An 11-year-old female spayed Domestic Shorthair cat presented to Cornell’s Cardiology Service for an annual echocardiogram recheck for hypertrophic cardiomyopathy (HCM). Eleven years before this presentation, she was diagnosed with HCM with a III/VI systolic heart murmur, the point of maximum intensity over the left apex, thickened interventricular septum and left ventricular free wall, systolic anterior motion of the mitral valve causing left ventricular outflow tract obstruction and mitral regurgitation, but no clinical signs of heart disease at home. She was treated with beta blockers. One year before this presentation, her HCM progressed with a large left atrium, so anticoagulants were added to her treatment. Since her last visit, she has been clinically healthy. On presentation, the patient had a regular heart rhythm with no murmur, and normal heart structure and function on echocardiogram. Anticoagulant therapy was stopped, and the beta blockers were continued because the patient has been doing well on them for 11 years.

Since HCM does not reverse itself, we suspect the patient had transient myocardial thickening (TMT) associated with a myocarditis of unknown origin. In humans, myocardial edema causing transient left ventricular wall thickening is well described. The cause of myocarditis is not usually identified, although infectious agents, drugs, and toxic agents have been reported to cause myocarditis. In animals, myocarditis is poorly understood, although antecedent general anesthesia, trauma, fever, and drugs have been associated.

Elevated serum cardiac troponin I (cTnI) is associated with TMT. In humans, elevated cTnI implies a myocardial infarction. However, in animals, elevated cTnI can be from infarction, myocarditis, HCM, and a number of other syndromes. Unfortunately, cTnI was not measured in the patient.

Recently, the patient was presented to the Cardiology Service in left sided heart failure with the HCM phenotype, dilated atria, and an elevated cTnI and was treated by adding a diuretic, positive inotrope, and anticoagulant, while stopping the beta blocker. This evidence further supports our suspicions of TMT.