Effects of pimobendan in cats with hypertrophic cardiomyopathy and recent congestive heart failure: Results of a prospective, double-blind, randomized, nonpivotal, exploratory field study.

BACKGROUND: The benefits of pimobendan in the treatment of congestive heart failure (CHF) in cats with hypertrophic cardiomyopathy (HCM) have not been evaluated prospectively. HYPOTHESIS/OBJECTIVES: To investigate the effects of pimobendan in cats with HCM and recent CHF and to identify possible endpoints for a pivotal study. We hypothesized that pimobendan would be well-tolerated and associated with improved outcome. ANIMALS: Eighty-three cats with HCM and recently controlled CHF: 30 with and 53 without left ventricular outflow tract obstruction. METHODS: Prospective randomized placebo-controlled double-blind multicenter nonpivotal field study. Cats received either pimobendan (0.30 mg/kg q12h, n = 43), placebo (n = 39), or no medication (n = 1) together with furosemide (<10 mg/kg/d) with or without clopidogrel. The primary endpoint was a successful outcome (ie, completing the 180-day study period without a dose escalation of furosemide). RESULTS: The proportion of cats in the full analysis set population with a successful outcome was not different between treatment groups (P = .75). For nonobstructive cats, the success rate was 32% in pimobendan-treated cats versus 18.2% in the placebo group (odds ratio [OR], 2.12; 95% confidence interval [CI], 0.54-8.34). For obstructive cats, the success rate was 28.6% and 60% in the pimobendan and placebo groups, respectively (OR, 0.27; 95% CI, 0.06-1.26). No difference was found between treatments for the secondary endpoints of time to furosemide dose escalation or death (P = .89). Results were similar in the per-protocol sets. Adverse events in both treatment groups were similar. CONCLUSIONS AND CLINICAL IMPORTANCE: In this study of cats with HCM and recent CHF, no benefit of pimobendan on 180-day outcome was identified.

Pilot study on cardiac troponin I levels in dogs with pericardial effusion.

OBJECTIVES: The aim of this pilot study was to assess cardiac troponin I (cTnI) levels in pericardial effusion (PE) and plasma from dogs with PE. BACKGROUND: A reliable marker for detecting the etiology of PE in dogs remains undetermined. cTnI is becoming the gold standard marker for detecting myocardial damage in humans. ANIMALS, MATERIALS AND METHODS: Twenty-five dogs with PE (21 and 4 secondary to neoplasia and non-neoplasia causes, respectively) and 37 control dogs were studied. RESULTS: The median cTnI plasma level from 37 normal dogs versus 15 (out of 25) with PE was 0.03ng/mL and 0.19ng/mL, respectively (p<0.0001). The level of cTnI in PE versus plasma showed a significant correlation (p<0.01) with a Spearman r coefficient of 0.7603. No significant difference could be found upon comparison of dogs with only right atrial tumors (n=14) versus other types of neoplasia (n=7), nor between the group with right atrial tumors (n=14) versus all other cases including neoplasia as well as non-neoplasia (n=11). The median cTnI level in PE from dogs with neoplasia and non-neoplasia was not significantly different. CONCLUSIONS: cTnI did rise significantly in both PE and plasma in dogs with PE, but cTnI levels did not help differentiate between etiologies according to this study. One of the study groups is too small to allow final conclusions, and thus further investigation is warranted.

Aneurysmal dilatation of the right auricle in two dogs.

An 8-year-old sexually intact male Golden Retriever with a history of collapse during exercise underwent an examination during which tachydysrhythmia was identified. At another institution, a 12.5-year-old spayed female Lhasa Apso was referred because of a cough and for evaluation of a heart murmur. In the Golden Retriever, radiographic examination revealed bulging of the craniodorsal aspect of the cardiac silhouette and echocardiography revealed right atrial dilatation. In the Lhasa Apso, a cranial mediastinal mass was suspected on the basis of radiographic findings, but no abnormalities were detected echocardiographically. In both dogs, nonselective angiography and contrast-enhanced computed tomography revealed a markedly enlarged, thin-walled right auricle. Exploratory thoracotomy in the Golden Retriever revealed a defect in the pericardium through which the right auricle and part of the atrium had herniated. In dogs, a right auricular aneurysm should be considered in differential diagnoses of a cranial mediastinal mass (detected radiographically) adjacent to the cardiac silhouette.

Patent ductus arteriosus ligation and pulmonary artery banding in a kitten.

Patent ductus arteriosus (PDA) and ventricular septal defect were diagnosed in a 2-month-old, 0.9-kg, male kitten. This combination of PDA and ventricular septal defect in a cat has not been previously described. Surgical ligation of the PDA, together with palliation of the ventricular septal defect by pulmonary artery banding with a silastic band, successfully improved the kitten's condition.

Appendicular arterial tumor embolization in two cats with pulmonary carcinoma.

A 13-year-old neutered male Persian cat and an 11-year-old neutered female Persian cat were examined because of an acute onset of lameness. In both cats, conscious proprioception and reflexes were diminished in the affected limb. In 1 cat, no blood flow was detected in the left brachial artery with a Doppler ultrasonic flow detector, whereas blood flow in the right brachial artery was easily documented. In the other cat, the right femoral pulse was not palpable. Neither cat had any echocardiographic evidence of cardiac disease. In both cats, treatment was primarily supportive. One cat died, and the other was euthanatized. At necropsy, lung lobe consolidation was seen. Microscopically, there was multifocal infiltration of the lung parenchyma with cuboidal to columnar neoplastic epithelial cells. Neoplastic epithelial cells of similar morphology were identified in nodular masses in sections of muscle, and intravascular tumor emboli were identified obliterating small and large arterioles. Immunohistochemical staining of pulmonary and muscular tissue for pan-cytokeratin antigen revealed intense cytoplasmic staining of neoplastic cells. Staining for factor VIII-related antigen confirmed that clusters of neoplastic cells represented intravascular emboli. Clinical signs in the cats were attributed to arterial occlusion by tumor emboli.

Echocardiography in the chinchilla.

Heart disease has been described in the chinchilla and, with increasing popularity as a pet, the demand for diagnostic evaluation and treatment has increased. The goal of this study was to determine reference values for echocardiographic measurements in chinchillas and the effect of anesthesia on these measurements. Seventeen clinically healthy adult chinchillas were studied. All animals were anesthetized with isoflurane by mask. Standard echocardiographic views were used. A difference was seen in the echocardiographic measurements for left ventricular systolic dimension, fractional shortening, aortic (Ao) diameter, left atrial (LA) diameter, ratio of LA diameter to Ao diameter, and peak flow velocities and ejection times for Ao and pulmonary artery flows between awake and anesthetized chinchillas.

Cardiac troponin I in feline hypertrophic cardiomyopathy.

Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.