.1102}, abstractNote={Abstract Objective —To identify clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and echocardiographic evidence of left ventricular systolic dysfunction. Design —Retrospective study. Animals —48 mature Boxers. Procedure —Medical records were reviewed for information on age; sex; physical examination findings; and results of electrocardiography, 24-hour ambulatory electrocardiography, thoracic radiography, and echocardiography. Results —Mean age of the dogs was 6 years (range, 1 to 11 years). Twenty (42%) dogs had a systolic murmur, and 9 (19%) had ascites. Congestive heart failure was diagnosed in 24 (50%) dogs. Seventeen (35%) dogs had a history of syncope. Mean fractional shortening was 14.4% (range, 1% to 23%). Mean left ventricular systolic and diastolic diameters were 4.5 cm (range, 3 to 6.3 cm) and 5.3 cm (range, 3.9 to 7.4 cm), respectively. Twenty-eight (58%) dogs had a sinus rhythm with ventricular premature complexes (VPCs), and 20 had supraventricular arrhythmias (15 with atrial fibrillation and 5 with sinus rhythm and atrial premature complexes). Sixteen of the dogs with supraventricular arrhythmias also had occasional VPCs. Morphology of the VPCs seen on lead II ECGs was consistent with left bundle branch block in 25 dogs, right bundle branch block in 8, and both in 11. Conclusions and Clinical Relevance —Results suggest that Boxers with cardiomyopathy and left ventricular dysfunction frequently have arrhythmias of supraventricular or ventricular origin. Whether ventricular dysfunction was preceded by electrical disturbances could not be determined from these data, and the natural history of myocardial disease in Boxers requires further study. ( J Am Vet Med Assoc 2005;226:1102–1104)}, number={7}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Baumwart, Ryan D. and Meurs, Kathryn M. and Atkins, Clarke E. and Bonagura, John D. and DeFrancesco, Teresa C. and Keene, Bruce W. and Koplitz, Shianne and Fuentes, Virginia Luis and Miller, Matthew W. and Rausch, William and et al.}, year={2005}, month={Apr}, pages={1102–1104} }
 @article{defrancesco_2003, title={Diagnosing congestive heart failure: Could a blood test increase our diagnostic accuracy in heart failure?}, volume={7}, journal={Abaxis VetCom}, author={DeFrancesco, T.C.}, year={2003}, month={Apr}, pages={1–4} }
 @book{defrancesco_atkins_hurley_devlin_2003, place={Lyon, France}, title={Getting to the heart of the matter : advances in the management of cardiac patients}, publisher={Merial}, author={DeFrancesco, Teresa and Atkins, Clarke and Hurley, Karyl and Devlin, Pauline}, editor={Hurley, Dr Karyl and Devlin, Dr PaulineEditors}, year={2003} }
 @article{defrancesco_hansen_atkins_sidley_keene_2003, title={Noninvasive transthoracic temporary cardiac pacing in dogs}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0663:NTTCPI>2.3.CO;2}, abstractNote={Temporary cardiac pacing is used in the emergency treatment of life-threatening bradyarrhythmias and for the support of heart rate and blood pressure of patients with sick sinus syndrome or high-grade atrioventricular (AV) block undergoing general anesthesia, typically for permanent pacemaker implantation. We retrospectively evaluated the safety and efficacy of a noninvasive transthoracic external cardiac pacing system in 42 dogs treated for bradyarrhythmias. Optimal placement of the patch electrodes on the skin of the thorax was initially established on 2 anesthetized normal dogs. The optimal electrode placement was determined to be on the right and left hemithoraces, directly over the heart. Afterward, by means of this electrode placement, all 42 dogs treated for bradyarrhythmias in this study were successfully paced with the noninvasive transthoracic system. Dogs ranged in age from 1 to 15 years and weighed between 3.2 and 40 kg. Miniature Schnauzers, German Shepherds, and mixed breeds were most common in the study population. Indications for noninvasive transthoracic pacing included emergency treatment of hemodynamically unstable 3rd-degree AV block (2 dogs); support of heart rate during general anesthesia for permanent pacemaker implantation or lead-wire adjustment (38 dogs); and support of heart rate during general anesthesia for ophthalmologic surgery in dogs with sick sinus syndrome (2 dogs). Complications included pain and skeletal muscle stimulation, which required general anesthesia. We conclude that the noninvasive transthoracic pacing system evaluated is satisfactory for clinical veterinary use.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={DeFrancesco, TC and Hansen, BD and Atkins, CE and Sidley, JA and Keene, BW}, year={2003}, pages={663–667} }
