Abstract
In feline hypertrophic cardiomyopathy (HCM), we hypothesized that a decrease in local release of prostacyclin (PGI2) and/or an unbalanced ratio of thromboxane A2 to PGI2 in the myocardium may induce microcirculatory disturbance, and aggravate the disease, we performed long-term treatment with beraprost sodium (BPS), a PGI2 derivative, on two cats with HCM, and made an echocardiographic examination of its effect morphologically and functionally. The left ventricular posterior wall and interventricular septum became thinner; The left ventricular end-systolic and end-diastolic diameters, left ventricular end-systolic and end-diastolic volumes, left ventricular fractional shortening, and left ventricular ejection fraction were remarkably improved, leading to an increase in cardiac output. Consequently, BPS might be an effective agent for feline HCM.
