@article{vereb_atkins_adin_blondel_coffman_lee_guillot_ward_2023, title={Efficacy of a mitral regurgitation severity index to predict long-term outcome in dogs with myxomatous mitral valve disease}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16923}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Vereb, Michelle and Atkins, Clarke E. and Adin, Darcy and Blondel, Thomas and Coffman, Melissa and Lee, Seunggon and Guillot, Emilie and Ward, Jessica L.}, year={2023}, month={Nov} }
 @article{adin_atkins_domenig_glahn_defrancesco_meurs_2023, title={Evaluation of Renin-Angiotensin-Aldosterone System Components and Enzymes in Systemically Hypertensive Cats Receiving Amlodipine}, volume={13}, ISSN={["2076-2615"]}, url={https://www.mdpi.com/2076-2615/13/22/3479}, DOI={10.3390/ani13223479}, abstractNote={Background: Chronic renin–angiotensin–aldosterone system (RAAS) activation is harmful. Amlodipine activates RAAS in humans and dogs, but contradictory data exist for systemically hypertensive (SHT) cats. Hypothesis: Cats with SHT and chronic kidney disease treated with amlodipine (SHT/CKD-A) are RAAS activated. Animals: Client-owned cats: unmedicated normotensive (NT) cats (n = 9); SHT/CKD-A cats (n = 5) with median systolic blood pressure of 170 mmHg (vs. 195 mmHg, pre-treatment), chronic kidney disease, and receiving no RAAS-suppressive therapy. Methods: Serum was frozen (−80 °C) until RAAS analysis via equilibrium analysis. The RAAS variables (reported as median (minimum–maximum)) were compared between groups, using Mann–Whitney U test. Results: Angiotensin 1, angiotensin 1,7, angiotensin III, and angiotensin 1,5, and angiotensin-converting enzyme (ACE)-2 activity were higher in SHT/CKD-A cats compared to NT cats, while ACE activity was lower in SHT/CKD-A cats compared to NT cats (p < 0.05 all). A marker for alternative RAAS influence (ALT-S) was significantly higher (69; 58–73 pmol/pmol) in SHT/CKD-A cats compared to NT cats (35; 14–63 pmol/pmol; p = 0.001). Aldosterone concentrations were significantly higher (393; 137–564 pmol/L) in SHT/CKD-A cats compared to NT cats (129; 28–206 pmol/L; p = 0.007). Conclusion and Clinical Importance: Circulating RAAS is activated in systemically hypertensive cats receiving amlodipine. Although this study did not parse out the individual contributions of SHT, chronic kidney disease, and amlodipine, the findings suggest that the use of concurrent RAAS-suppressant therapy, specifically aldosterone antagonism, in amlodipine-treated SHT cats with chronic kidney disease might be indicated.}, number={22}, journal={ANIMALS}, author={Adin, Darcy and Atkins, Clarke and Domenig, Oliver and Glahn, Catherine and Defrancesco, Teresa and Meurs, Kathryn}, year={2023}, month={Nov} }
 @article{ames_vaden_atkins_palerme_langston_grauer_shropshire_bove_webb_2022, title={Prevalence of aldosterone breakthrough in dogs receiving renin-angiotensin system inhibitors for proteinuric chronic kidney disease}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16573}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ames, Marisa K. and Vaden, Shelly L. and Atkins, Clarke E. and Palerme, Jean-Sebastien and Langston, Catherine E. and Grauer, Gregory F. and Shropshire, Sarah and Bove, Christina and Webb, Tracy}, year={2022}, month={Nov} }
 @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={Summary}, 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{coffman_guillot_blondel_garelli-paar_feng_heartsill_atkins_2021, title={Clinical efficacy of a benazepril and spironolactone combination in dogs with congestive heart failure due to myxomatous mitral valve disease: The BEnazepril Spironolactone STudy (BESST)}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16155}, abstractNote={Abstract}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Coffman, Melissa and Guillot, Emilie and Blondel, Thomas and Garelli-Paar, Catherine and Feng, Shuo and Heartsill, Susanne and Atkins, Clarke E.}, year={2021}, month={May} }
 @article{adin_atkins_londono_del nero_2021, title={Correction of serum chloride concentration in dogs with congestive heart failure}, volume={35}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.15998}, abstractNote={Abstract}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Adin, Darcy and Atkins, Clarke and Londono, Leonel and Del Nero, Bruna}, year={2021}, month={Jan}, pages={51–57} }
 @article{adin_atkins_wallace_klein_2021, title={Effect of spironolactone and benazepril on furosemide-induced diuresis and renin-angiotensin-aldosterone system activation in normal dogs}, volume={35}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.16097}, abstractNote={Abstract}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Adin, Darcy and Atkins, Clarke and Wallace, Gabrielle and Klein, Allison}, year={2021}, month={May}, pages={1245–1254} }
 @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={Dear Editors, 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 trial 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 angiotensinconverting 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. 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. 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 amlodipine; with ACEI in natural MMVD before CHF (without furosemide); and in MMVD with CHF in dogs receiving ACEI and furosemide. Furthermore, inclusion of MRAs in therapeutic protocols has improved survival in CHF caused by MMVD. 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. 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. For this Received: 11 January 2021 Accepted: 12 January 2021}, 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={Abstract}, 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{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={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. Thirty-two client-owned cats with subclinical HCM and 27 healthy control cats. 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. 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. 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{ames_vanvranken_evans_atkins_2020, title={Non-Arsenical heartworm adulticidal therapy using topical moxidectin-imidacloprid and doxycycline: A prospective case series}, volume={282}, ISSN={["1873-2550"]}, DOI={10.1016/j.vetpar.2020.109099}, abstractNote={Abstract This prospective case series evaluated the adulticidal efficacy of topical 10 % moxidectin/2.5 % imidacloprid (M/I; Advantage Multi®, Bayer, Shawnee Mission, KS, USA) and doxycycline in dogs with naturally occurring heartworm infection (HWI). Twenty-two dogs with HWI whose owners declined melarsomine were treated with M/I at the preventive dosage twice monthly for 90 days then monthly thereafter and doxycycline (median [interquartile range; IQR] dosage 12.6 [12.0–16.1] mg/kg/day) for the first 15 days. Although strict activity restriction was not imposed, owners were asked to prevent their dogs from exercising strenuously. This protocol was referred to as the MOXY protocol. Antigen testing was performed every 30–60 days, until dogs had ‘no antigen detected’ (NAD). Twenty-one of the 22 dogs ultimately converted to NAD by 434 days (median [IQR]), 234 (179–303). One dog remained positive 701 days after MOXY initiation and was considered a treatment failure. All sera which converted to NAD on HW antigen testing were retested after heat-treatment. Twelve dogs had NAD on the heat-treated test on the same day as having their first NAD on the conventional test. Six of 9 dogs testing positive after heat-treatment were retested and all 6 had NAD on a heat-treated test within 2–3 months. Microfilaremia was cleared in all 8 dogs re-tested. Four dogs required treatment for cough, thought due to heartworm (HW) death, an average of 89 days after initiation of MOXY. This cough was most likely due to pneumonitis with heartworm-pulmonary thromboembolism. One dog required hospitalization for 24 -h and recovered fully with corticosteroid therapy and supportive care and 2 dogs were treated in an outpatient fashion with steroids. The MOXY protocol was tolerated and 96 % (21/22) of dogs converted to NAD, though 2 dogs required greater than 1 year to achieve this result. Nonaresenical-adulticide therapy may result in pneumonitis and heartworm-pulmonary thromboembolism at unpredictable times, potentially months after initiation of macrocyclic lactone therapy and exercise restriction should be considered when using a nonarsenical protocol. Although not currently recommended by the American Heartworm Society (AHS), non-arsenical strategies are in use and the goal of this study was to evaluate the efficacy, duration of therapy, and safety of an accelerated dosing protocol of M/I with doxycycline.}, journal={VETERINARY PARASITOLOGY}, author={Ames, Marisa K. and VanVranken, Philip and Evans, Chelsea and Atkins, Clarke E.}, year={2020}, month={Jun} }
 @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={Abstract}, 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{ames_atkins_2020, title={Treatment of dogs with severe heartworm disease}, volume={283}, ISSN={["1873-2550"]}, DOI={10.1016/j.vetpar.2020.109131}, abstractNote={Fortunately, the majority of dogs diagnosed with heartworm infection are asymptomatic (or have only mild symptoms such as intermittent cough) and go through adulticide therapy without complication. Complications occurring with heartworm infection and during its treatment most often directly reflect the pulmonary vascular and parenchymal injury inflicted by Dirofilaria immitis. Clinical signs may include exercise intolerance, frequent cough, hemoptysis, tachypnea, and dyspnea. Severe manifestations such as heart failure and caval syndrome may prove fatal. Acute hypersensitivity reactions after initiation of macrocyclic lactone preventive therapy in microfilaremic dogs or after melarsomine injection during adulticide therapy do occur, but are uncommon. This article reviews complications associated with heartworm infection.}, journal={VETERINARY PARASITOLOGY}, author={Ames, Marisa K. and Atkins, Clarke E.}, year={2020}, month={Jul} }
 @article{keene_atkins_bonagura_fox_haggstrom_fuentes_oyama_rush_stepien_uechi_et al._2019, title={ACVIM consensus guidelines for the diagnosis and treatment of myxomatous mitral valve disease in dogs}, volume={33}, ISSN={["1939-1676"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85064530654&partnerID=MN8TOARS}, DOI={10.1111/jvim.15488}, abstractNote={Abstract}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Keene, Bruce W. and Atkins, Clarke E. and Bonagura, John D. and Fox, Philip R. and Haggstrom, Jens and Fuentes, Virginia Luis and Oyama, Mark A. and Rush, John E. and Stepien, Rebecca and Uechi, Masami and et al.}, year={2019}, month={May}, pages={1127–1140} }
 @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{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} }
 @misc{ames_atkins_pitt_2019, title={The renin-angiotensin-aldosterone system and its suppression}, volume={33}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.15454}, abstractNote={Chronic activation of the renin‐angiotensin‐aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro‐fibrotic, ‐inflammatory, and ‐hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ames, Marisa K. and Atkins, Clarke E. and Pitt, Bertram}, year={2019}, pages={363–382} }