 @article{meurs_spier_wright_atkins_defrancesco_gordon_hamlin_keene_miller_moise_et al._2002, title={Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers}, volume={221}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2002.221.522}, DOI={10.2460/javma.2002.221.522}, abstractNote={Abstract Objective —To evaluate the effect of 4 antiarrhythmic treatment protocols on number of ventricular premature complexes (VPC), severity of arrhythmia, heart rate (HR), and number of syncopal episodes in Boxers with ventricular tachyarrhythmias. Design —Randomized controlled clinical trial. Animals —49 Boxers. Procedure —Dogs with > 500 VPC/24 h via 24-hour ambulatory ECG (AECG) were treated with atenolol (n = 11), procainamide (11), sotalol (16), or mexiletine and atenolol (11) for 21 to 28 days. Results of pre- and posttreatment AECG were compared with regard to number of VPC/24 h; maximum, mean, and minimum HR; severity of arrhythmia; and occurrence of syncope. Results —Significant differences between pre- and posttreatment number of VPC, severity of arrhythmia, HR variables, or occurrence of syncope were not observed in dogs treated with atenolol or procainamide. Significant reductions in number of VPC, severity of arrythmia, and maximum and mean HR were observed in dogs treated with mexiletineatenolol or sotalol; occurrence of syncope was not significantly different between these 2 treatment groups. Conclusions and Clinical Relevance —Treatment with sotalol or mexiletine-atenolol was well tolerated and efficacious. Treatment with procainamide or atenolol was not effective. ( J Am Vet Med Assoc 2002;221:522–527)}, number={4}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Meurs, K. M. and Spier, A. W. and Wright, N. A. and Atkins, C. E. and DeFrancesco, Teresa and Gordon, S. G. and Hamlin, R. L. and Keene, B. W. and Miller, M. W. and Moise, N. S. and et al.}, year={2002}, month={Aug}, pages={522–527} }
 @article{atkins_brown_coats_crawford_defrancesco_edwards_fox_keene_lehmkuhl_luethy_et al._2002, title={Effects of long-term administration of enalapril on clinical indicators of renal function in dogs with compensated mitral regurgitation}, volume={221}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2002.221.654}, DOI={10.2460/javma.2002.221.654}, abstractNote={To determine the effect of long-term administration of enalapril on renal function in dogs with severe, compensated mitral regurgitation.Randomized controlled trial.139 dogs with mitral regurgitation but without overt signs of heart failure.Dogs were randomly assigned to be treated with enalapril (0.5 mg/kg [0.23 mg/lb], PO, q 24 h) or placebo, and serum creatinine and urea nitrogen concentrations were measured at regular intervals for up to 26 months.Adequate information on renal function was obtained from 132 dogs; follow-up time ranged from 0.5 to 26 months (median, 12 months). Mean serum creatinine and urea nitrogen concentrations were not significantly different between dogs receiving enalapril and dogs receiving the placebo at any time, nor were concentrations significantly different from baseline concentrations. Proportions of dogs that developed azotemia or that had a +/- 35% increase in serum creatinine or urea nitrogen concentration were also not significantly different between groups.And Clinical Relevance: Results suggest that administration of enalapril for up to 2 years did not have any demonstrable adverse effects on renal function in dogs with severe, compensated mitral regurgitation.}, number={5}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Atkins, Clarke E. and Brown, William A. and Coats, Julie R. and Crawford, Mary Ann and DeFrancesco, Teresa C. and Edwards, Joel and Fox, Philip R. and Keene, Bruce W. and Lehmkuhl, Linda and Luethy, Michael and et al.}, year={2002}, month={Sep}, pages={654–658} }
 @article{sidley_atkins_keene_defrancesco_2002, title={Percutaneous Balloon Pericardiotomy as a Treatment for Recurrent Pericardial Effusion in 6 Dogs}, volume={16}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2002.tb02384.x}, DOI={10.1892/0891-6640(2002)016<0541:PBPAAT>2.3.CO;2}, abstractNote={Percutaneous balloon pericardiotomy (PBP) has been performed in people and in a small number of dogs as a treatment for recurrent pericardial effusion with tamponade (PET). We performed this technique on 6 dogs with recurrent PET (5 with heart base tumors and 1 with no identifiable mass). Under general anesthesia and fluoroscopic guidance, a balloon-dilating catheter (diameters 14-20 mm) was introduced percutaneously at the 5th intercostal space through a sheath-introducing catheter, positioned across the parietal pericardium, and inflated 3 times. No dog experienced serious complications. The procedure was considered successful in 4 of 6 dogs. One dog is still alive without recurrence of PET 1 year after the procedure. Three dogs died of unrelated disease without recurrence of PET 5. 