Naturally occurring torsades de pointes and QT interval prolongation in a domestic cat.

A 10-year-old male American Shorthair cat was presented after a witnessed syncopal event. A Holter monitor demonstrated a long QT interval and revealed a rhythm characteristic of torsades de pointes (TdP) coincident with a bout of syncope. On subsequent Holter monitor recordings, sotalol did not prolong the QT interval further and did not reduce the severity of the underlying ventricular tachyarrhythmias, but no TdP was identified. When another syncopal event occurred, sotalol was discontinued, and oral amiodarone and magnesium were started. This resulted in improvement in the ventricular tachyarrhythmia. No syncopal events occurred in the ensuing 3 months, but the cat died of an unrelated disease shortly after. This is the first report of naturally occurring torsades de pointes in a domestic cat.

Assisted reproduction mediated resurrection of a feline model for Chediak-Higashi syndrome caused by a large duplication in LYST.

Chediak-Higashi Syndrome (CHS) is a well-characterized, autosomal recessively inherited lysosomal disease caused by mutations in lysosomal trafficking regulator (LYST). The feline model for CHS was originally maintained for ~20 years. However, the colonies were disbanded and the CHS cat model was lost to the research community before the causative mutation was identified. To resurrect the cat model, semen was collected and cryopreserved from a lone, fertile,  CHS carrier male. Using cryopreserved semen, laparoscopic oviductal artificial insemination was performed on three queens, two queens produced 11 viable kittens. To identify the causative mutation, a fibroblast cell line, derived from an affected cat from the original colony, was whole genome sequenced. Visual inspection of the sequence data identified a candidate causal variant as a ~20 kb tandem duplication within LYST, spanning exons 30 through to 38 (NM_001290242.1:c.8347-2422_9548 + 1749dup). PCR genotyping of the produced offspring demonstrated three individuals inherited the mutant allele from the CHS carrier male. This study demonstrated the successful use of cryopreservation and assisted reproduction to maintain and resurrect biomedical models and has defined the variant causing Chediak-Higashi syndrome in the domestic cat.

Echocardiographic Features of Giant Right Atrial Diverticulum in a Dog.

A 12-year-old spayed female miniature Poodle presented for coughing, respiratory distress, and anorexia. After thoracentesis for pleural effusion, radiography revealed an enlarged cardiac silhouette with a bulge in the area of the body of the right atrium. Echocardiography revealed an anechoic chamber-like cavity lateral to the right atrium that communicated with the right atrium through a 13 mm defect in the right atrial free wall. Contrast echocardiography and color flow Doppler were used to prove that the cavity communicated with the right atrium. The cavity was diagnosed as a giant right atrial diverticulum.

Naturally Occurring Biventricular Noncompaction in an Adult Domestic Cat.

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non-human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth-eaten appearance to the inner wall of the mid- to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial-lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.

Balloon Valvuloplasty of Tricuspid Stenosis: A Retrospective Study of 5 Labrador Retriever Dogs.

BACKGROUND: There are limited reports of severe tricuspid valve stenosis in dogs and limited data regarding treatment and outcome. OBJECTIVE: To evaluate clinical signs, echocardiographic features, and outcome of balloon valvuloplasty (BV) in dogs with severe tricuspid valve stenosis (TVS) in which BV was attempted. ANIMALS: Five client-owned dogs with severe TVS. METHODS: Records were retrospectively reviewed and data collected regarding signalment, clinical signs, diagnostic findings, procedures, and outcome. RESULTS: All dogs were Labrador Retrievers. Presenting complaints included episodic weakness/syncope (4/5), abdominal distension (4/5), lethargy (2/5), and exercise intolerance (2/5). The median and range of measurements before BV were as follows: TV mean velocity 1.5 m/s (range 1.4-1.7 m/s); velocity-time integral (VTI) 79.8 cm (42.4-99.1 cm); and TV maximum velocity 2.9 m/s (2.3-3.2 m/s). Measurements (available for 3 of 5 dogs) after BV were as follows: TV mean velocity 1.15 m/s (0.9-1.4 m/s); VTI 44.95 cm (41.4-54.8 cm); and TV maximum velocity 1.15 m/s (1.9-2.3 m/s). The procedure was attempted in all dogs and completed in 4/5 dogs. The largest balloon diameter ranged from 15 mm to 25 mm, and length ranged from 4 cm to 5 cm. Right atrial pressure decreased in 4/5 dogs. All but 1 dog had clinical improvement after BV, but recurrence of clinical signs occurred (2/5). Tricuspid regurgitation worsened in 1 dog culminating in right heart failure and euthanasia. CONCLUSIONS AND CLINICAL IMPORTANCE: BV can be an effective treatment; however, clinical signs can recur. Right heart failure due to worsened TR is a potential complication in dogs with pre-existing moderate-to-severe TR.

