Ventricular Tachyarrhythmias in 106 Cats: Associated Structural Cardiac Disorders

Background: Ventricular tachyarrhythmias occur in association with cardiac and extracardiac disorders in many species of animals, but information identifying concurrent disorders in cats with such arrhythmias is scarce. Methods: We investigated coexisting diseases by retrospectively evaluating medical records of cats with ventricular tachyarrhythmias seen during a 51‐month period at 1 institution. For comparative purposes, we evaluated records of dogs with similar arrhythmias during the same time period. All cats and dogs had premature ventricular complexes, accelerated idioventricular rhythm, ventricular tachycardia, or some combination of these arrhythmias, and all had undergone echocardiography during the same visit that led to the diagnosis of ventricular tachyarrhythmia. Results and Conclusions: Most (102/106; 96%) cats had at least 1 echocardiographically apparent abnormality concurrent with ventricular tachyarrhythmias. Ventricular tachyarrhythmias in cats were most commonly associated with myocardial disease (eg, left ventricular concentric hypertrophy [n = 66], restrictive or unclassified cardiomyopathy [n = 17], and dilated cardiomyopathy [n = 6]). When comparing dogs and cats that had ventricular tachyarrhythmias and were diagnosed on the same clinical service of the same institution, an echocardiographically apparent cardiac lesion was seen more often in cats (102/106, 96%) than in dogs (95/138, 69%) (P < .001).     

Bradycardia-Associated Syncope in 7 Boxers with Ventricular Tachycardia (2002–2005)

Background: Syncope is a recognized problem in Boxers and often is the result of rapid ventricular tachycardia (VT). Affected dogs may have echocardiographic evidence of dilated cardiomyopathy, but frequently have normal echocardiograms. Although VT is probably the most common cause of syncope in Boxers, neurocardiogenic bradycardia can also occur.
Objective: We describe 7 Boxers with comorbid VT and neurocardiogenic bradycardia, wherein the syncope was secondary to bradycardia rather than VT.
Animals: Seven Boxers were selected from a larger population of Boxers with Holter-documented VT because these dogs had documented bradycardia at the time of syncope.
Methods: Retrospective study.
Results: Although all dogs had Holter-documented VT, the etiology of the syncopal episodes was consistent with neurocardiogenic bradycardia.
Clinical Importance: Neurocardiogenic bradycardia or VT can occur as isolated problems in Boxers. In some Boxers, VT and potential or manifest neurocardiogenic bradycardia coexist. The administration of a β-blocker or sotalol to such dogs can aggravate or precipitate neurocardiogenic bradycardia-related syncope.     

Cardioversion of supraventricular tachycardia using lidocaine in five dogs

Sustained supraventricular tachycardia (SVT) may lead to life-threatening complications such as tachycardia-induced myocardial failure. We report the use of intravenous lidocaine in 5 dogs with SVT. Two dogs had evidence of an accessory conduction pathway, 2 were suspected of having an accessory pathway, and the mechanism of SVT was unknown in the remaining dog, which subsequently developed dilated cardiomyopathy 2 years later. In all cases there was rapid conversion to normal sinus rhythm, which was then maintained with oral mexilitene (4 dogs) or mexilitene combined with propranolol (1 dog).     

Evaluation of plasma C-terminal atrial natriuretic peptide in healthy cats and cats with heart disease

BACKGROUND: The clinical implications of evaluating C-terminal atrial natriuretic peptide (ANP) concentration in cats are still controversial. HYPOTHESIS: The objective of this study was to investigate the relationship between plasma C-terminal ANP concentration and left atrial pressure (LAP) in healthy cats with volume overload (study 1), and to compare plasma C-terminal ANP in normal cats and cats with cardiomyopathy (study 2). ANIMALS: Five healthy adult cats were used in study 1, and clinically healthy cats (n=8) and cats with cardiomyopathy (n=14) were used in study 2. METHODS: In study 1, cats were anesthetized and given acetated Ringer's solution (100 mL/kg/h for 60 minute) via the cephalic vein. Hemodynamic measurements and blood samples, collected from the jugular vein, were performed at 10-min intervals. In study 2, blood samples from normal cats and cats with cardiomyopathy were collected from the cephalic vein. The plasma C-terminal ANP concentration was determined by radioimmunoassay for human alpha-ANP. RESULTS: In study 1, volume overload significantly increased the C-terminal ANP concentration and LAP from baseline. The C-terminal ANP concentration was strongly correlated with the mean LAP. In study 2, age, E wave velocity, and the ratios of the left atrium to aorta were significantly higher in the cats with cardiomyopathy compared with the normal cats. The C-terminal ANP concentration was significantly higher in the cats with cardiomyopathy compared with the normal cats. CONCLUSIONS AND CLINICAL IMPORTANCE: Our results suggest that the measurement of plasma C-terminal ANP in cats may provide additional information for the diagnosis of heart disease.     

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.     

Distinguishing cardiac and noncardiac dyspnea in 48 dogs using plasma atrial natriuretic factor, B-type natriuretic factor, endothelin, and cardiac troponin-I

BACKGROUND: It is challenging to differentiate congestive heart failure (CHF) from noncardiac cause of dyspnea. HYPOTHESIS: Circulating concentrations of atrial natriuretic peptide (NT-proANP), B-type natriuretic peptide (BNP), endothelin-I (ET-1), and cardiac troponin-I (cTnI) can be used to help distinguish between cardiac and noncardiac causes of dyspnea in dogs. ANIMALS: Forty-eight client-owned dogs admitted to a veterinary teaching hospital for respiratory distress. METHODS: Blood samples from patients were prospectively obtained. The etiology of dyspnea was determined by using physical examination, thoracic radiographs, and echocardiography. RESULTS: CHF was diagnosed in 22 dogs, and dyspnea of noncardiac origin (noHD group) was diagnosed in 26 dogs. Analyses revealed significant difference between groups for NT-proANP (geometric mean, 95% confidence [CI]; no HD: 0.26 nmol/mL, 95% CI 0.17-1.09; CHF: 1.38 nmol/mL, 95% CI 1.09-1.74 nmol/mL; P < .0001), BNP (noHD: 12.18 pg/mL, 95% CI 10.91-16.17 pg/mL; CHF: 34.97 pg/mL, 95% CI 23.51-52.02 pg/mL; P < .0001), and ET-1 (noHD: 0.32 fmol/mL, 95% CI 0.23-0.46 fmol/mL; CHF: 1.26 fmol/mL, 95% CI 0.83-1.91 fmol/mL; P < .0001). Plasma cTnI concentrations were not significantly different between groups (noHD: 0.29 ng/mL, 95% CI 0.12-0.72 ng/mL; CHF: 0.42 ng/mL, 95% CI 0.18-0.97, P = .53). Receiver operating curves indicated areas under the curve for NT-proANP, BNP, and ET-1 of 0.946, 0.886, and 0.849, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Plasma NT-proANP, BNP, and ET-1, but not cTnI, appear useful for distinguishing between dogs with cardiac and noncardiac causes of dyspnea, with plasma NT-proANP having the highest sensitivity (95.5%) and specificity (84.6%).