19, and 32 months after the procedure. The procedure was not beneficial in 1 dog that was euthanized 9 weeks later because of recurrence of pleural and abdominal effusion thought to be secondary to PET. One dog may have temporarily benefited but developed symptomatic PET 6 months after PBP. PBP appears to be a safe, economical, and potentially effective palliative treatment for recurrent PET and is a reasonable, less invasive alternative to surgery for dogs with recurrent PET, especially effusions caused by heart base tumors and possibly idiopathic pericardial effusion. Premature closure of the stoma is a potential cause for long-term failure and was thought to have been responsible for the recurrence of clinical signs in 2 dogs.}, number={5}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Sidley, J.A. and Atkins, C.E. and Keene, B.W. and DeFrancesco, T.C.}, year={2002}, month={Sep}, pages={541–546} }
 @article{defrancesco_atkins_keene_coats_hauck_2002, title={Prospective clinical evaluation of serum cardiac troponin T in dogs admitted to a veterinary teaching hospital}, volume={16}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2002)016<0553:PCEOSC>2.3.CO;2}, abstractNote={The purpose of this study was to measure serum cardiac troponin T (cTnT) with a commercially available human enzyme-linked immunoassay (ELISA) test in various groups of dogs, including those undergoing doxorubicin chemotherapy. Serum samples were obtained from 6 groups of dogs: (1) normal adult dogs (n = 15); (2) dogs with asymptomatic dilated cardiomyopathy (n = 5); (3) dogs with congestive heart failure (n = 10); (4) dogs with untreated neoplasia (n = 20); (5) dogs with skeletal muscle trauma (n = 10); and (6) dogs with neoplasia receiving doxorubicin chemotherapy (n = 4). One serum sample was obtained from each of the normal dogs, those with asymptomatic cardiomyopathy, those with congestive heart failure, and those with untreated neoplasia. Serum samples were obtained serially from the dogs that were undergoing doxorubicin chemotherapy; samples were collected before doxorubicin (30 mg/m2) administration and then 1, 5, 7, and 14 days after administration throughout 6 cycles for a cumulative total dose of 180 mg/m2. All normal dogs, dogs with untreated neoplasia, and dogs with asymptomatic dilated cardiomyopathy had cTnT concentrations below the lower limits of detection for the assay used (<0.05 ng/mL). Detectable concentrations of cTnT were found in 3 dogs with congestive heart failure and in 2 dogs with skeletal muscle trauma. Detectable concentrations also were found in both dogs that had received 180 mg/m2 of doxorubicin. We conclude that dogs with congestive heart failure and those with skeletal muscle trauma and dogs with neoplasia receiving high-dose doxorubicin chemotherapy may have increased serum cTnT concentration, which may be suggestive of myocardial damage.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={DeFrancesco, TC and Atkins, CE and Keene, BW and Coats, JR and Hauck, ML}, year={2002}, pages={553–557} }
 @article{hansen_defrancesco_2002, title={Relationship between hydration estimate and body weight change after fluid therapy in critically ill dogs and cats}, volume={12}, ISSN={["1534-6935"]}, DOI={10.1046/j.1435-6935.2002.t01-1-00050.x}, abstractNote={Objective: To characterize the relationship between clinical estimates of hydration in dogs and cats admitted to an intensive care unit (ICU) and changes in their body weight following 24–48 hours of fluid therapy. Design: Outcome study. Setting: ICU at a veterinary teaching hospital (VTH). Animals: A total of 151 dogs and 42 cats with various medical disorders that had not had surgery within 48 hours of admission into the ICU were consecutively admitted into the study. Animals with any condition predisposing to excess fluid loss or retention were excluded: heart disease, sepsis, trauma, pancreatitis, pleural or pericardial effusion, ascites, and pathologic oliguria. Animals that acquired any of the following during the observation period were excluded: gastrointestinal fluid loss, edema or diseases predisposing to edema, oliguria, diuretic therapy, and body fluid drainage or hemorrhage. Fluid therapy