 @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{adin_atkins_papich_2018, title={Pharmacodynamic assessment of diuretic efficacy and braking in a furosemide continuous infusion model}, volume={20}, ISSN={["1875-0834"]}, url={https://doi.org/10.1016/j.jvc.2018.01.003}, DOI={10.1016/j.jvc.2018.01.003}, abstractNote={Diuretic failure is a potential life-ending event but is unpredictable and poorly understood. The objectives of this study were to evaluate pharmacodynamic markers of furosemide-induced diuresis and to investigate mechanisms of diuretic braking in dogs receiving constant rate infusion (CRI) of furosemide. Six healthy male dogs. Raw data and stored samples from one arm of a previously published study were further analyzed to mechanistically investigate causes of diuretic braking in these dogs. Urine volume was recorded hourly during a 5-h furosemide CRI. Urine and blood samples were collected hourly to measure serum and urine electrolytes, urine aldosterone, and plasma and urine furosemide. Serum electrolyte fractional excretion was calculated. Urine sodium concentration was indexed to urine potassium (uNa:uK) and urine furosemide (uNa:uFur) concentrations, plasma furosemide concentration was indexed to urine furosemide concentration (pFur:uFur), and urine aldosterone was indexed to urine creatinine (UAldo:C). Temporal change and the relationship to urine volume were evaluated for these measured and calculated variables. Urine volume was significantly correlated with urine electrolyte amounts and with uNa:uK. The ratio of pFur:uFur decreased during the infusion, whereas furosemide excretion was unchanged. There was a strong relationship between urine volume and absolute urine electrolyte excretion. Urine volume was strongly correlated to uNa:uK, giving it potential as a spot indicator of urine production during diuresis. The decrease in uNa:uK over time during the infusion is consistent with mineralocorticoid modification of urinary electrolyte excretion, supporting renin–angiotensin–aldosterone activation as a cause of diuretic braking in this model.}, number={2}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, publisher={Elsevier BV}, author={Adin, D. and Atkins, C. and Papich, M. G.}, year={2018}, month={Apr}, pages={92–101} }
 @article{ames_atkins_eriksson_hess_2017, title={Aldosterone breakthrough in dogs with naturally occurring myxomatous mitral valve disease}, volume={19}, ISSN={["1875-0834"]}, DOI={10.1016/j.jvc.2017.03.001}, abstractNote={Aldosterone breakthrough (ABT) is the condition in which angiotensin converting enzyme inhibitors (ACEIs) and/or angiotensin receptor blockers fail to effectively suppress the activity of the renin angiotensin aldosterone system. The objective of this study was to determine if ABT occurs in dogs with naturally occurring myxomatous mitral valve disease receiving an ACEI, using the urine aldosterone to creatinine ratio (UAldo:C) as a measure of renin angiotensin aldosterone system activation.This study includes 39 dogs with myxomatous mitral valve disease. A UAldo:C cut-off definition (derived from a normal population of healthy, adult, and client-owned dogs) was used to determine the prevalence of ABT in this population. Spearman analysis and univariate logistic regression were used to evaluate the relationship between UAldo:C and ABT (yes/no) and eight variables (age, serum K+ concentration, serum creatinine concentration, ACEI therapy duration and ACEI dosage, furosemide therapy duration and furosemide dosage, and urine sample storage time). Finally, the UAldo:C in dogs receiving spironolactone, as part congestive heart failure (CHF) therapy, was compared to dogs with CHF that were not receiving spironolactone.The prevalence of ABT was 32% in dogs with CHF and 30% in dogs without CHF. There was no relationship between either the UAldo:C or the likelihood of ABT and the eight variables. Therapy with spironolactone lead to a significant elevation of the UAldo:C.Using the UAldo:C and a relatively stringent definition of ABT, it appears that incomplete RAAS blockade is common in dogs with MMVD receiving an ACEI. The prevalence of ABT in this canine population mirrors that reported in humans. While the mechanism of ABT is likely multifactorial and still poorly understood, the proven existence of ABT in dogs offers the potential to improve the prognosis for MMVD with the addition of a mineralocorticoid receptor blocker to current therapeutic regimens.Approximately 30% of dogs being treated for heart disease and CHF satisfied the definition of ABT. Identifying patient subpopulations experiencing ABT may help guide future study design and clinical decision-making.}, number={3}, journal={JOURNAL OF VETERINARY CARDIOLOGY}, author={Ames, M. K. and Atkins, C. E. and Eriksson, A. and Hess, A. M.}, year={2017}, month={Jun}, pages={218–227} }
 @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"]}, url={https://europepmc.org/articles/PMC5843865}, DOI={10.1177/1470320317737184}, abstractNote={Objective: 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. Methods: 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). Results: 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. Conclusion: 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{mathews_coleman_atkins_2017, title={ECG of the month}, volume={250}, DOI={10.2460/javma.250.2.166}, number={2}, journal={Journal of the American Veterinary Medical Association}, author={Mathews, J. S. and Coleman, A. E. and Atkins, C. E.}, year={2017}, pages={166–168} }
 @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{ames_atkins_lantis_brunnen_2016, title={Evaluation of subacute change in RAAS activity (as indicated by urinary aldosterone: creatinine, after pharmacologic provocation) and the response to ACE inhibition}, volume={17}, ISSN={["1752-8976"]}, DOI={10.1177/1470320316633897}, abstractNote={Objective: The objective of this study was to evaluate subacute changes in renin–angiotensin–aldosterone system (RAAS) activity during angiotensin-converting enzyme inhibitor (ACEI) therapy in dogs with experimental RAAS activation. Methods: Analysis of data (urine aldosterone:creatinine ratio (UAldo:C) and serum angiotensin-converting enzyme activity), in 31 healthy dogs with furosemide or amlodipine-activated RAAS that received an ACEI. When furosemide or amlodipine activation of RAAS preceded ACEI administration, incomplete RAAS blockade (IRB) was defined as a UAldo:C greater than (a) the dog’s ‘activated’ baseline value or (b) a population-derived cut-off value (mean + 2 SD (>1.0 μg/g) of pretreatment UAldo:C from our population of research dogs). In studies where RAAS activation occurred concurrently with ACEIs, IRB was defined as (a) a UAldo:C greater than either twofold the dog’s prestimulation baseline value or (b) 1.0 µg/g. Dogs were followed for 7–17 days. Results: Serum angiotensin-converting enzyme activity was measured in 19 dogs and was significantly reduced (P<0.0001) after ACEI administration. The overall incidence of IRB, when RAAS activation preceded ACEI administration, was 33% and 8% for definitions (a) and (b), respectively. The overall incidence of IRB, when ACEIs were concurrent with RAAS activation, was 65% and 61% for definitions (a) and (b), respectively. Conclusion: Increases in UAldo:C, despite ACEI administration, is evidence of IRB in this subacute model of experimental RAAS activation and suppression.}, number={1}, journal={JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM}, author={Ames, Marisa K. and Atkins, Clarke E. and Lantis, Andrea C. and Brunnen, James}, year={2016} }
 @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{pouchelon_atkins_bussadori_oyama_vaden_bonagura_chetboul_cowgill_elliot_francey_et al._2015, title={Cardiovascular-renal axis disorders in the domestic dog and cat: a veterinary consensus statement}, volume={56}, ISSN={["1748-5827"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84940504868&partnerID=MN8TOARS}, DOI={10.1111/jsap.12387}, abstractNote={OBJECTIVESThere is a growing understanding of the complexity of interplay between renal and cardiovascular systems in both health and disease. The medical profession has adopted the term “cardiorenal syndrome” (CRS) to describe the pathophysiological relationship between the kidney and heart in disease. CRS has yet to be formally defined and described by the veterinary profession and its existence and importance in dogs and cats warrant investigation. The CRS Consensus Group, comprising nine veterinary cardiologists and seven nephrologists from Europe and North America, sought to achieve consensus around the definition, pathophysiology, diagnosis and management of dogs and cats with “cardiovascular‐renal disorders” (CvRD). To this end, the Delphi formal methodology for defining/building consensus and defining guidelines was utilised.}, number={9}, journal={JOURNAL OF SMALL ANIMAL PRACTICE}, author={Pouchelon, J. L. and Atkins, C. E. and Bussadori, C. and Oyama, M. A. and Vaden, S. L. and Bonagura, J. D. and Chetboul, V. and Cowgill, L. D. and Elliot, J. and Francey, T. and et al.}, year={2015}, month={Sep}, pages={537–552} }
 @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={BackgroundTransvenous 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.}, 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{ames_atkins_lee_lantis_zumbrunnen_2015, title={Effects of high doses of enalapril and benazepril on the pharmacologically activated renin-angiotensin-aldosterone system in clinically normal dogs}, volume={76}, ISSN={["1943-5681"]}, DOI={10.2460/ajvr.76.12.1041}, abstractNote={Abstract}, number={12}, journal={AMERICAN JOURNAL OF VETERINARY RESEARCH}, author={Ames, Marisa K. and Atkins, Clarke E. and Lee, Seunggon and Lantis, Andrea C. and zumBrunnen, James R.}, year={2015}, month={Dec}, pages={1041–1050} }
 @article{schneider_ames_dicicco_savage_atkins_wood_gookin_2015, title={Recovery of normal esophageal function in a kitten with diffuse megaesophagus and an occult lower esophageal stricture}, volume={17}, ISSN={["1532-2750"]}, DOI={10.1177/1098612x14542451}, abstractNote={ An 8-week-old male domestic shorthair was presented to the Internal Medicine Service at North Carolina State University for regurgitation. Radiographic diagnosis of generalized esophageal dilation and failure of esophageal peristalsis were compatible with diagnosis of congenital megaesophagus. Endoscopic examination of the esophagus revealed a fibrous stricture just orad to the lower esophageal sphincter. Conservative management to increase the body condition and size of the kitten consisted of feeding through a gastrostomy tube, during which time the esophagus regained normal peristaltic function, the stricture orifice widened in size and successful balloon dilatation of the stricture was performed. Esophageal endoscopy should be considered to rule out a stricture near the lower esophageal sphincter in kittens with radiographic findings suggestive of congenital megaesophagus. Management of such kittens by means of gastrostomy tube feeding may be associated with a return of normal esophageal motility and widening of the esophageal stricture, and facilitate subsequent success of interventional dilation of the esophageal stricture. }, number={6}, journal={JOURNAL OF FELINE MEDICINE AND SURGERY}, author={Schneider, Jaycie and Ames, Marisa and DiCicco, Michael and Savage, Mason and Atkins, Clarke and Wood, Michael and Gookin, Jody L.}, year={2015}, month={Jun}, pages={557–561} }