Use of Anti-Thymocyte Globulin for Induction Therapy in Cardiac Transplantation: A Review.

The most common causes of death after heart transplantation (HTx) include acute rejection and multi-organ failure in the early period and malignancy and cardiac allograft vasculopathy (CAV) in the late period. Polyclonal antibody preparations such as rabbit anti-thymocyte globulin (ATG) may reduce early acute rejection and the later occurrence of CAV after HTx. ATG therapy depletes T cells, modulates adhesion and cell-signaling molecules, interferes with dendritic cell function, and induces B-cell apoptosis and regulatory and natural killer T-cell expansion. Evidence from animal studies and from retrospective clinical studies in humans indicates that ATG can be used to delay calcineurin inhibitor (CNI) exposure after HTx, thus benefiting renal function, and to reduce the incidence of CAV and ischemia-reperfusion injury in the transplanted heart. ATG may reduce de novo antibody production after HTx. ATG does not appear to increase cytomegalovirus infection rates with longer prophylaxis (6-12 months). In addition, ATG may reduce the risk of lymphoproliferative disease and does not appear to confer an additive effect on acquiring lymphoma after HTx. Randomized, controlled trials may provide stronger evidence of ATG association with patient survival, graft rejection, renal protection through delayed CNI initiation, as well as other benefits. It can also help establish optimal dosing and patient criteria to maximize treatment benefits.

Combined Heart and Kidney Transplantation: A 23-Year Experience.

BACKGROUND: We report clinical experience with combined heart and kidney transplantation (HKTx) over a 23-year time period. METHODS: From June 1992 to August 2015, we performed 83 combined HKTx procedures at our institution. We compared the more recent cohort of 53 HKTx recipients (group 2, March 2009 to August 2015) with the initial 30 previously reported HKTx recipients (group 1, June 1992 to February 2009). Pre-operative patient characteristics, peri-operative factors, and post-operative outcomes including survival were examined. RESULTS: The baseline characteristics of the two groups were similar, except for a lower incidence of ethanol use and higher pre-operative left-ventricular ejection fraction, cardiac output, and cardiac index in group 2 when compared with group 1 (P = .007, .046, .037, respectively). The pump time was longer in group 2 compared with group 1 (153.30 ± 38.68 vs 129.60 ± 37.60 minutes; P = .007), whereas the graft ischemic time was not significantly different between the groups, with a trend to a longer graft ischemic time in group 2 versus group 1 (195.17 ± 45.06 vs 178.07 ± 52.77 minutes; P = .056, respectively). The lengths of intensive care unit (ICU) and hospital stay were similar between the groups (P = .083 and .39, respectively). In addition, pre-operative and post-operative creatinine levels at peak, discharge, 1 year, and 5 years and the number of people on post-operative dialysis were similar between the groups (P = .37, .75, .54, .87, .56, and P = .139, respectively). Overall survival was not significantly different between groups 2 and 1 for the first 5 years after transplant, with a trend toward higher survival in group 2 (P = .054). CONCLUSIONS: The most recent cohort of combined heart and kidney transplant recipients had similar ICU and hospital lengths of stay and post-operative creatinine levels at peak, discharge, and 1 and 5 years and a similar number of patients on post-operative dialysis when compared with the initial cohort. Overall survival was not significantly different between the later and earlier groups, with a trend toward higher overall survival at 5 years in the more recent cohort of patients. In selected patients with co-existing heart and kidney failure, combined heart and kidney transplantation is safe to perform and has excellent outcomes.