was ordered based on estimate of hydration at admission. Other treatments were not modified or withheld. Interventions: Physiologic data were collected at the time of admission and 24–48 hours later. Measurements and main results: Hydration was estimated on admission to the ICU using clinical judgement with no supporting laboratory data. Each admitting clinician used this estimate to plan fluid therapy. Fluid therapy was defined as the administration of any enteral or parenteral fluids as well as any decision to withhold fluids. Paired measurements taken on admission and at 24–48 hours included packed cell volume (PCV), total plasma solids (TS), and body weight. Amount and type of fluids or blood products administered were noted. Neither clinician estimates of dehydration nor baseline PCV or TS predicted clinically significant changes in body weight following fluid therapy, and there was no relationship between weight change and changes in PCV or TS. Conclusions: A clinical diagnosis of dehydration in our ICU does not predict weight gain following fluid therapy. Neither baseline PCV/TS nor changes in these measurements following 24–48 hours of fluid therapy predicted changes in body weight.}, number={4}, journal={JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE}, author={Hansen, B and DeFrancesco, T}, year={2002}, month={Dec}, pages={235–243} }
 @article{defrancesco_2002, title={The case of the fainting Boxer: review of Boxer cardiomyopathy}, volume={12}, number={3}, journal={Waltham FOCUS}, author={DeFrancesco, T.C.}, year={2002}, pages={28–30} }
 @article{baty_malarkey_atkins_defrancesco_sidley_keene_2001, title={Natural history of hypertrophic cardiomyopathy and aortic thromboembolism in a family of domestic shorthair cats}, volume={15}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2001)015<0595:NHOHCA>2.3.CO;2}, abstractNote={A feline domestic shorthair queen and her 3 offspring were all diagnosed with asymptomatic hypertrophic cardiomyopathy (HCM). The family has been followed for 13 years, and 3 cats have died of aortic thromboembolism (ATE). This communication documents the long-term progression of HCM in these cats that presented with mild left ventricular hypertrophy and hyperdynamic systolic ventricular function, developed progressive left atrial enlargement, and eventually resulted in hypodynamic left ventricular systolic function with relative left ventricular chamber dilation at the time of ATE.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Baty, CJ and Malarkey, DE and Atkins, CE and DeFrancesco, TC and Sidley, J and Keene, BW}, year={2001}, pages={595–599} }
 @article{defrancesco_atkins_miller_meurs_keene_2001, title={Use of echocardiography for the diagnosis of heartworm disease in cats: 43 cases (1985-1997)}, volume={218}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2001.218.66}, DOI={10.2460/javma.2001.218.66}, abstractNote={Abstract Objective —To determine the usefulness of echocardiography in the diagnosis of heartworm disease in cats and to compare this modality with other tests. Design —Retrospective study. Animals —43 cats with heartworm infection that had echocardiographic examinations at 2 veterinary teaching hospitals between 1985 and 1997. Twenty-two of these 43 cats also underwent radiography of the thorax and heartworm antibody and heartworm antigen testing. Procedure —Cats were determined to be infected with Dirofilaria immitis infection on the basis of 1 or more of the following findings: positive modified Knott or antigen test result, echocardiographic evidence of heartworm disease, or confirmation of the disease on postmortem examination. The percentage of echocardiographs in which heartworms were evident was compared with the percentage of radiographs in which pulmonary artery enlargement was evident and results of antigen or antibody tests in cats in which all tests were performed. Results —Overall, heartworms were detectable by use of echocardiography in 17 of 43 cats, most often in the pulmonary arteries. In the 22 cats in which all tests were performed, antibody test results were positive in 18, antigen test results were positive in 12, and pulmonary artery enlargement was evident radiographically and heartworms were identifiable echocardiographically in 14. Heartworm infection was diagnosed exclusively by use of echocardiography in 5 cats in which the antigen test result was negative. Conclusions and Clinical Relevance —Although echocardiography was less sensitive than antigen testing, it was a useful adjunctive test in cats that had negative antigen test results in which there was a suspicion of heartworm disease. The pulmonary arteries should be evaluated carefully to increase the likelihood of detection of heartworms echocardiographically. ( J Am Vet Med Assoc2001;218:66–69)}, number={1}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={DeFrancesco, Teresa C. and Atkins, Clarke E. and Miller, Matthew W. and Meurs, Kathryn M. and Keene, Bruce W.}, year={2001}, month={Jan}, pages={66–69} }