 @article{lantis_ames_werre_atkins_2015, title={The effect of enalapril on furosemide-activated renin-angiotensin-aldosterone system in healthy dogs}, volume={38}, ISSN={["1365-2885"]}, DOI={10.1111/jvp.12216}, abstractNote={Studies in our laboratory have revealed that furosemide‐induced RAAS activation, evaluated via the urine aldosterone‐to‐creatinine ratio (UAldo:C), was not attenuated by the coadministration of benazepril, while enalapril successfully suppressed amlodipine‐induced urinary aldosterone excretion. This study was designed to evaluate the efficacy of enalapril in suppressing ACE activity and furosemide‐induced circulating RAAS activation. Failure to do so would suggest that this failure may be a drug class effect. We hypothesized that enalapril would suppress ACE activity and furosemide‐induced circulating RAAS activation. Sixteen healthy hound dogs. The effect of furosemide (2 mg/kg PO, q12 h; Group F) and furosemide plus enalapril (0.5 mg/kg PO, q12 h; Group FE) on circulating RAAS was determined by plasma ACE activity, 4–6 h post‐treatment, and urinary A:C on days −1, −2, 1, 4, and 7. There was a significant increase in the average urine aldosterone‐to‐creatinine ratio (UAldo:C) after administration of furosemide (P < 0.05). Enalapril inhibited ACE activity (P < 0.0001) but did not significantly reduce aldosterone excretion. A significant (P < 0.05) increase in the UAldo:C was maintained for the 7 days of the study in both groups. Enalapril decreased plasma ACE activity; however, it did not suppress furosemide‐induced RAAS activation, as determined by the UAldo:C. While enalapril blunts ACE activity, the absence of circulating RAAS suppression may be due to angiotensin II reactivation, alternative RAAS pathways, and furosemide overriding concurrent ACE inhibition, all indicating the existence of aldosterone breakthrough (ABT). Along with similar findings with benazepril, it appears that failure to suppress aldosterone suppression with furosemide stimulation may be a drug class effect. The discrepancy between the current data and the documented benefits of enalapril likely reflects the efficacy of this ACE inhibitor in suppressing tissue RAAS, variable population responsiveness to ACE‐inhibition, and/or providing additional survival benefits, possibly through as yet unknown mechanisms.}, number={5}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Lantis, A. C. and Ames, M. K. and Werre, S. and Atkins, C. E.}, year={2015}, month={Oct}, pages={513–517} }
 @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"]}, url={https://doi.org/10.2460/javma.245.5.534}, DOI={10.2460/javma.245.5.534}, abstractNote={Abstract}, 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} }
 @article{atkins_murray_olavessen_burton_marshall_brooks_2014, title={Heartworm 'lack of effectiveness' claims in the Mississippi delta: Computerized analysis of owner compliance-2004-2011}, volume={206}, ISSN={["1873-2550"]}, DOI={10.1016/j.vetpar.2014.08.013}, abstractNote={A retrospective medical record review was conducted to identify factors from veterinary clinic medical records that may have contributed to suspected ineffectiveness of a heartworm preventive product. Patient records of 271 dogs, comprising 301 instances of positive heartworm antigen test results while the dogs were receiving heartworm preventive were evaluated. Nineteen veterinary practices in 17 counties and parishes in Arkansas, Louisiana, Mississippi, and Tennessee participated in the study. Records were selected by the veterinary clinics as representative of cases of suspected lack of effectiveness for a heartworm preventive, and for which an owner satisfaction claim had been filed with the manufacturer. Medical record data were entered into a software program, and a graphic representation was created to facilitate analysis of whether pet owners had purchased sufficient heartworm preventive for the dog to be compliant during the period when infection with Dirofilaria immitis could have led to the positive heartworm antigen test result for that patient (“window of infection”). In 243 (80.7%) cases, there was insufficient heartworm preventive purchased, leading to a gap in protection during the “window of infection”. In only five cases (1.7%) there were no purchase lapses or extenuating circumstances (underdosing of medication, multiple purchase gaps outside the established window of infection, or dogs have been diagnosed with heartworm infection more than once during the period studied). Half the cases were from multiple-dog households, and in many of these households, sharing of product between pets was acknowledged. In another 28% of the cases from multiple-dog households, more product was purchased than was needed for one dog, suggesting that the product was being shared between more than one pet. In most cases, there was at least one reason that a dog did not receive sufficient heartworm preventive product, placing the dog at risk of developing an infection with mature heartworms. Several actions were identified that veterinary clinics can take to improve heartworm disease prevention in their patients.}, number={1-2}, journal={VETERINARY PARASITOLOGY}, author={Atkins, Clarke E. and Murray, Michael J. and Olavessen, Lauren J. and Burton, K. Wade and Marshall, James W. and Brooks, Christopher C.}, year={2014}, month={Nov}, pages={106–113} }
 @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"]}, url={https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/jvim.12163}, DOI={10.1111/jvim.12163}, abstractNote={BackgroundMyocardial 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.}, 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{ames_atkins_lantis_were_2013, title={Effect of furosemide and high-dosage pimobendan administration on the renin-angiotensin-aldosterone system in dogs}, volume={74}, DOI={10.2460/ajvr.74.8.1084}, abstractNote={Abstract}, number={8}, journal={American Journal of Veterinary Research}, author={Ames, M. K. and Atkins, C. E. and Lantis, A. C. and Were, S. R.}, year={2013}, pages={1084–1090} }
 @article{lefebvre_ollivier_atkins_combes_concordet_kaltsatos_baduel_2013, title={Safety of Spironolactone in Dogs with Chronic Heart Failure because of Degenerative Valvular Disease: A Population-Based, Longitudinal Study}, volume={27}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.12141}, abstractNote={BackgroundSpironolactone treatment in humans is associated with an increased risk of hyperkalemia and renal dysfunction.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Lefebvre, H. P. and Ollivier, E. and Atkins, C. E. and Combes, B. and Concordet, D. and Kaltsatos, V. and Baduel, L.}, year={2013}, month={Sep}, pages={1083–1091} }
 @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} }
 @article{atkins_vaden_arther_ciszewski_davis_ensley_chopade_2011, title={Renal effects of Dirofilaria immitis in experimentally and naturally infected cats}, volume={176}, ISSN={["1873-2550"]}, DOI={10.1016/j.vetpar.2011.01.016}, abstractNote={Canine heartworm infection has been associated with glomerular disease and proteinuria. We hypothesized that proteinuria, likely due to glomerular damage, would also be found in cats experimentally and naturally infected with Dirofilaria immitis. Two populations of cats were evaluated, including 80 that were each experimentally infected with 60 infective heartworm larvae as part of a drug safety study, and 31 that were naturally infected with D. immitis. Each had a control population with which to be compared. In the experimentally infected group, we evaluated urine from 64 cats. Ten of these cats were shown to have microalbuminuria 8 months post infection. No cat refractory to infection with larvae and no cats from the control group demonstrated microalbuminuria. All 10 microalbuminuric cats were shown to have significant proteinuria, as measured by the urine protein:creatinine ratio. There was a subtle, but significant, association between worm burden and proteinuria, and although the presence of adult heartworms was required for the development of proteinuria, both microfilaremic and amicrofilaremic cats were affected. Neither the presence of circulating heartworm antibodies and antigen nor the presence of antigenuria predicted the development of proteinuria. Both heavily infected cats (5–25 adult heartworms) and cats with worm burdens compatible with natural infections (1–4 adult heartworms) developed proteinuria, and the relative numbers of cats so affected were similar between heavily and more lightly infected cats. Naturally infected cats, for which only dipstick protein determinations were available, were shown to have a significantly greater incidence of proteinuria (90% vs 35%) than did those in an age- and gender-matched control population. Additionally, the proteinuria in heartworm-infected cats was 3- to 5-fold greater in severity. We conclude that cats infected with mature adult heartworms are at risk for developing proteinuria and that this is recognized relatively soon after infection. While heavier infections may predispose cats to developing proteinuria, this complication is seen in naturally infected cats and experimental cats with worm burdens similar to those seen in natural infections (i.e., “clinically appropriate” worm burdens). The clinical relevance of heartworm-associated proteinuria is yet to be determined.}, number={4}, journal={VETERINARY PARASITOLOGY}, author={Atkins, C. E. and Vaden, S. L. and Arther, R. G. and Ciszewski, D. K. and Davis, W. L. and Ensley, S. M. and Chopade, N. H.}, year={2011}, month={Mar}, pages={317–323} }
 @misc{lee_atkins_2010, title={Understanding Feline Heartworm Infection Disease, Diagnosis, and Treatment}, volume={25}, ISSN={["1946-9837"]}, DOI={10.1053/j.tcam.2010.09.003}, abstractNote={Feline heartworm disease is a very different clinical entity from canine heartworm disease. In cats, the arrival and death of immature heartworms in the pulmonary arteries can cause coughing and dyspnea as early as 3 months postinfection. Adult heartworms suppress the function of pulmonary intravascular macrophages and thus reduce clinical disease in chronic feline heartworm infection. Approximately 80% of asymptomatic cats self-cure. Median survival time for symptomatic cats is 1.5 years, or 4 years if only cats living beyond the day of presentation are considered. Aberrant worm migration is more frequent than it is in dogs, and sudden death can occur with no prior clinical signs. The bacterial endosymbiont Wolbachia likely contributes to the inflammatory pathology of heartworm disease, but its role is not yet fully clear. Unfortunately, the diagnosis, treatment, and management of feline heartworm disease are far from simple. Antemortem diagnosis is hampered by low worm burdens, the frequency of all-male infections, and nonspecific radiographic lesions. It is up to the veterinarian to determine the correct index of suspicion and choose the right combination of diagnostic tests to achieve an answer. Treatment is symptomatic because adulticide therapy is risky and does not increase survival time. Despite the dangers of feline heartworm disease, less than 5% of cats in the United States are on chemoprophylaxis. It is important for veterinarians to take a proactive preventive stance because heartworm infection in cats is a multisystemic disease that has no easy cure.}, number={4}, journal={TOPICS IN COMPANION ANIMAL MEDICINE}, author={Lee, Alice C. Y. and Atkins, Clarke E.}, year={2010}, month={Nov}, pages={224–230} }