Atrial Fibrillation as a Prognostic Indicator in Medium to Large-Sized Dogs with Myxomatous Mitral Valvular Degeneration and Congestive Heart Failure.

BACKGROUND: The prevalence and prognostic importance of atrial fibrillation (AF) on survival in nonsmall breed dogs with myxomatous mitral valvular disease (MMVD) and congestive heart failure (CHF) remain unknown. AIM: To identify the prevalence of AF in nonsmall breed dogs with CHF because of MMVD and to characterize the impact of AF on survival outcome. ANIMAL: Sixty-four client-owned dogs (>15 kg) with MMVD and CHF. METHODS: Retrospective review of medical records for dogs weighing >15 kg with MMVD treated for CHF. RESULTS: Thirty-three dogs presented with AF or developed AF during follow-up examinations, and 31 dogs were free of AF until cardiac-related death. For dogs with AF, median survival time (MST) was 142 days (range: 9-478) while dogs without AF lived 234 days (range: 13-879 days). AF increased risk of cardiac-related death (HR = 2.544; 95% CI = 1.41-4.59; P = .0019) when compared to dogs without AF. MST was significantly prolonged for dogs with AF whose rates were adequately controlled (<160 bpm; 171 days; n = 13) when compared to dogs that failed to respond to negative chronotropic agents (61 days; n = 20; P = .032). The administration of combination treatment (diltiazem and digoxin) significantly decreased median HR to 144 bpm (range: 84-218 bpm) in dogs with AF and significantly prolonged MST (diltiazem+digoxin: 130 days versus diltiazem: 35 days, P = .0241) when compared to diltiazem alone. CONCLUSIONS AND CLINICAL IMPORTANCE: Inadequately controlled AF is associated with a higher rate of mortality. Optimization of therapeutic strategies for the rate control of AF remains determined.

Toxoplasma gondii Serology and Outcomes After Heart Transplantation: Contention in the Literature.

BACKGROUND: Toxoplasma gondii is an endemic pathogen to which approximately half of healthy patients develop antibodies. Toxoplasma serology is routinely assessed prior to heart transplantation. It has been suggested that donor or recipient toxoplasma serologic status may be associated with poor long-term outcomes post-transplantation, but current literature reveals conflicting results. METHODS: From 1995 to 2012 at our single center, we retrospectively reviewed 785 heart transplant patients for pre-transplantation T. gondii serology. Patients were divided into T. gondii seronegative and seropositive groups. Subgroups in each group were created based on whether the donor was seropositive or seronegative. We assessed survival, freedom from nonfatal major adverse cardiac events, and freedom from cardiac allograft vasculopathy at 5 years post-transplantation. RESULTS: No significant difference was found between 5-year outcomes of pre-transplant T. gondii seronegative and T. gondii seropositive recipients post-heart transplantation. However, in the donor-seropositive/recipient-seronegative subgroup (D+/R-), there was a significantly lower 5-year survival rate compared to the cohort of donor-seronegative/recipient-seronegative (D-/R-) patients (60% vs 87%, P = .04). After adjustment by multivariate analysis, D+/R- status conferred a trend towards increased mortality (HR 3.0, P = .06). CONCLUSIONS: Toxoplasma serology prior to heart transplantation does not appear to impact post-transplantation outcome. However, toxoplasma seronegative patients who receive toxoplasma seropositive hearts appear to have poorer 5-year survival compared to toxoplasma seronegative patients who received toxoplasma seronegative hearts. Due to the small sample size, the association between T. gondii serology mismatch and long-term survival warrants further study.

Anti-thymocyte gamma-globulin may prevent antibody production after heart transplantation.

