@article{ward_lisciandro_ware_viall_aona_kurtz_reina-doreste_defrancesco_2018, title={Evaluation of point-of-care thoracic ultrasound and NT-proBNP for the diagnosis of congestive heart failure in cats with respiratory distress}, volume={32}, ISSN={["1939-1676"]}, url={https://doi.org/10.1111/jvim.15246}, DOI={10.1111/jvim.15246}, abstractNote={BackgroundThe diagnosis of congestive heart failure (CHF) in cats is challenging. Point‐of‐care (POC) thoracic ultrasound and NT‐proBNP testing are emerging tools that may aid in diagnosis.Hypothesis/ObjectivesTo assess the diagnostic accuracy of POC lung ultrasound (LUS), focused cardiac ultrasound (FCU), and NT‐proBNP in predicting a final diagnosis of CHF.AnimalsFifty‐one cats in respiratory distress.MethodsBlood NT‐proBNP, LUS, and FCU evaluating left atrial (LA) size and presence of pericardial effusion (PCEFF) were performed in all cats. Lung ultrasound findings including pleural effusion (PLEFF), number of B‐lines, and sub‐pleural abnormalities were noted. Medical records were evaluated for final diagnosis.ResultsThirty‐three of 51 (65%) cats were diagnosed with CHF. Lung ultrasound and blood NT‐proBNP were significant predictors of CHF in a multivariate model. The LUS criterion that maximized accuracy for CHF diagnosis was presence of >1 site strongly positive for B‐lines (>3 B‐lines per site), resulting in sensitivity of 78.8%, specificity of 83.3%, and area under the curve (AUC) of 0.833. Subjective LA enlargement was 97.0% sensitive and 100% specific for CHF (AUC 0.985). Presence of PCEFF also was 100% specific, but only 60.6% sensitive, for CHF (AUC 0.803). A positive blood NT‐proBNP test was 93.9% sensitive and 72.2% specific for the diagnosis of CHF (AUC 0.831).Conclusions and Clinical ImportancePoint‐of‐care diagnostic techniques of LUS, FCU, and NT‐proBNP are useful to diagnose CHF in cats with respiratory distress.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ward, Jessica L. and Lisciandro, Gregory R. and Ware, Wendy A. and Viall, Austin K. and Aona, Brent D. and Kurtz, Kari A. and Reina-Doreste, Yamir and DeFrancesco, Teresa C.}, year={2018}, pages={1530–1540} }
 @article{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{meurs_stern_reina-doreste_maran_chdid_lahmers_keene_mealey_2015, title={Impact of the canine double-deletion beta 1 adrenoreceptor polymorphisms on protein structure and heart rate response to atenolol, a beta 1-selective beta-blocker}, volume={25}, ISSN={["1744-6880"]}, url={https://doi.org/10.1097/FPC.0000000000000152}, DOI={10.1097/fpc.0000000000000152}, abstractNote={Objective &bgr;-Adrenergic receptor antagonists are widely utilized for the management of cardiac diseases in dogs. We have recently identified two deletion polymorphisms in the canine adrenoreceptor 1 (ADRB1) gene. We hypothesized that canine ADRB1 deletions would alter the structure of the protein, as well as the heart rate response to the &bgr;-adrenergic receptor antagonist, atenolol. The objectives of this study were to predict the impact of these deletions on the predicted structure of the protein and on the heart rate response to atenolol in a population of healthy adult dogs. Methods Eighteen apparently healthy, mature dogs with (11) and without (seven) ADRB1 deletions were evaluated. The heart rate of the dogs was evaluated with a baseline ambulatory ECG before and 14–21 days after atenolol therapy (1 mg/kg orally q12 h). Minimum, average, and maximum heart rates were compared between groups of dogs (deletions, controls) using an unpaired t-test and within each group of dogs using a paired t-test. The protein structure of ADRB1 was predicted by computer modeling. Results Deletions were predicted to alter the structure of the ADRB1 protein. The heart rates of the dogs with deletions were lower than those of the control dogs (the average heart rates were significantly lower). Conclusion ADRB1 deletions appear to have structural and functional consequences. Individual genome-based treatment recommendations could impact the management of dogs with heart disease.}, number={9}, journal={PHARMACOGENETICS AND GENOMICS}, author={Meurs, Kathryn M. and Stern, Josh A. and Reina-Doreste, Yamir and Maran, Brian A. and Chdid, Lhoucine and Lahmers, Sunshine and Keene, Bruce W. and Mealey, Katrina L.}, year={2015}, month={Sep}, pages={427–431} }