 @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.}, 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{litster_atkins_atwell_2009, title={Acute death in heartworm-infected cats: Unraveling the puzzle (vol 158, pg 196, 2008)}, volume={163}, number={4}, journal={Veterinary Parasitology}, author={Litster, A. and Atkins, C. and Atwell, R.}, year={2009}, pages={376–376} }
 @article{lantis_atkins_2009, title={ECG of the Month}, volume={235}, ISSN={["1943-569X"]}, DOI={10.2460/javma.235.5.514}, number={5}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Lantis, Andrea C. and Atkins, Clarke E.}, year={2009}, month={Sep}, pages={514–516} }
 @misc{atkins_bonagura_ettinger_fox_gordon_haggstrom_hamlin_keene_luis-fuentes_stepien_2009, title={Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease}, volume={23}, ISSN={["1939-1676"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-70350430448&partnerID=MN8TOARS}, DOI={10.1111/j.1939-1676.2009.0392.x}, abstractNote={his is the report of the American College of Veteri-nary Internal Medicine (ACVIM) Specialty ofCardiology consensus panel convened to formulateguidelines forthe diagnosis andtreatment ofchronicval-vularheartdisease (CVHD, also knownas endocardiosisand myxomatous valve degeneration) in dogs. It is esti-mated that approximately 10% of dogs presented toprimary care veterinary practices have heart disease, andCVHD is the most common heart disease of dogs inmany parts of the world, accounting for approximately75% of canine cases of heart disease cases seen by veter-inary practices in North America.CVHD most commonly affects the left atrioventricu-lar or mitral valve, although in approximately 30% ofcases the right atrioventricular (tricuspid) valve also isinvolved. The disease is approximately 1.5 times morecommon in males than in females. Its prevalence is alsohigher in smaller (o20kg) dogs, although large breedsoccasionally are affected.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Atkins, C. and Bonagura, J. and Ettinger, S. and Fox, P. and Gordon, S. and Haggstrom, J. and Hamlin, R. and Keene, B. and Luis-Fuentes, V. and Stepien, R.}, year={2009}, pages={1142–1150} }
 @article{bowman_atkins_2009, title={Heartworm Biology, Treatment, and Control}, volume={39}, ISSN={["1878-1306"]}, DOI={10.1016/j.cvsm.2009.06.003}, abstractNote={This article is a review of the systematics, taxonomy, biology, prevention, control, and treatment of the canine heartworm, Dirofilaria immitus. This filarioid parasite remains one of the most important and dangerous diseases of the dog throughout the United States. The geographic range of the parasite is expanding, and in many parts of the country it has emerged as a threat to canine welfare only in the last 50 or so years. The article also discusses the pathophysiological mechanisms behind the disease induced, the means for diagnosing the disease, and the means of assessing the success of therapy. The treatment of potential complications of heartworm infection, such as post-adulticide thromboembolism, eosinophilic granulomatous pneumonitis, and caval syndrome, is also discussed.}, number={6}, journal={VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE}, author={Bowman, Dwight D. and Atkins, Clarke E.}, year={2009}, month={Nov}, pages={1127-+} }
 @article{atkins_arther_ciszewski_davis_ensley_guity_chopade_hoss_settje_2008, title={Echocardiographic quantification of Dirofilaria immitis in experimentally infected cats}, volume={158}, ISSN={["0304-4017"]}, DOI={10.1016/j.vetpar.2008.09.003}, abstractNote={The safety of heartworm preventives in heartworm-positive cats has traditionally been evaluated using adult Dirofilaria immitis removed from infected dogs and surgically implanted into the cats. An alternate study model uses infective larvae to establish adult infections in cats. Unfortunately, the number of adult worms resulting from the latter method varies widely from none to more than 30, both unacceptable for studies of natural heartworm infection and for studies evaluating product safety in heartworm-infected cats. We sought to determine infection severity in experimental infections via echocardiography to reduce the chances of enrolling uninfected and heavily infected cats into a study. Eighty adult cats were each inoculated with 60 infective D. immitis larvae and maintained for 8 months to allow for the development of adult worms. Antigen and antibody testing, as well as echocardiographic imaging, were performed to confirm and estimate adult worm burdens. Approximately 8 and 12 months post-infection, echocardiographic examination was performed to confirm and enumerate adult D. immitis populations in the cardiovascular system. Worm burdens were stratified as 0, 1-3, 4-11, and > 11 adults, with 0 being considered uninfected and more than 11 considered too heavily infected to be relevant for anthelmintic studies. Cats with clinically relevant infections (1-10 adults) subsequently received multiple treatments with the investigational drug, and worm burdens were confirmed by necropsy 30 days following the final treatment. Worm burden estimated with echocardiography correlated well, but not precisely, with post-mortem counts (p < 0.001, r2 = 0.67). Echocardiography under-, over-, and exactly estimated heartworm burden 53%, 27%, and 22% of the time, respectively. Although the correct category (0-4) was determined by echocardiography in only 54% of cats, positive cats were distinguished from negative cats 88% of the time and the heaviest infections (> 11) were correctly categorized 95% of the time. Both false negative and false positive results were observed. We conclude that echocardiography is useful for detecting mature experimental heartworm infections, identifying cats that have rejected mature infection, and detecting very heavy heartworm burdens, but it is only moderately accurate in classifying lesser burdens. While echocardiography cannot be relied upon to consistently determine the exact heartworm burden in experimentally infected cats, it is useful in stratifying worm burdens for anthelmintic safety studies.}, number={3}, journal={VETERINARY PARASITOLOGY}, author={Atkins, C. E. and Arther, R. G. and Ciszewski, D. K. and Davis, W. L. and Ensley, S. M. and Guity, P. S. and Chopade, H. and Hoss, H. and Settje, T. L.}, year={2008}, month={Dec}, pages={164–170} }
 @misc{atkins_2008, title={Questions terminology in heartworm infection commentary - The author responds}, volume={232}, number={2}, journal={Journal of the American Veterinary Medical Association}, author={Atkins, C. E.}, year={2008}, pages={194–194} }
 @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={Abstract}, 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} }
 @article{small_atkins_gordon_birkenheuer_booth-sayer_keene_fujii_miller_2008, title={Use of a nitinol gooseneck snare catheter for removal of adult Dirofilaria immitis in two cats}, volume={233}, ISSN={["0003-1488"]}, DOI={10.2460/javma.233.9.1441}, abstractNote={Abstract}, number={9}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Small, Merrilee T. and Atkins, Clarke E. and Gordon, Sonya G. and Birkenheuer, Adam J. and Booth-Sayer, Margaret A. and Keene, Bruce W. and Fujii, Yoko and Miller, Matthew W.}, year={2008}, month={Nov}, pages={1441–1445} }
 @article{johansson_gardner_atkins_lafevers_breuhaus_2007, title={Cardiovascular effects of acute pulmonary obstruction in horses with recurrent airway obstruction}, volume={21}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2007)21[302:CEOAPO]2.0.CO;2}, abstractNote={Recurrent airway obstruction (RAO) is common in horses. Although pulmonary artery (PA) pressure increases during RAO, cardiac function in horses with RAO has received limited attention.The purpose of this study was to noninvasively determine the cardiovascular effects of acute pulmonary obstruction (APO) in horses with RAO and their reversibility.Five geldings with RAO, inducible by exposure to moldy hay, were studied.Pulmonary mechanics, echocardiography, serum troponin I concentrations, arterial blood gases, and hematocrit were obtained before and after 7 days of APO. Heart rate, PA diameter and flow characteristics, right and left ventricular luminal dimensions and wall thicknesses, global cardiac performance, and evidence of myocardial damage were evaluated. Pulmonary mechanics and echocardiography were reevaluated during remission.[corrected] Severe, transient APO did not induce chronic cor pulmonale in horses, because cardiac anatomy and function were normal between episodes. An acute episode of APO produced anatomical and functional cardiac changes in both the right and left heart (including increased PA diameter, abnormal septal motion, and decreased left ventricular diameter and estimated stroke volume), possibly because of the development of pulmonary hypertension, without apparent myocardial damage. The decrease in stroke volume was offset by the increase in heart rate.With APO of 7 days' duration, cardiovascular abnormalities and the functional airway changes that produce them are reversible when the offending allergens are removed.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, Anna M. and Gardner, Sarah Y. and Atkins, Clarke E. and LaFevers, D. Heath and Breuhaus, Babetta A.}, year={2007}, pages={302–307} }
 @article{arther_atkins_ciszewski_davis_settje_2007, title={Design and testing of a natural dirofilaria immitis infection model to evaluate the safety of an imidacloprid plus moxidectin combination in cats}, volume={101}, ISSN={["1432-1955"]}, DOI={10.1007/s00436-007-0613-9}, journal={PARASITOLOGY RESEARCH}, author={Arther, R. G. and AtkinS, C. and Ciszewski, D. K. and Davis, W. L. and Settje, T. L.}, year={2007}, month={Aug}, pages={S69–S76} }
 @misc{brown_atkins_bagley_carr_cowgill_davidson_egner_elliott_henik_labato_et al._2007, title={Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats}, volume={21}, DOI={10.1111/j.1939-1676.2007.tb03005.x}, abstractNote={Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide veterinarians with guidelines regarding the pathophysiology, diagnosis, or treatment of animal diseases. The foundation of the Consensus Statement is evidence‐based medicine, but if such evidence is conflicting or lacking, the panel provides interpretive recommendations on the basis of their collective expertise. The Consensus Statement is intended to be a guide for veterinarians, but it is not a statement of standard of care or a substitute for clinical judgment. Topics of statements and panel members to draft the statements are selected by the Board of Regents with input from the general membership. A draft prepared and input from Diplomates is solicited at the ACVIM Forum and via the ACVIM Web site and incorporated in a final version. This Consensus Statement was approved by the Board of Regents of the ACVIM before publication.}, number={3}, journal={Journal of Veterinary Internal Medicine}, author={Brown, S. and Atkins, C. and Bagley, R. and Carr, A. and Cowgill, L. and Davidson, M. and Egner, B. and Elliott, J. and Henik, R. and Labato, M. and et al.}, year={2007}, pages={542–558} }
 @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={Background:B-type natriuretic peptide (BNP) is increased in dogs with congestive heart failure (CHF). 
 
 
 
Hypothesis: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. 
 
 
 
Animals:Three hundred and thirty dogs from 2 large university teaching hospitals. 
 
 
 
Methods: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. 