BACKGROUND: Rabbit anti-thymocyte globulin (RATG) has been used as induction therapy in heart transplantation. RATG is polyclonal and has been postulated to have anti-humoral properties by preventing the production of circulating antibodies after heart transplant. Thus, we reviewed our patients who received RATG induction therapy and compared them with those who did not receive therapy for post-transplant de novo antibody production. METHODS: Between January 1, 2006, and January 1, 2013, we assessed 196 non-sensitized heart transplant recipients and divided them into those who received 3 to 5 days of RATG induction therapy mostly due to renal insufficiency (n = 35) versus patients who did not receive therapy (n = 161). All patients were given tacrolimus, mycophenolate mofetil, and corticosteroids. Post-transplant circulating antibodies were routinely monitored at 1, 3, 6, and 12 months after heart transplantation; 1-year and 3-year end points were assessed. RESULTS: The RATG-treated group had a significantly higher 12-month freedom from de novo antibody production compared with the patients who did not receive RATG induction (89% vs 71%, log-rank P = .043); however there was no significant difference for 12-month freedom from de novo donor-specific antibody production (91% vs 88%, log-rank P = .541). Treated rejection rates in the first-year were comparable in both groups; 3-year actuarial survival, freedom from cardiac allograft vasculopathy, and freedom from non-fatal major adverse cardiac events were also similar between both groups. CONCLUSIONS: RATG induction therapy appears to reduce the production of de novo circulating antibodies in non-sensitized patients during the first year after heart transplantation. Although there were no short-term clinical differences between groups, there were imbalances in group characteristics and relatively short follow-up, which are limitations to this study. A randomized, clinical trial with longer follow-up in a larger cohort of patients is warranted.

Selecting oversized donor cardiac allografts for patients with pulmonary hypertension may be unnecessary.

INTRODUCTION: There is a tendency to favor oversized donor hearts for heart transplant candidates affected by mild to moderate pulmonary hypertension (PHTN). We hypothesize that both undersized and oversized donor hearts fare equally well in this setting. METHODS: A total of 107 cases from 2003 to 2008 were retrospectively reviewed and subsequently divided into those receiving organs from undersized donors (group 1: donor weight/recipient weight ≤ 0.90, n = 37) and oversized donors (group 2: donor weight/recipient weight ≥ 1.2, n = 70). PHTN was identified in the perioperative period in those patients with systolic pulmonary artery pressure (SPAP) ≥ 40 mm Hg. Endpoints of mortality and hemodynamic data were investigated. RESULTS: Of 107 patients, 37 received undersized donor allografts, with a mean donor-to-recipient weight ratio of 0.8, and 70 received oversized donors allografts, with a mean donor-to-recipient ratio of 1.4. Perioperative PAH was diagnosed in 20 of the 37 (54%) patients from the undersized group (mean SPAP = 45.9 mm Hg) and 41 of 70 (59%) patients from the oversized group (mean SPAP = 46.5 mm Hg). There was no significant difference in right ventricular function at 1 week, 1 month, or 6 months. Left ventricular function was similar between both groups at 6 months (P = .22). The mean SPAP in the undersized group was 45.9, 33.4, 31.8, and 23.1 mm Hg at the perioperative, 1 week, 1 month, and 6 month time points, respectively. Corresponding mean SPAP for the oversized group was 46.5, 35.0, 29.4, and 26.1 mm Hg. The 1 month, 1 year, and 3 year survivals were similar in both groups. CONCLUSIONS: Oversized and undersized donor hearts fared equally well in the setting of mild to moderate perioperative PAH. This in addition to the propensity for resolution of pulmonary hypertension over time suggests that the current practice of favoring oversized donor hearts for patients with pre-transplantation PAH may be unwarranted.

Platelet activation in cats with hypertrophic cardiomyopathy.