 @inbook{defrancesco_2000, title={AMBULATORY ELECTROCARDIOGRAPHY}, ISBN={9781560533528}, url={http://dx.doi.org/10.1016/b978-1-56053-352-8.50024-9}, DOI={10.1016/b978-1-56053-352-8.50024-9}, booktitle={Small Animal Cardiology Secrets}, publisher={Elsevier}, author={DeFrancesco, Teresa C.}, year={2000}, pages={115–118} }
 @inbook{defrancesco_2000, title={CVT update: Infectious endocarditis}, ISBN={0721655238}, booktitle={Kirk's current veterinary therapy : small animal practice (13th Ed.)}, publisher={Philadelphia, PA : W.B. Saunders}, author={DeFrancesco, T. C.}, year={2000}, pages={768} }
 @inbook{defrancesco_2000, place={Philadelphia, PA}, edition={7th}, title={Cardiac Emergencies, Hypertension, Electrocution, and Exam of the Cardiovascular System}, booktitle={Kirk and Bistner's handbook of veterinary procedures and emergency treatment}, publisher={WB Saunders}, author={DeFrancesco, T.C.}, editor={Bistner, S. and Ford, R.B. and Raffe, M.R. and Kirk, R.W.Editors}, year={2000}, pages={54–74, 282–313} }
 @article{atkins_defrancesco_coats_sidley_keene_2000, title={Heartworm infection in cats: 50 cases (1985-1997)}, volume={217}, DOI={10.2460/javma.2000.217.355}, abstractNote={To characterize risk factors, clinical findings, usefulness of diagnostic tests, and prognosis in cats with naturally occurring heartworm infection (HWI).Retrospective study.50 cats with Dirofilaria immitis infection.Medical records, thoracic radiographs, and echocardiograms were reviewed and findings compared with appropriate reference populations.Findings suggested that male cats were not predisposed to HWI, domestic shorthair cats were at increased risk, and indoor housing was only partially protective. Fewer cases of HWI were identified in the final quarter of the year, compared with other periods, and prevalence is not apparently increasing. Signs of respiratory tract disease were most common, followed by vomiting. Infection was diagnosed incidentally in > 25% of cats; conversely, 10% of infected cats died suddenly without other clinical signs. Serologic tests were most useful for diagnosis, followed by radiography and echocardiography. Eosinophilia supported the diagnosis. Overall median survival time was 1.5 years but exceeded 4 years in cats surviving beyond the day of diagnosis.Sex does not appear to be a risk factor for HWI in cats, and indoor housing provides only incomplete protection. Signs of respiratory tract disease (dyspnea and cough) are the strongest indicators of HWI in cats, and some radiographic evidence of infection is detected in most cases. Antibody screening for HWI in cats is efficacious, and antigen testing and echocardiography are most useful for making a definitive antemortem diagnosis.}, number={3}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Atkins, CE and DeFrancesco, TC and Coats, JR and Sidley, JA and Keene, BW}, year={2000}, month={Aug}, pages={355–358} }
 @article{maggio_defrancesco_atkins_pizzirani_gilger_davidson_2000, title={Ocular lesions associated with systemic hypertension in cats: 69 cases (1985-1998)}, volume={217}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2000.217.695}, abstractNote={Abstract Objective —To characterize clinical and clinicopathologic findings, response to treatment, and causes of systemic hypertension in cats with hypertensive retinopathy. Design —Retrospective study. Animals —69 cats with hypertensive retinopathy. Procedure —Medical records from cats with systemic hypertension and hypertensive retinopathy were reviewed. Results —Most cats (68.1%) were referred because of vision loss; retinal detachment, hemorrhage, edema, and degeneration were common findings. Cardiac abnormalities were detected in 37 cats, and neurologic signs were detected in 20 cats. Hypertension was diagnosed concurrently with chronic renal failure (n = 22), hyperthyroidism (5), diabetes mellitus (2), and hyperaldosteronism (1). A clearly identifiable cause for hypertension was not detected in 38 cats; 26 of these cats had mild azotemia, and 12 did not have renal abnormalities. Amlodipine decreased blood pressure in 31 of 32 cats and improved ocular signs in 18 of 26 cats. Conclusions and Clinical