 
 
 
Results: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) 
 
 
 
Conclusion and Clinical Importance: 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_2007, title={Reassessing the definition of heartworm infection in cats}, volume={231}, ISSN={["0003-1488"]}, DOI={10.2460/javma.231.9.1338}, abstractNote={JAVMA, Vol 231, No. 9, November 1, 2007 R studies by Browne et al and Dillon et al have corroborated earlier findings of Selcer et al, who reported radiographic evidence of pulmonary disease in cats experimentally exposed to heartworm infective larvae, but which did not develop mature heartworm infection (dirofilariasis). Importantly, the two more recent aforementioned studies identified histologic lesions in the pulmonary arteries or in airways and pulmonary parenchyma, as well as pulmonary arteries in cats with natural or experimental infections, respectfully. While it remains to be proven that naturally infected cats (with presumably lesser L 3 exposure) develop pulmonary parenchymal and airway lesions, it seems clear that naturally exposed cats that resist mature infection develop, at the very least, pulmonary vascular disease. These three landmark works broaden our understanding of the pathophysiology of the respiratory tract signs associated with exposure to various stages of Dirofilaria immitis. Their findings also raise questions as to appropriately descriptive terminology, particularly regarding the use of the word exposure. In 2005, I was an investigator on a study of heartworm risk in nondomestic cats in the southeastern United States. In that article, we defined antibodypositive cats as those exposed to, but negative for, heartworm infection if they were heartworm antigen negative and if no heartworms were found on necropsy. During the peer review process, one reviewer challenged this definition conceptually, arguing that antibody-positive cats indeed were infected. While acknowledging that exposed cats might well have pulmonary lesions, we argued that a cat without mature (L 5 ) heartworms did not meet the requirements for a diagnosis of heartworm infection. Our arguments were convincing enough that the manuscript was published with this distinction intact. Perhaps, in light of recent work, this point should be reconsidered. Conceptually, this represents a thorny problem. In an ideal world, cats would either have heartworm infection or not, but there is now a recognized gray zone in which cats that have successfully rejected an infection (probably at the young L 5 stage) may develop lesions (ie, disease) induced by D immitis. New terminology is Reassessing the definition of heartworm infection in cats}, number={9}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Atkins, Clarke E.}, year={2007}, month={Nov}, pages={1338–1338} }
 @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}, 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.}, 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{atkins_moresco_litster_2005, title={Prevalence of naturally occurring Dirofilaria immitis infection amona nondomestic cats housed in an area in which heartworms are endemic}, volume={227}, ISSN={["0003-1488"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-22244446809&partnerID=MN8TOARS}, DOI={10.2460/javma.2005.227.139}, abstractNote={Abstract}, number={1}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Atkins, C and Moresco, A and Litster, A}, year={2005}, month={Jul}, pages={139–143} }
 @article{cote_harpster_laste_macdonald_kittleson_bond_barrett_ettinger_atkins_2004, title={Atrial fibrillation in cats: 50 cases (1979-2002)}, volume={225}, ISSN={["1943-569X"]}, DOI={10.2460/javma.2004.225.256}, abstractNote={Abstract}, number={2}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Cote, E and Harpster, NK and Laste, NJ and MacDonald, KA and Kittleson, MD and Bond, BR and Barrett, KA and Ettinger, SJ and Atkins, CE}, year={2004}, month={Jul}, pages={256–260} }
 @article{gardner_atkins_sams_schwabenton_papich_2004, title={Characterization of the Pharmacokinetic and Pharmacodynamic Properties of the Angiotensin-Converting Enzyme Inhibitor, Enalapril, in Horses}, volume={18}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2004.tb00166.x}, DOI={10.1111/j.1939-1676.2004.tb00166.x}, abstractNote={The pharmacokinetics of enalapril (0.5 mg/kg IV) and the pharmacodynamics of enalapril (0.5 mg/kg PO) in 5 mares were investigated. After single IV dosing, concentrations of enalapril and enalaprilat, its active metabolite, were measured. Two weeks later, enalapril was administered by nasogastric tube. Potassium, creatinine, blood urea nitrogen (BUN), enalapril, and enalaprilat concentrations and angiotensin converting enzyme (ACE) activity were measured in serum. In addition, heart rate, blood pressure, digital venous blood gases, and lactate were measured. Two weeks later, enalapril was again administered by nasogastric tube. To mimic activation of the renin‐angiotensin‐aldosterone system, angiotensin I (0.5 μg/kg) was administered at fixed intervals, followed by blood‐pressure and heart‐rate measurement. The elimination half lives of enalapril and enalaprilat were 0.59 and 1.25 hours, respectively, after IV administration. After PO administration, enalapril and enalaprilat were not detectable in serum. There was a tendency(P= .0625) toward a decrease in ACE activity 45–120 minutes after enalapril administration, but ACE activity suppression was never >16%. There was a tendency(P= .0625) toward a decrease in mean arterial pressure (MAP) 6–8 hours after enalapril administration. Serum concentrations of potassium, creatinine, and BUN and digital venous blood gases and lactate concentrations did not change. In response to angiotensin I, there was a tendency(P= .0625) toward a decrease in the MAP response 4–24 hours after enalapril administration. Single‐dose enalapril at 0.5 mg/kg PO did not demonstrate significant availability, pharmacodynamic effect, or substantial suppression of ACE activity.}, number={2}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Gardner, Sarah Y. and Atkins, Clarke E. and Sams, Richard A. and Schwabenton, A. Brooke and Papich, Mark G.}, year={2004}, month={Mar}, pages={231–237} }
 @article{atkins_2004, title={Feline heartworm infection}, ISBN={1542-4014}, journal={NAVC Clinician's Brief}, author={Atkins, C. E.}, year={2004}, pages={15} }
 @article{johansson_gardner_levine_papich_lafevers_goldman_sheets_atkins_2004, title={Pharmacokinetics and pharmacodynamics of furosemide after oral administration to horses}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<739:PAPOFA>2.0.CO;2}, abstractNote={Furosemide is the most common diuretic drug used in horses. Furosemide is routinely administered as IV or IM bolus doses 3-4 times a day. Administration PO is often suggested as an alternative, even though documentation of absorption and efficacy in horses is lacking. This study was carried out in a randomized, crossover design and compared 8-hour urine volume among control horses that received placebo, horses that received furosemide at 1 mg/kg PO, and horses that received furosemide at 1 mg/kg IV. Blood samples for analysis of plasma furosemide concentrations, PCV, and total solids were obtained at specific time points from treated horses. Furosemide concentrations were determined by reversed-phase high-performance liquid chromatography with fluorescent detection. Systemic availability of furosemide PO was poor, erratic, and variable among horses. Median systemic bioavailability was 5.4% (25th percentile, 75th percentile: 3.5, 9.6). Horses that received furosemide IV produced 7.4 L (7.1, 7.7) of urine over the 8-hour period. The maximum plasma concentration of 0.03 microg/mL after administration PO was not sufficient to increase urine volume compared with control horses (1.2 L [1.0, 1.4] PO versus 1.2 L [1.0, 1.4] control). There was a mild decrease in urine specific gravity within 1-2 hours after administration of furosemide PO, and urine specific gravity was significantly lower in horses treated with furosemide PO compared with control horses at the 2-hour time point. Systemic availability of furosemide PO was poor and variable. Furosemide at 1 mg/kg PO did not induce diuresis in horses.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Levine, JF and Papich, MG and LaFevers, DH and Goldman, RB and Sheets, MK and Atkins, CE}, year={2004}, pages={739–743} }
 @article{atkins_2003, title={Comparison of results of three commercial heartworm antigen test kits in dogs with low heartworm burdens}, volume={222}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2003.222.1221}, abstractNote={Abstract}, number={9}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Atkins, CE}, year={2003}, month={May}, pages={1221–1223} }
 @article{johansson_gardner_levine_papich_lafevers_fuquay_reagan_atkins_2003, title={Furosemide continuous rate infusion in the horse: Evaluation of enhanced efficacy and reduced side effects}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0887:FCRIIT>2.3.CO;2}, abstractNote={Journal of Veterinary Internal MedicineVolume 17, Issue 6 p. 887-895 Open Access Furosemide Continuous Rate Infusion in the Horse: Evaluation of Enhanced Efficacy and Reduced Side Effects Anna M. Johansson, Anna M. Johansson Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSarah Y. Gardner, Corresponding Author Sarah Y. Gardner Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, Department of Clinical Sciences, College of Veterinary Medicine, Hillsborough Street 4700, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorJay F. Levine, Jay F. Levine Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorMark G. Papich, Mark G. Papich Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorVirginia H. Reagan, Virginia H. Reagan Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this author Anna M. Johansson, Anna M. Johansson Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSarah Y. Gardner, Corresponding Author Sarah Y. Gardner Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, Department of Clinical Sciences, College of Veterinary Medicine, Hillsborough Street 4700, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorJay F. Levine, Jay F. Levine Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorMark G. Papich, Mark G. Papich Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorVirginia H. Reagan, Virginia H. Reagan Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02529.xCitations: 32AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Continuous rate infusion (CRI) of furosemide in humans is considered superior to