BACKGROUND: Cats with hypertrophic cardiomyopathy (HCM) are at risk for development of systemic thromboembolic disease. However, the relationship between platelet activation state and cardiovascular parameters associated with HCM is not well described. OBJECTIVES: To characterize platelet activation by flow cytometric evaluation of platelet P-selectin and semiquantitative Western blot analysis of soluble platelet-endothelial cell adhesion molecule-1 (sPECAM-1). ANIMALS: Eight normal healthy cats (controls) owned by staff and students of the School of Veterinary Medicine and 36 cats from the UC Davis Feline HCM Research Laboratory were studied. METHODS: Platelet-rich plasma (PRP) was used for all flow cytometry studies. Platelet surface CD41 and P-selectin expression were evaluated before and after ADP stimulation. sPECAM-1 expression was evaluated by Western blot analysis of platelet-poor plasma that had been stabilized with aprotinin. Standard echocardiographic studies were performed. RESULTS: Resting platelets from cats with severe HCM had increased P-selectin expression compared to controls, and expressed higher surface density of P-selectin reflected by their increased mean fluorescence intensities (MFI). Stimulation with ADP also resulted in significantly increased P-selectin MFI of platelets from cats with severe HCM. Increased P-selectin expression and MFI correlated with the presence of a heart murmur and end-systolic cavity obliteration (ESCO). sPECAM-1 expression from cats with moderate and severe HCM was significantly increased above those of control cats. CONCLUSIONS AND CLINICAL IMPORTANCE: P-selectin and sPECAM expression may be useful biomarkers indicating increased platelet activation in cats with HCM.

Association of dilated cardiomyopathy with the striatin mutation genotype in boxer dogs.

BACKGROUND: Myocardial disease in the Boxer dog is characterized by 1 of 2 clinical presentations, dilated cardiomyopathy (DCM) characterized by ventricular systolic dysfunction, dilatation and tachyarrhythmias, and arrhythmogenic right ventricular cardiomyopathy (ARVC) characterized by ventricular tachyarrhythmias, syncope, and sudden death. Boxer ARVC has been associated with a deletion in the striatin gene in some families. HYPOTHESIS/OBJECTIVES: We hypothesized that both presentations represent a single disease, and the development of DCM in the Boxer is associated with the striatin deletion. ANIMALS: Thirty-three adult Boxer dogs with DCM, 29 adult Boxer dogs with the striatin deletion and ARVC, and 16 Boxers without cardiac disease. METHODS: DNA samples were evaluated for the striatin deletion. Association of the deletion with the DCM phenotype was tested by a Fisher's exact test. T-tests were used to evaluate potential differences between the positive heterozygous and positive homozygous groups with DCM with regard to age, LVIDD, LVIDS, and FS%. RESULTS: Thirty of 33 dogs with DCM were positive for the striatin deletion. The striatin mutation and the homozygous genotype were strongly associated with the DCM phenotype (P < .001 and P = .005). There was no statistical difference between the heterozygous and homozygous groups with regard to age and echocardiographic measurements. CONCLUSIONS AND CLINICAL IMPORTANCE: This study demonstrates an association between DCM in the Boxer dog and the striatin mutation, particularly with the homozygous genotype. The observation that 3/33 dogs developed DCM and lacked the striatin mutation suggests that there is at least 1 other cause of DCM in the Boxer dog.

Myosin-binding protein C DNA variants in domestic cats (A31P, A74T, R820W) and their association with hypertrophic cardiomyopathy.

BACKGROUND: Two mutations in the MYBPC3 gene have been identified in Maine Coon (MCO) and Ragdoll (RD) cats with hypertrophic cardiomyopathy (HCM). OBJECTIVE: This study examined the frequency of these mutations and of the A74T polymorphism to describe their worldwide distribution and correlation with echocardiography. ANIMALS: 1855 cats representing 28 breeds and random-bred cats worldwide, of which 446 underwent echocardiographic examination. METHODS: This is a prospective cross-sectional study. Polymorphisms were genotyped by Illumina VeraCode GoldenGate or by direct sequencing. The disease status was defined by echocardiography according to established guidelines. Odds ratios for the joint probability of having HCM and the alleles were calculated by meta-analysis. Functional analysis was simulated. RESULTS: The MYBPC3 A31P and R820W were restricted to MCO and RD, respectively. Both purebred and random-bred cats had HCM and the incidence increased with age. The A74T polymorphism was not associated with any phenotype. HCM was most prevalent in MCO homozygote for the A31P mutation and the penetrance increased with age. The penetrance of the heterozygote genotype was lower (0.08) compared with the P/P genotype (0.58) in MCO. CONCLUSIONS AND CLINICAL IMPORTANCE: A31P mutation occurs frequently in MCO cats. The high incidence of HCM in homozygotes for the mutation supports the causal nature of the A31P mutation. Penetrance is incomplete for heterozygotes at A31P locus, at least at a young age. The A74T variant does not appear to be correlated with HCM.