 @article{meurs_chdid_reina-doreste_stern_2015, title={Polymorphisms in the canine and feline renin-angiotensin-aldosterone system genes}, volume={46}, ISSN={["1365-2052"]}, url={https://doi.org/10.1111/age.12260}, DOI={10.1111/age.12260}, abstractNote={Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.}, number={2}, journal={ANIMAL GENETICS}, author={Meurs, Kathryn M. and Chdid, Lhoucine and Reina-Doreste, Yamir and Stern, Joshua A.}, year={2015}, month={Apr}, pages={226–226} }
 @article{ware_reina-doreste_stern_meurs_2015, title={Sudden Death Associated with QT Interval Prolongation and KCNQ1 Gene Mutation in a Family of English Springer Spaniels}, volume={29}, ISSN={["1939-1676"]}, url={https://europepmc.org/articles/PMC4895492}, DOI={10.1111/jvim.12550}, abstractNote={BackgroundA 5‐year‐old, healthy English Springer Spaniel died suddenly 4 months after delivering a litter of 7 puppies. Within 4 months of the dam's death, 3 offspring also died suddenly.HypothesisAbnormal cardiac repolarization, caused by an inherited long QT syndrome, is thought to be responsible for arrhythmias leading to sudden death in this family.AnimalsFour remaining dogs from the affected litter and 11 related dogs.MethodsPhysical examination and resting ECG were done on the littermates and 9 related dogs. Additional tests on some or all littermates included echocardiogram with Doppler, Holter monitoring, and routine serum biochemistry. Blood for DNA sequencing was obtained from all 15 dogs.ResultsThree of 4 littermates examined, but no other dogs, had prolonged QT intervals with unique T‐wave morphology. DNA sequencing of the KCNQ1 gene identified a heterozygous single base pair mutation, unique to these 3 dogs, which changes a conserved amino acid from threonine to lysine and is predicted to change protein structure.Conclusions and Clinical ImportanceThis family represents the first documentation in dogs of spontaneous familial QT prolongation, which was associated with a KCNQ1 gene mutation and sudden death. Although the final rhythm could not be documented in these dogs, their phenotypic manifestations of QT interval prolongation and abnormal ECG restitution suggested increased risk for sudden arrhythmic death. The KCNQ1 gene mutation identified is speculated to impair the cardiac repolarizing current IKs, similar to KCNQ1 mutations causing long QT syndrome 1 in humans.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Ware, W. A. and Reina-Doreste, Y. and Stern, J. A. and Meurs, K. M.}, year={2015}, pages={561–568} }
 @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
Objective—To assess survival time and adverse events related to the administration of pimobendan to cats with congestive heart failure (CHF) secondary to hypertrophic cardiomyopathy (HCM) or hypertrophic obstructive cardiomyopathy (HOCM).
Design—Retrospective case-control study.
Animals—27 cats receiving treatment with pimobendan and 27 cats receiving treatment without pimobendan.
Procedures—Medical records between 2003 and 2013 were reviewed. All cats with HCM or HOCM treated with a regimen that included pimobendan (case cats) were identified. Control cats (cats with CHF treated during the same period with a regimen that did not include pimobendan) were selected by matching to case cats on the basis of age, sex, body weight, type of cardiomyopathy, and manifestation of CHF. Data collected included signalment, physical examination findings, echocardiographic data, serum biochemical values, and survival time from initial diagnosis of CHF. Kaplan-Meier survival curves were constructed and compared by means of a log rank test.
Results—Cats receiving pimobendan had a significant benefit in survival time. Median survival time of case cats receiving pimobendan was 626 days, whereas median survival time for control cats not receiving pimobendan was 103 days. No significant differences were detected for any other variable.
Conclusions and Clinical Relevance—The addition of pimobendan to traditional treatment for CHF may provide a substantial clinical benefit in survival time for HCM-affected cats with CHF and possibly HOCM-affected cats with CHF.}, number={5}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Reina-Doreste, Yamir and Stern, Joshua A. and Keene, Bruce W. and Tou, Sandra P. and Atkins, Clarke E. and DeFrancesco, Teresa C. and Ames, Marisa K. and Hodge, Timothy E. and Meurs, Kathryn M.}, year={2014}, month={Sep}, pages={534–539} }