intermittent administration (IA). This study examined whether furosemide CRI, compared with IA, would increase diuretic efficacy with decreased fluid and electrolyte fluctuations and activation of the renin-angiotensin-aldosterone system (RAAS) in the horse. Five mares were used in a crossover-design study. During a 24-hour period, each horse received a total of 3 mg/kg furosemide by either CRI (0.12 mg/kg/h preceded by a loading dose of 0.12 mg/kg IV) or IA (1 mg/kg IV q8h). There was not a statistically significant difference in urine volume over 24 hours between methods; however, urine volume was significantly greater after CRI compared with IA during the first 8 hours ([median 25th percentile, 75th percentile]: 9.6 L [8.9, 14.4] for CRI versus 5.9 L [5.3, 6.0] for IA). CRI produced a more uniform urine flow, decreased fluctuations in plasma volume, and suppressed renal concentrating ability throughout the infusion period. Potassium, Ca, and Cl excretion was greater during CRI than IA (1,133 mmol [1,110, 1,229] versus 764 mmol [709, 904], 102.7 mmol [96.0, 117.2] versus 73.3 mmol [65.0, 73.5], and 1,776 mmol [1,657, 2,378] versus 1,596 mmol [1,457, 1,767], respectively). Elimination half-lives of furosemide were 1.35 and 0.47 hours for CRI and IA, respectively. The area under the excretion rate curve was 1,285.7 and 184.2 mL mg/mL for CRI and IA, respectively. Furosemide CRI (0.12 mg/kg/h) for 8 hours, preceded by a loading dose (0.12 mg/kg), is recommended when profound diuresis is needed acutely in horses. References 1 Jackson EK. Diuretics. In: JG Hardman, LE Limbird, PB Molinoff, RW Ruddon, AG Gilman, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. New York , NY : The McGraw-Hills Companies; 1995: 685–715. Web of Science®Google Scholar 2 Rose BD. Diuretics. Kidney Int 1991; 39: 336–352. 10.1038/ki.1991.43 CASPubMedWeb of Science®Google Scholar 3 Tobin T, Roberts BL, Swerczek TW, et al. The pharmacology of furosemide in the horse. III. Dose and time response relationships, effects of repeated dosing, and performance effects. J Equine Med Surg 1978; 2: 216–226. CASWeb of Science®Google Scholar 4 Hinchcliff KW, McKeever KH, Muir WW, 3rd. Furosemide-in-duced changes in plasma and blood volume of horses. J Vet Pharmacol Ther 1991; 14: 411–417. 10.1111/j.1365-2885.1991.tb00855.x CASPubMedWeb of Science®Google Scholar 5 Muir WW, McGuirk SM. Pharmacology and pharmacokinetics of drugs used to treat cardiac disease in horses. Vet Clin North Am Equine Pract 1985; 1: 335–352. 10.1016/S0749-0739(17)30759-9 CASPubMedWeb of Science®Google Scholar 6 Muir WW, Kohn CW, Sams R. Effects of furosemide on plasma volume and extracellular fluid volume in horses. Am J Vet Res 1978; 39: 1688–1691. CASPubMedWeb of Science®Google Scholar 7 Freestone JF, Carlson GP, Harrold DR, et al. Influence of furo-semide treatment on fluid and electrolyte balance in horses. Am J Vet Res 1988; 49: 1899–1902. CASPubMedWeb of Science®Google Scholar 8 Van Meyel JJ, Smits P, Russel FG, et al. Diuretic efficiency of furosemide during continuous administration versus bolus injection in healthy volunteers. Clin Pharmacol Ther 1992; 51: 440–444. 10.1038/clpt.1992.44 PubMedWeb of Science®Google Scholar 9 Lahav M, Regev A, Ra'anani P, et al. Intermittent administration of furosemide vs continuous infusion preceded by a loading dose for congestive heart failure. Chest 1992; 102: 725–731. 10.1378/chest.102.3.725 CASPubMedWeb of Science®Google Scholar 10 Acara MA. Renal pharmacology–Diuresis. In: CM Smith, AM Reynard, eds. Textbook of Pharmacology. Philadelphia , PA : WB Saunders Company; 1992: 554–588. Google Scholar 11 Baggot JD. The pharmacological basis of cardiac drug selection for use in horses. Equine Vet J Suppl 1995: 97–100. CASPubMedGoogle Scholar 12 Guthrie GP Jr, Cecil SG, Darden ED, et al. Dynamics of renin and aldosterone in the thoroughbred horse. Gen Comp Endocrinol 1982; 48: 296–299. 10.1016/0016-6480(82)90140-X CASPubMedWeb of Science®Google Scholar 13 Lee MG, Li T, Chiou WL. Effect of intravenous infusion time on the pharmacokinetics and pharmacodynamics of the same total dose of furosemide. Biopharm Drug Dispos 1986; 7: 537–547. 10.1002/bdd.2510070603 CASPubMedWeb of Science®Google Scholar 14 Pivac N, Rumboldt Z, Sardelic S, et al. Diuretic effects of fu-rosemide infusion versus bolus injection in congestive heart failure. Int J Clin Pharmacol Res 1998; 18: 121–128. CASPubMedWeb of Science®Google Scholar 15 Yelton SL, Gaylor MA, Murray KM. The role of continuous infusion loop diuretics. Ann Pharmacother 1995; 29: 1010–1014; quiz 1060–1011. 10.1177/106002809502901011 CASPubMedWeb of Science®Google Scholar 16 Gwilt PR. Pharmacokinetics. In: CR Craig, RE Stitzel, eds. Modern Pharmacology. Boston , MA : Little, Brown and Company; 1990: 68–81. Google Scholar 17 Chay S, Woods WE, Rowse K, et al. The pharmacology of furosemide in the horse. V. Pharmacokinetics and blood levels of fu-rosemide after intravenous administration. Drug Metab Dispos 1983; 11: 226–231. CASPubMedWeb of Science®Google Scholar 18 Harrison MH. Effects on thermal stress and exercise on blood volume in humans. Physiol Rev 1985; 65: 149–209. 10.1152/physrev.1985.65.1.149 CASPubMedWeb of Science®Google Scholar 19 Yamaoka K, Nakagawa T, Uno T. Application of Akaike's information criterion (AIC) in the evaluation of linear pharmacokinetic equations. J Pharmacokinet Biopharm 1978; 6: 165–175. 10.1007/BF01117450 CASPubMedWeb of Science®Google Scholar 20 Campbell MJ, Machin D. Non-parametric tests. In: MJ Campbell, D Machin, eds. Medical Statistics–A Commonsense Approach, 3rd ed. Chichester , UK : John Wiley & Sons Ltd; 1999: 163–165. Web of Science®Google Scholar 21 Chennavasin P, Seiwell R, Brater DC, et al. Pharmacodynamic analysis of the furosemide-probenecid interaction in man. Kidney Int 1979; 16: 187–195. 10.1038/ki.1979.120 CASPubMedWeb of Science®Google Scholar 22 Kaojarern S, Day B, Brater DC. The time course of delivery of furosemide into urine: An independent determinant of overall response. Kidney Int 1982; 22: 69–74. 10.1038/ki.1982.134 CASPubMedWeb of Science®Google Scholar 23 Hammarlund MM, Odlind B, Paalzow LK. Acute tolerance to furosemide diuresis in humans. Pharmacokinetic-pharmacodynamic modeling. J Pharmacol Exp Ther 1985; 233: 447–453. CASPubMedWeb of Science®Google Scholar 24 Streeten DH, Tomycz N, Anderson GH. Reliability of screening methods for the diagnosis of primary aldosteronism. Am J Med 1979; 67: 403–413. 10.1016/0002-9343(79)90786-1 CASPubMedWeb of Science®Google Scholar 25 Roberts BL, Blake JW, Tobin T. The pharmacology of furose-mide in the horse. II. Its detection, pharmacokinetics, and clearance from urine. J Equine Med Surg 1978; 2: 185–194. CASWeb of Science®Google Scholar Citing Literature Volume17, Issue6November 2003Pages 887-895 ReferencesRelatedInformation}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Levine, JF and Papich, MG and LaFevers, DH and Fuquay, LR and Reagan, VH and Atkins, CE}, year={2003}, pages={887–895} }
 @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{atkins_miller_2003, title={Is there a better way to administer heartworm adulticidal therapy?}, volume={98}, number={4}, journal={Veterinary Medicine}, author={Atkins, C. E. and Miller, M. W.}, year={2003}, pages={310-} }
 @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={Journal of Veterinary Internal MedicineVolume 17, Issue 5 p. 663-667 Open Access Noninvasive Transthoracic Temporary Cardiac Pacing in Dogs Teresa C. DeFrancesco, Corresponding Author Teresa C. DeFrancesco Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC. College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorBernard D. Hansen, Bernard D. Hansen Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this authorJennifer A. Sidley, Jennifer A. Sidley Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this authorBruce W. Keene, Bruce W. Keene Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this author Teresa C. DeFrancesco, Corresponding Author Teresa C. DeFrancesco Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC. College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorBernard D. Hansen, Bernard D. Hansen Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this authorJennifer A. Sidley, Jennifer A. Sidley Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this authorBruce W. Keene, Bruce W. Keene Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02497.xCitations: 33AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract 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. References 1 Yoshioka MM, Tilley LP, Harvey HJ, et al. Permanent pacemaker implantation in the dog. J Am Anim Hosp Assoc 1981; 17: 746–750. 2 Bonagura JD, Helphrey ML, Muir WW. Complications associated with permanent pacemaker implantation in the dog. J Am Vet Med Assoc 1983; 182: 149–155. 3 Klement P., Del-Nido PJ, Wilson GJ. The use of cardiac pacemakers in veterinary practice. Compendium 1984; 6: 893–902. 4 Fox PR, Matthiesen DT, Purse D., et al. Ventral abdominal, trans-diaphragmatic approach for implantation of cardiac pacemakers in the dog. J Am Vet Med Assoc 1986; 189: 1303–1308. 5 Sisson D., Thomas WP, Woodfield J., et al. Permanent transvenous pacemaker implantation in forty dogs. J Vet Intern Med 1991; 5: 322–331. 6 Flanders JA, Moise NS, Gelzer ARM, et al. Introduction of an endocardial pacing lead through the costocervical vein in six dogs. J Am Vet Med Assoc 1999; 215: 46–48. 7 Cote E., Laste NJ. Transvenous cardiac pacing. Clin Tech Small Anim Pract 2000; 15: 165–176. 8 Hynes JK, Holmes DR, Harrison CE. Five-year experience with temporary pacemaker therapy in the coronary care unit. Mayo Clin Proc 1983; 58: 122–126. 9 Hildick-Smith DJR, Petch MC. Temporary pacing before per-manent pacing should be avoided unless essential. Br Med J 1999; 317: 79–80. 10 Murphy JJ. Problems with temporary cardiac pacing. Br Med J 2001; 323: 527. 11 Zoll PM. Resuscitation of the heart in ventricular standstill by external electric stimulation. N Engl J Med 1952; 13: 768–771. 12 Zoll PM, Zoll RH, Belgard AH. External noninvasive electric stimulation of the heart. Crit Care Med 1981; 9: 393–394. 13 Falk RH, Zoll PM, Zoll RH. Safety and efficacy of noninvasive cardiac pacing. N Engl J Med 1983; 309: 1166–1168. 14 Zoll PM, Zoll RH, Falk RH, et al. External noninvasive temporary cardiac pacing: Clinical trials. Circulation 1985; 71: 937–944. 15 White JD, Brown CG. Immediate transthoracic pacing for cardiac asystole in an emergency department setting. Am J Emerg Med 1985; 3: 125–128. 16 Allen PW, OToole JJ. External transthoracic pacemaking. Anaesthesia 1988; 43: 895–896. 