Bronchomalacia in dogs with myxomatous mitral valve degeneration.

BACKGROUND: Cough in the geriatric small breed dog with myxomatous mitral valve degeneration (MMVD), a large left atrium, and absence of heart failure often is attributed to compression of the left mainstem bronchus by the left atrium. Studies investigating this syndrome are lacking in dogs. HYPOTHESIS: Airway collapse is independent of left atrial enlargement. ANIMALS: A total of 16 dogs presenting with chronic cough in the absence of congestive heart failure. Group 1 dogs (n = 10) had moderate-to-severe left atrial enlargement based on an echocardiographically calculated left atrial:aortic surface area [LA:Ao(a)] > 6. Group 2 dogs (n = 6) had no to mild left atrial enlargement [LA:Ao(a) ≤ 6]. METHODS: Dogs were prospectively evaluated. CBC, biochemistry, urinalysis, cervical and thoracic radiographs, fluoroscopy, echocardiography, and bronchoscopy were performed. Bronchoscopic abnormalities were compared between groups using Fisher's Exact Test. P < .05 was considered significant. RESULTS: Fluoroscopy identified airway collapse in both groups. Bronchoscopic evidence of airway collapse >50% was observed in multiple bronchi with no difference between groups. All dogs had inflammation on airway cytology with respiratory infection in 1 dog in group 2. Left atrial size was interpreted radiographically as enlarged in 9 of 10 group 1 dog and in 2 of 6 group 2 dogs. VHS was above normal in both groups of dogs regardless of echocardiographic evidence of cardiomegaly. CONCLUSIONS: Results failed to identify an association between left atrial enlargement and airway collapse in dogs with MMVD, but did suggest that airway inflammation is common in dogs with airway collapse.

Occlusion devices and approaches in canine patent ductus arteriosus: comparison of outcomes.

BACKGROUND: A comparison of transvascular occlusion methods for closing patent ductus arteriosus (PDA) in dogs has not been done. OBJECTIVES: To determine if clinically important differences exist between the approaches and devices currently used. ANIMALS: A total of 112 client-owned dogs with left-to-right shunting PDA. METHODS: Retrospective study. Records from dogs that underwent attempted transvascular PDA occlusion from January 2006 to December 2009 were examined. Dogs were placed into 4 groups: Group 1: Amplatz Canine Duct Occluder (ACDO) (transarterial) - 36 dogs; Group 2: Gianturco or MReye Flipper Detachable Embolization (Flipper) coil (transarterial) - 38 dogs; Group 3: Amplatzer Vascular Plug (AVP) (transarterial) - 23 dogs; Group 4: Flipper coil (transvenous) - 15 dogs. RESULTS: The overall success rate of the procedures was high (92%) with comparable success rates among groups (87-97%). There were significantly fewer complications (P < .0001) in dogs receiving an ACDO than in the remaining groups (3% for ACDO versus 26-33% for the other groups). Fluoroscopy time for the transvenous method was significantly longer (median, 13 minutes) than for the other groups (median, 6 minutes) (P < .0001). Severity of residual flow 24 hours postprocedure was significantly less in the ACDO group than in the remaining groups (P = .0001-.05). CONCLUSIONS: The ACDO appears superior in ease of use, complication rate, and completeness of occlusion. The remaining limiting factor with this device is patient size. Until a smaller ACDO device is marketed, coils remain the only choice for interventional closure in very small dogs.

The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study.

BACKGROUND: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long-term prognosis, and in monitoring the response to therapy in humans. HYPOTHESIS: Circulating concentrations of the biomarkers N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure. ANIMALS: Six Maine Coon or Maine Coon cross cats with severe HCM. METHODS: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT-proBNP and cTnI were assayed before and on the last day of drug administration. RESULTS: There was no statistically significant change in NT-proBNP (median before, 394 pmol/L; range, 71-1,500 pmol/L; median after, 439 pmol/L; range, 24-1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10-0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09-1.0 ng/mL; P = .69) after administration of atenolol. CONCLUSIONS: Atenolol administration did not decrease NT-proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings.