BackgroundCats 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.ObjectivesTo 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).AnimalsEight 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.MethodsPlatelet‐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.ResultsResting 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 ImportanceP‐selectin and sPECAM expression may be useful biomarkers indicating increased platelet activation in cats with HCM.

A domestic shorthaired cat was presented with a 1-month history of cardiomegaly and recurrent chylothorax. The heart rate was 130 beats/min and no P waves were present on a surface electrocardiogram. Thoracic radiographs and an echocardiogram demonstrated severe biatrial dilatation, pleural effusion and restrictive pleural disease. Permanent atrial standstill was suspected. Pleurocentesis was performed and therapy was started with enalapril, frusemide and aspirin. Intracardiac electrograms revealed no atrial activity, and atrial pacing failed to elicit atrial or ventricular depolarisations. The patient was euthanased. Necropsy showed severe atrial wall thinning with marked cardiocyte loss. Persistent atrial standstill is a rare disease in the cat. Clinical signs may have been due to loss of atrial function, ventricular diastolic dysfunction, bradycardia, neurohormonal activation and reduced atrial natriuretic peptide plasma concentrations.

A 4.5-year-old, Holstein-Friesian cow presented with a 1-month history of severe exercise intolerance. Rectal examination and transrectal ultrasonography revealed a large mass in the left retroperitoneum. The heart rate was 70 to 80/min. Premature ventricular complexes and ventricular bigeminy were present on an electrocardiogram. Erythrocytosis was present and blood gas analysis revealed marked hypoxaemia. An echocardiogram demonstrated a large ventricular septal defect, a partially dextroposed aorta, and concentric hypertrophy of the right ventricular free wall. Colour flow Doppler echocardiography and a contrast echocardiographic study demonstrated a right-to-left shunt through the ventricular septal defect. Eisenmenger's complex was diagnosed. The patient was euthanased. Necropsy confirmed the gross cardiac lesions identified by echocardiography and an abscess in the apex of the left ventricle. Severe pulmonary arterial lesions were present, consistent with a marked increased in pulmonary vascular resistance. Actinomyces pyogenes was cultured from abscesses of the retroperitoneum and the ventricular apex.