17 Madsen JK, Meibom J., Videbak R., et al. Transcutaneous pacing: Experience with the Zoll noninvasive temporary pacemaker. Am Heart J 1988; 116: 7–10. 18 Normal myocardial enzymes and normal echocardiographic findings during noninvasive transcutaneous pacing Pacing Clin Elec-trophysiol 1988; 11: 1188–1193. 19 Kirschenbaum LP, Eisenkraft JB, Mitchell J., Hillel Z. Transtho-racic pacing for the treatment of severe bradycardia during induction of anesthesia. J Cardiothorac Anesth 1989; 3: 329–332. 20 Wood M., Ellenbogen KA. Bradyarrhythmias, emergency pacing and implantable defibrillation devices. Crit Care Clin 1989; 5: 551–568. 21 Hedges JR, Feero S., Shultz B., et al. Prehospital transcutaneous cardiac pacing for symptomatic bradycardia. Pacing Clin Electrophy-siol 1991; 14: 1473–1478. 22 Gammage MD. Temporary cardiac pacing. Heart 2000; 83: 715–720. 23 Syverud SA, Dalsey WC, Hedges JR, et al. Transcutaneous cardiac pacing: Determination of myocardial injury in the canine model. Ann Emerg Med 1983; 12: 745–748. 24 Kicklighter EJ, Syverud SA, Dalsey WC, et al. Pathological aspects of transcutaneous cardiac pacing. Am J Emerg Med 1985; 3: 108–113. 25 Syverud SA, Hedges JR, Dalsey WC, et al. Hemodynamics of transcutaneous cardiac pacing. Am J Emerg Med 1986; 4: 17–20. 26 Niemann JT, Rosborough JP, Garner D., et al. External nonin-vasive cardiac pacing; comparative hemodynamic study of two techniques with conventional endocardial pacing. Pacing Clin Electrophy-siol 1988; 11: 575–582. 27 Hedges JR, Syverud SA, Dalsey WC, et al. Threshold, enzymatic, and pathologic changes associated with prolonged transcuta-neous pacing in a chronic heart block model. J Emerg Med 1989; 7: 1–4. 28 Oyama MA, Sisson DD, Lehmkuhl LB. Practices and outcomes of artificial cardiac pacing in 154 dogs. J Vet Intern Med 2001; 15: 229–239. Citing Literature Volume17, Issue5September 2003Pages 663-667 ReferencesRelatedInformation}, 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}, 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={Abstract}, 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{rausch_atkins_2002, title={Treatment of canine pulmonic stenosis with percutaneous balloon valvuloplasty}, volume={97}, number={11}, journal={Veterinary Medicine}, author={Rausch, W. P. and Atkins, C.}, year={2002}, pages={819–821} }
 @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{maxson_meurs_lehmkuhl_magnon_weisbrode_atkins_2001, title={Polymerase chain reaction analysis for viruses in paraffin-embedded myocardium from dogs with dilated cardiomyopathy or myocarditis}, volume={62}, ISSN={0002-9645}, url={http://dx.doi.org/10.2460/ajvr.2001.62.130}, DOI={10.2460/ajvr.2001.62.130}, abstractNote={Abstract}, number={1}, journal={American Journal of Veterinary Research}, publisher={American Veterinary Medical Association (AVMA)}, author={Maxson, Tracy R. and Meurs, Kathryn M. and Lehmkuhl, Linda B. and Magnon, Alex L. and Weisbrode, Steven E. and Atkins, Clarke E.}, year={2001}, month={Jan}, pages={130–135} }
 @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}, 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} }
 @article{wey_atkins_2000, title={Aortic dissection and congestive heart failure associated with systemic hypertension in a cat}, volume={14}, DOI={10.1111/j.1939-1676.2000.tb02239.x}, abstractNote={Journal of Veterinary Internal MedicineVolume 14, Issue 2 p. 208-213 Open Access Aortic Dissection and Congestive Heart Failure Associated with Systemic Hypertension in a Cat Aaron C. Wey, Corresponding Author Aaron C. Wey Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC Veterinary Medical Teaching Hospital, University of California, Davis, CA. Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606; e-mail: clarke-atkins @ ncsu. edu.Search for more papers by this authorClarke E. Atkins, Corresponding Author Clarke E. Atkins Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC Veterinary Medical Teaching Hospital, University of California, Davis, CA. Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606; e-mail: clarke-atkins @ ncsu. edu.Search for more papers by this author Aaron C. Wey, Corresponding Author Aaron C. Wey Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC Veterinary Medical Teaching Hospital, University of California, Davis, CA. Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606; e-mail: clarke-atkins @ ncsu. edu.Search for more papers by this authorClarke E. Atkins, Corresponding Author Clarke E. Atkins Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC Veterinary Medical Teaching Hospital, University of California, Davis, CA. Department of Companion Animals and Special Species, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606; e-mail: clarke-atkins @ ncsu. edu.Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2000.tb02239.xCitations: 31AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 Liu S. Postmortem examination of the heart. Vet Clin North Am 1983; 13: 379– 394. 2 Heritage ME, Gorman NT, Jeffries AR. Coarctation of the aorta in a dog. Vet Radiol Ultrasound 1992; 33: 25– 30. 3 Hamir AN. Perforation of the thoracic aorta in a dog associated with Spirocerca lupi infection. Aust Vet J 1984; 61: 64. 4 Potter KA, Besser TE. Cardiovascular lesions in bovine Marfan syndrome. Vet Pathol 1994; 31: 501– 509. 5 Lester GD, Lombard CW, Ackerman N. Echocardiographic detection of a dissecting aortic root aneurysm in a thoroughbred stallion. Vet Radiol Ultrasound 1992; 33: 202– 205. 6 Marr CM, Reef VB, Brazil TJ, et al. Aorto-cardiac fistulas in seven horses. Vet Radiol Ultrasound 1998; 39: 22– 31. 7 Pretre R, VonSesser LK. Aortic dissection. Lancet 1997; 349: 1462– 1464. Citing Literature Volume14, Issue2March 2000Pages 208-213 ReferencesRelatedInformation}, number={2}, journal={Journal of Veterinary Internal Medicine}, author={Wey, A. C. and Atkins, C. E.}, year={2000}, pages={208–213} }
 @inbook{atkins_ryan_2000, title={CVT update: Diagnosis and prevention of heartworm disease in cats}, ISBN={0721655238}, booktitle={Kirk's current veterinary therapy : small animal practice (13th Ed.)}, publisher={Philadelphia, PA : W.B. Saunders}, author={Atkins, C. E. and Ryan, W. G.}, year={2000}, pages={782} }
 @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={Abstract}, 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}, 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} }
 @article{schatzberg_olby_steingold_keene_atkins_meurs_solomon_goedegebuure_wilton_sharp_1999, title={A polymerase chain reaction screening strategy for the promoter of the canine dystrophin gene}, volume={60}, number={9}, journal={American Journal of Veterinary Research}, author={Schatzberg, S. and Olby, N. and Steingold, S. and Keene, B. and Atkins, C. and Meurs, K. and Solomon, G. and Goedegebuure, S. A. and Wilton, S. and Sharp, N.}, year={1999}, pages={1040–1046} }
 @article{breitschwerdt_atkins_brown_kordick_snyder_1999, title={Bartonella vinsonii subsp berkhoffi and related members of the alpha subdivision of the Proteobacteria in dogs with cardiac arrhythmias, endocarditis, or myocarditis}, volume={37}, number={11}, journal={Journal of Clinical Microbiology}, author={Breitschwerdt, E. B. and Atkins, C. E. and Brown, T. T. and Kordick, D. L. and Snyder, P. S.}, year={1999}, pages={3618–3626} }
 @article{gookin_atkins_1999, title={Evaluation of the effect of pleural effusion on central venous pressure in cats}, volume={13}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(1999)013<0561:EOTEOP>2.3.CO;2}, abstractNote={This study was undertaken to determine if pleural effusion (PEF) increases central venous pressure (CVP) in cats, to define any relationship between volume of PEF and CVP and to ascertain the significance of CVP alterations in cats having PEF and suspected right heart failure (RHF). CVP was measured from a jugular vein before (CVPpre) and after (CVPpost) bilateral thoracentesis in 9 cats with naturally occurring PEF and under experimental conditions in 3 spontaneously breathing anesthetized cats receiving graded intrathoracic infusion of saline. Volumes of introduced and recovered fluid were recorded. A significant decrease occurred in CVP after thoracentesis in cats with naturally occurring PEF (mean difference, 4.5 cm H2O; range, 0-7.0 cm H2O, P .05) over the range of volumes recovered (range, 95-450 mL or 16.4-90 mL/kg). Five cats had CVPpre suggestive of RHF (range, 8.16-20.4 cm H2O). After thoracentesis, RHF was ruled out in 1 cat (CVPpost, 4.08 cm H2O) and the CVP declined but remained abnormally high (9.52 cm H2O) in 1 cat with a mediastinal mass. In 2 cats with confirmed RHF (CVPpre, 20.4 and 16.3 cm H2O), CVP decreased after thoracentesis but remained abnormally high (CVPpost, 14.96 and 10.88 cm H2O). In 1 cat with noncardiogenic PEF and inadequate removal of fluid, CVPpost (8.16 cm H2O) did not decrease. Experimentally, a positive linear relationship was observed between CVP and volume of PEF. The threshold volume required to increase CVP (17 mL/kg) approximated that suggested by clinical observation (22 mL/kg). PEF increases CVP and can cause abnormally high CVP in the absence of RHF.}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Gookin, JL and Atkins, CE}, year={1999}, pages={561–563} }
 @article{atkins_1999, title={The diagnosis of feline heartworm infection}, volume={35}, ISSN={["0587-2871"]}, DOI={10.5326/15473317-35-3-185}, abstractNote={Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation C Atkins; The diagnosis of feline heartworm infection. J Am Anim Hosp Assoc 1 May 1999; 35 (3): 185–187. doi: https://doi.org/10.5326/15473317-35-3-185 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search}, number={3}, journal={JOURNAL OF THE AMERICAN ANIMAL HOSPITAL ASSOCIATION}, author={Atkins, C}, year={1999}, pages={185-+} }
 @article{atkins_1998, title={Complications of heartworm disease}, volume={12}, number={1998}, journal={North American Veterinary Conference. Veterinary Proceedings}, author={Atkins, C. E.}, year={1998}, pages={556–558} }
 @article{atkins_1998, title={Feline heartworm disease}, volume={12}, number={1998}, journal={North American Veterinary Conference. Veterinary Proceedings}, author={Atkins, C. E.}, year={1998}, pages={551–553} }
 @article{atkins_1998, title={Heartworm disease: An update on testing and prevention in dogs and cats}, volume={93}, number={1}, journal={Veterinary Medicine}, author={Atkins, C.}, year={1998}, pages={15} }
 @article{atkins_1998, title={Heartworm disease: an update}, volume={12}, number={1998}, journal={North American Veterinary Conference. Veterinary Proceedings}, author={Atkins, C. E.}, year={1998}, pages={553–556} }
