BackgroundHypertrophic cardiomyopathy is the most prevalent heart disorder in cats and principal cause of cardiovascular morbidity and mortality. Yet, the impact of preclinical disease is unresolved.Hypothesis/ObjectivesObservational study to characterize cardiovascular morbidity and survival in cats with preclinical nonobstructive (HCM) and obstructive (HOCM) hypertrophic cardiomyopathy and in apparently healthy cats (AH).AnimalsOne thousand seven hundred and thirty client‐owned cats (430 preclinical HCM; 578 preclinical HOCM; 722 AH).MethodsRetrospective multicenter, longitudinal, cohort study. Cats from 21 countries were followed through medical record review and owner or referring veterinarian interviews. Data were analyzed to compare long‐term outcomes, incidence, and risk for congestive heart failure (CHF), arterial thromboembolism (ATE), and cardiovascular death.ResultsDuring the study period, CHF, ATE, or both occurred in 30.5% and cardiovascular death in 27.9% of 1008 HCM/HOCM cats. Risk assessed at 1, 5, and 10 years after study entry was 7.0%/3.5%, 19.9%/9.7%, and 23.9%/11.3% for CHF/ATE, and 6.7%, 22.8%, and 28.3% for cardiovascular death, respectively. There were no statistically significant differences between HOCM compared with HCM for cardiovascular morbidity or mortality, time from diagnosis to development of morbidity, or cardiovascular survival. Cats that developed cardiovascular morbidity had short survival (mean ± standard deviation, 1.3 ± 1.7 years). Overall, prolonged longevity was recorded in a minority of preclinical HCM/HOCM cats with 10% reaching 9‐15 years.Conclusions and Clinical ImportancePreclinical HCM/HOCM is a global health problem of cats that carries substantial risk for CHF, ATE, and cardiovascular death. This finding underscores the need to identify therapies and monitoring strategies that decrease morbidity and mortality.

Double-chambered right ventricle (DCRV) is possibly an emerging congenital cardiac anomaly in dogs. The defect causes clinical and pathophysiologic signs similar to those of congenital pulmonic stenosis in dogs but has distinct diagnostic features, breed predilections, and implications for treatment. The defect is often associated with clinical signs early in life. Surgical correction of DCRV can be undertaken with the aid of cardiopulmonary bypass and offers the prospect of an improved clinical outcome.

West Nile virus (WNV)-associated disease has a range of clinical manifestations among avian taxa, the reasons for which are not known. Species susceptibility varies within the avian family Corvidae, with estimated mortality rates ranging from 50 to 100%. We examined and compared virologic, immunologic, pathologic, and clinical responses in 2 corvid species, the American crow (Corvus brachyrhynchos) and the fish crow (C ossifragus), following experimental WNV inoculation. Unlike fish crows, which remained clinically normal throughout the study, American crows succumbed to WNV infection subsequent to dehydration, electrolyte and pH imbalances, and delayed or depressed humoral immune responses concurrent with marked, widespread virus replication. Viral titers were approximately 3,000 times greater in blood and 30,000 to 50,000 times greater in other tissues (eg, pancreas and small intestine) in American crows versus fish crows. Histologic lesion patterns and antigen deposition supported the differing clinical outcomes, with greater severity and distribution of lesions and WNV antigen in American crows. Both crow species had multiorgan necrosis and inflammation, although lesions were more frequent, severe, and widespread in American crows, in which the most commonly affected tissues were small intestine, spleen, and liver. American crows also had inflammation of vessels and nerves in multiple tissues, including heart, kidney, and the gastrointestinal tract. WNV antigen was most commonly observed within monocytes, macrophages, and other cells of the reticuloendothelial system of affected tissues. Collectively, the data support that WNV-infected American crows experience uncontrolled systemic infection leading to multiorgan failure and rapid death.

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Obstruction to pulmonary blood flow as a result of neoplasia in the right ventricular outflow tract is described in two dogs. Whereas one dog had exertional syncope and a systolic ejection murmur, the other had signs of congestive failure and hypoxia. In both animals the mass was detected in the right ventricle with two-dimensional echocardiography and confirmed angiographically. Although rare, primary right ventricular neoplasia represents a potentially treatable form of cardiac disease and should be considered as a cause of acquired outflow tract obstruction. (Journal of Veterinary Internal Medicine 1990; 4:12-16) PRIMARY tumors of the heart, although uncommon, occur with sufficient frequency in dogs that clinicians should be aware of the manifestations of cardiac neoplasia and should consider neoplasia in the differential diagnosis of heart disease.'.' However, the clinical manifestations of cardiac neoplasia are highly variable making antemortern diagnosis difficult. This study describes the clinical, echocardiographic, hemodynamic, and angiographic features of primary right ventricular neoplasia in two dogs. In both dogs the tumor produced obstruction of the right ventricular outflow tract. Case Reports Dog IAn eight-year-old, spayed female Bassett Hound cross weighing 30 kg was referred to the University of Tennessee Veterinary Teaching Hospital for evaluation and treatment of anasarca and dyspnea of two weeks duration. The dyspnea and edema had improved with furosemide therapy. Tests for circulating microfilaria and heartworm antigen were negative.During physical examination the heart rate was slightly elevated ( 180 beats per minute), but auscultation of the heart was otherwise normal. The jugular veins were distended. and the liver was palpably enlarged. The dog was tachypneic (60 breaths per minute).An electrocardiogram showed abnormally deep S waves in leads 11, 111, aVF, CV6LL, and CV6LU and a right axis deviation in the frontal plane (mean electrical axis, 260"). These ECG changes were suggestive of right ventricular enlargement.Survey thoracic radiographs revealed an enlarged right heart and caudal vena cava. The main pulmonary artery and peripheral pulmonary vasculature were unremarkable. The dog's packed cell volume and red blood cell count (RBC) were high normal (PCV = 5096, RBC = 8.66 X 106/pl), and there was a slight increase of the alkaline phosphatase (189 units/L). The central venous pressure was 20 cm HzO (normal < 7 cm HzO) indicating right heart failure.Two-dimensional and M-mode echocardiographic examination* demonstrated normal left heart structure and function. However, the right atrium and right ventricle were eccentrically hypertrophied, and there was an echodense mass located within the right ventricular outflow tract (Fig. I). The mass was best seen using left cranial and left caudal long-axis views.3Right heart catheterization revealed right ventricular systolic hypertension consistent with right ventricular outflow obstruction or pulmonary hypertension (peak systolic pressure = ...