Relevance —Retinal lesions, caused predominantly by choroidal injury, are common in cats with hypertension. Primary hypertension in cats may be more common than currently recognized. Hypertension should be considered in older cats with acute onset of blindness; retinal edema, hemorrhage, or detachment; cardiac disease; or neurologic abnormalities. Cats with hypertensioninduced ocular disease should be evaluated for renal failure, hyperthyroidism, diabetes mellitus, and cardiac abnormalities. Blood pressure measurements and funduscopic evaluations should be performed routinely in cats at risk for hypertension (preexisting renal disease, hyperthyroidism, and age > 10 years). Amlodipine is an effective antihypertensive agent in cats.( J Am Vet Med Assoc 2000;217:695–702)}, number={5}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Maggio, F and DeFrancesco, TC and Atkins, CE and Pizzirani, S and Gilger, BC and Davidson, MG}, year={2000}, month={Sep}, pages={695–702} }
 @misc{atkins_defrancesco_2000, title={Untitled}, volume={14}, number={5}, journal={Journal of Veterinary Internal Medicine}, author={Atkins, C. E. and DeFrancesco, T.}, year={2000}, pages={471} }
 @inbook{defrancesco_2000, place={Philadelphia, PA}, title={Update: Infectious Endocarditis}, booktitle={Kirk’s Current Veterinary Therapy XIII}, publisher={WB Saunders}, author={DeFrancesco, T.C.}, editor={Bonagura, J.D. and Kirk, R.W.Editors}, year={2000}, pages={768–771} }
 @article{ward_forrester_defrancesco_troy_1999, title={Treatment of severe chronic digoxin toxicosis in a dog with cardiac disease, using ovine digoxin-specific immunoglobulin G Fab fragments}, volume={215}, number={12}, journal={Journal of the American Veterinary Medical Association}, author={Ward, D. M. and Forrester, S. D. and DeFrancesco, T. C. and Troy, G. C.}, year={1999}, pages={1808–1812} }
 @article{atkins_defrancesco_miller_meurs_keene_1998, title={Prevalence of heartworm infection in cats with signs of cardiorespiratory abnormalities}, volume={212}, number={4}, journal={Journal of the American Veterinary Medical Association}, author={Atkins, C. E. and DeFrancesco, T. C. and Miller, M. W. and Meurs, K. M. and Keene, B.}, year={1998}, pages={517–520} }
 @misc{defrancesco_1997, place={Cardiopet}, title={Feline Heartworm Disease: Should I be concerned?}, journal={Cardiopet Educator}, publisher={Little Falls, NJ}, author={DeFrancesco, T.C.}, year={1997}, month={Oct} }
 @book{defrancesco_1997, place={Baltimore}, title={Taurine Deficiency in The 5 Minute Veterinary Consult Canine and Feline}, journal={The 5 Minute Veterinary Consult Canine and Feline}, publisher={Williams and Wilkins}, author={DeFrancesco, T.C.}, editor={Tilley, L.P. and Smith, F.W.K.Editors}, year={1997}, pages={1093} }
 @article{defrancesco_atkins_keene_1996, title={Myocardial infarction complicating management of congestive heart failure in a dog}, volume={32}, ISSN={["0587-2871"]}, DOI={10.5326/15473317-32-1-68}, abstractNote={A 7.5-kg, 10-year-old, spayed female, mixed-breed dog was evaluated for sudden onset of weakness, tachypnea, and an irregular cardiac rhythm. Congestive heart failure secondary to mitral valve regurgitation had been diagnosed six weeks earlier. The dog was stable on furosemide, enalapril, and hydralazine. Complex ventricular tachycardia, altered QRS conformation of sinus complexes, echocardiographic evidence of a hypokinetic left-ventricular free wall, and elevated creatine kinase suggested a diagnosis of myocardial infarction. Despite antiarrhythmic therapy, the dog developed ventricular fibrillation and died 36 hours after admission. Postmortem examination confirmed the myocardial infarction. Although a rare diagnosis in the veterinary patient, myocardial infarction must be considered in the differential diagnosis for sudden onset of weakness, tachypnea, and ventricular tachycardia.}, number={1}, journal={JOURNAL OF THE AMERICAN ANIMAL HOSPITAL ASSOCIATION}, author={DeFrancesco, TC and Atkins, CE and Keene, BW}, year={1996}, pages={68–72} }
 @inbook{moise_defrancesco_1995, place={Philadelphia}, title={Ambulatory (Holter) Electrocardiography}, booktitle={Kirk’s Current Veterinary Therapy XII}, publisher={WB Saunders}, author={Moise, N.S. and DeFrancesco, T.C.}, editor={Bonagura, J.D. and Kirk, R.W.Editors}, year={1995}, pages={792–799} }
 @article{schulz_baruffaldi_carrig_defrancesco_1993, title={What Is Your Diagnosis?}, volume={203}, number={5}, journal={Journal of the American Veterinary Medical Association}, author={Schulz, K. and Baruffaldi, J. and Carrig, C. and DeFrancesco, T.C.}, year={1993}, pages={645–646} }