 @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} }
 @article{atkins_atwell_dillon_genchi_hayasaki_holmes_knight_lukof_mccall_slocombe_1997, title={American Heartworm Society guidelines: Guidelines for the diagnosis, treatment, and prevention of heartworm (Dirofilaria immitis) infection in cats}, volume={19}, number={4}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={Atkins, C. E. and Atwell, R. B. and Dillon, R. and Genchi, C. and Hayasaki, M. and Holmes, R. A. and Knight, D. H. and Lukof, D. K. and McCall, J. W. and Slocombe, J. O. D.}, year={1997}, pages={422–429} }
 @article{bliss_atkins_1997, title={ECG of the month. Sinus arrhythmia in a dog}, volume={211}, number={9}, journal={Journal of the American Veterinary Medical Association}, author={Bliss, S. P. and Atkins, C. E.}, year={1997}, pages={1126–1127} }
 @article{dillon_atkins_clekis_genchi_knight_mccall_miller_1997, title={Feline heartworm disease}, volume={25}, number={2}, journal={Feline Practice}, author={Dillon, R. and Atkins, Clarke E. and Clekis, T. and Genchi, C. and Knight, D. H. and McCall, J. and Miller, M. W.}, year={1997}, pages={12} }
 @article{frank_nutter_kyles_atkins_sellon_1997, title={Systemic arterial dirofilariasis in five dogs}, volume={11}, ISSN={["0891-6640"]}, DOI={10.1111/j.1939-1676.1997.tb00089.x}, abstractNote={Systemic arterial dirofilariasis is an unusual manifestation of heartworm disease of dogs that results from aberrant migration ofDirofilaria immitisinto the peripheral arterial circulation. To expand the clinical characterization of systemic arterial dirofilariasis, 5 dogs evaluated at the North Carolina State University's College of Veterinary Medicine were reviewed. Common clinical presentations included hindlimb lameness, paresthesia of hindlimbs, and interdigital ischemic necrosis resulting from thromboembolic disease. Visualization of heartworms with angiography or ultrasonography confirmed the diagnosis in all cases. All 5 dogs were treated with an adulticide; 3 dogs were treated with thiacetarsamide sodium and 2 with melarsomine dihydrochloride. Four of the 5 dogs survived the initial treatment period; 1 dog died of severe thromboembolic complications after thiacetarsamide sodium therapy. The treatment of systemic arterial dirofilariasis creates a therapeutic challenge because of multiple potential complications resulting from thromboembolic disease.}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Frank, JR and Nutter, FB and Kyles, AE and Atkins, CE and Sellon, RK}, year={1997}, pages={189–194} }
 @book{goodwin_atkins_tilley_1995, place={Guelph, Ontario}, title={Diagnostic cardiology}, publisher={Lifelearn V}, author={Goodwin, John-Karl and Atkins, Clarke and Tilley, Larry}, year={1995} }
 @article{atkins_kanter_wright_saba_baty_swanson_bai_keene_1995, title={ORTHODROMIC RECIPROCATING TACHYCARDIA AND HEART-FAILURE IN A DOG WITH A CONCEALED POSTEROSEPTAL ACCESSORY PATHWAY}, volume={9}, ISSN={["1939-1676"]}, DOI={10.1111/j.1939-1676.1995.tb03271.x}, abstractNote={A 4‐month‐old male Labrador Retriever was presented for recurrent bouts of pulmonary edema associated with tachycardia. Initial physical examination and echocardiography were unremarkable, and the electrocardiogram revealed only an intraventricular conduction disturbance. Subsequent recordings showed paroxysmal supraventricular tachycardia (SVT) (340 beats/min), which consistently produced pulmonary edema. The supraventricular tachycardia was unresponsive to adenosine, esmolol, and propranolol; was variably and transiently responsive to various vagal maneuvers and precordial thumps; and was always responsive to IV diltiazem. Multiple life‐threatening episodes of SVT occurred, however, despite the chronic administration of oral diltiazem, propranolol, and procainamide. Diastolic cardiac dysfunction was documented by Doppler echocardiography and was thought to contribute to the development of pulmonary edema. A subsequent electrophysiologic study confirmed the presence of an atrioventricular posteroseptal accessory pathway that participated in orthodromic reciprocating tachycardia. This pathway was determined to conduct only in the retrograde direction (“concealed accessory pathway”). Intraoperative IV procainamide titration terminated the arrhythmia, which could not be reinduced when procainamide blood concentration approximated 20 μg/dL. Increasing the oral procainamide dose to achieve such plasma concentrations was successful in eliminating orthodromic reciprocating tachycardia, preventing heart failure, and returning Doppler indices of diastolic function to normal.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={ATKINS, CE and KANTER, R and WRIGHT, K and SABA, Z and BATY, C and SWANSON, C and BAI, S and KEENE, BW}, year={1995}, pages={43–49} }
 @article{atkins_keene_mcguirk_sato_1994, title={Acute effect of hydralazine administration on pulmonary artery hemodynamics in dogs with chronic heartworm disease}, volume={55}, number={2}, journal={American Journal of Veterinary Research}, author={Atkins, C. E. and Keene, B. W. and McGuirk, S. M. and Sato, T.}, year={1994}, pages={262} }
 @article{atkins_cali_lombardo_1994, title={ECG of the month [Supraventricular tachycardia in a dog]}, volume={205}, number={7}, journal={Journal of the American Veterinary Medical Association}, author={Atkins, C. E. and Cali, J. V. and Lombardo, P. S.}, year={1994}, pages={983} }
 @article{riond_riviere_duckett_atkins_jernigan_rikihisa_spurlock_1992, title={CARDIOVASCULAR EFFECTS AND FATALITIES ASSOCIATED WITH INTRAVENOUS ADMINISTRATION OF DOXYCYCLINE TO HORSES AND PONIES}, volume={24}, ISSN={["0425-1644"]}, DOI={10.1111/j.2042-3306.1992.tb02777.x}, abstractNote={Summary}, number={1}, journal={EQUINE VETERINARY JOURNAL}, author={RIOND, JL and RIVIERE, JE and DUCKETT, WM and ATKINS, CE and JERNIGAN, AD and RIKIHISA, Y and SPURLOCK, SL}, year={1992}, month={Jan}, pages={41–45} }
 @article{atkins_gallo_kurzman_cowen_1992, title={Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases (1985-1989)}, volume={201}, number={4}, journal={Journal of the American Veterinary Medical Association}, author={Atkins, C. E. and Gallo, A. M. and Kurzman, I. D. and Cowen, P.}, year={1992}, pages={613} }
 @article{atkins_snyder_1992, title={SYSTOLIC-TIME INTERVALS AND THEIR DERIVATIVES FOR EVALUATION OF CARDIAC-FUNCTION}, volume={6}, ISSN={["0891-6640"]}, DOI={10.1111/j.1939-1676.1992.tb03152.x}, abstractNote={Systolic time intervals provide a noninvasive indication of global left ventricular performance, are relatively sensitive, and are easily obtained from an M‐mode echocardiogram. This paper defines systolic time intervals (preejection period, left ventricular ejection time, and total electromechanical systole) and their derivatives (preejection period/left ventricular ejection time and velocity of circumferential fiber shortening). Their utility and weaknesses, as well as the effects of heart rate, loading conditions, cardiac contractility, and drug therapies on systolic time intervals are discussed. Normal values for systolic time intervals for the dog and cat are provided.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={ATKINS, CE and SNYDER, PS}, year={1992}, pages={55–63} }
 @article{atkins_curtis_mcguirk_kittleson_sato_snyder_1992, title={THE USE OF M-MODE ECHOCARDIOGRAPHY IN DETERMINING CARDIAC-OUTPUT IN DOGS WITH NORMAL, LOW, AND HIGH OUTPUT STATES - COMPARISON TO THERMODILUTION METHOD}, volume={33}, ISSN={["1058-8183"]}, DOI={10.1111/j.1740-8261.1992.tb00147.x}, abstractNote={The utility of M‐mode echocardiographic determination of left ventricular volume and cardiac output was evaluated by comparing four commonly used formulae for ventricular volume, derived from end‐systolic (ESD) and end‐diastolic (EDD) ventricular dimensions. Cardiac index (CI) was calculated by the following formulae, where HR = heart rate and BSA = body surface area (M2): 1. (EDD3‐ ESD3) * HR/BSA; 2. (0.85 * EDD3 ‐ 1.2 *ESD3) * HR/BSA; 3. (EDD3.16 ‐ ESD3.16) * HR/BSA; and 4. {[7/(2.4 + EDD)] * [EDD3] ‐ [7/(2.4 + ESD)] * [ESD3)}* HR/BSA. Cardiac index, obtained invasively by thermodilution, was compared to values determined echocardiographically in normal dogs (Group 1) and in three states of altered cardiac function: after positive inotropic stimulation with graded doses (0,5,10, and 15 μg/kg/min) of intravenous dobutamine (Group 2); with experimentally induced heartworm disease (Group 3); and with spontaneous dilated cardiomyopathy (Group 4). Cardiac index, determined echocardiographically, was plotted against CI, determined with thermodilution, and regression equations calculated. In Group 1 (n = 15), a significant relationship (P < 0.01) was observed with each of the four formulae (r2= 0.54‐0.68), however, individual estimates of CI were often inaccurate. With inotropic stimulation (Group 2;3 normal dogs, n = 12 data points), the relationship was significant (P < 0.05), but the coefficients of determination were less than in the unstimulated normal dogs (r2= 0.41‐0.47). No significant relationship was seen between CI, determined echocardiographically and CI, determined by thermodilution, when overt cardiac disease was present (Groups 3 and 4; n = 7 and 13, r2= 0.13‐0.21, respectively). Specific formulae were evaluated for accuracy by comparing their coefficients of determination and their ability to predict mean and individual measured CI. Using the paired Student's t‐test, CI determined noninvasively were shown to differ significantly (P < 0.05) between methods and between formulae in many instances. No one formula was found to be consistently more accurate than the others. We conclude that, in normal dogs, while echocardiographic estimation of CI is significantly related to CI measured with thermodilution, individual variation diminishes clinical utility. However, this noninvasive technique should prove useful in comparing populations with minimal or no cardiac dysfunction. Secondly, the relationship is diminished, but not lost, after inotropic stimulation. M‐mode echocardiographic estimation of CI offers little promise for accurate assessment of cardiac performance in cardiac disease states. Lastly, although none of the four formulae for CI compared herein were found to be consistently superior to the other three, formulae 3 and 4 appear to be most useful in estimating CI in normal dogs.}, number={5}, journal={VETERINARY RADIOLOGY & ULTRASOUND}, author={ATKINS, CE and CURTIS, MB and MCGUIRK, SM and KITTLESON, MD and SATO, T and SNYDER, PS}, year={1992}, pages={297–304} }