A 58-year-old man with a history of hypertension was admitted to our institution with progressively increasing dyspnea on exertion and bilateral leg edema. He did not use alcohol, tobacco, or recreational drugs. On physical examination, jugular venous distention 12 cm above the sternal angle of Lewis was noted, along with bibasilar crackles, S3 and S4 gallops, 2+ bilateral lower-extremity pitting edema, and papular, brown, non-tender skin lesions on his legs and forearms. Electrocardiography revealed sinus tachycardia, left atrial enlargement, and an intraventricular conduction defect with nonspecific ST-T wave abnormalities. Chest radiography showed cardiomegaly and pulmonary congestion. Two-dimensional echocardiography revealed a severely dilated left atrium (LA) and left ventricle (LV), severe left ventricular systolic dysfunction (LV ejection fraction, 0.20), mild right ventricular (RV) enlargement, and mild RV systolic dysfunction (Fig. 1). The left ventricular end-diastolic dimension was 6.84 cm and the end-systolic dimension was 5.83 cm (Fig. 2). The patient underwent coronary angiography, which showed normal epicardial coronary arteries. An endomyocardial biopsy was performed; results revealed non-caseating granulomas and multinucleated giant cells (arrows), with active myocyte damage and focal interstitial fibrosis (Figs. 3 and 4; H + E, orig. ×100, ×400). Acid-fast bacilli and Gomori methena-mine silver stains for organisms were negative. Similar non-caseating granulomas were identified in punch biopsies of the skin lesions. Computed tomography of the chest showed diffuse mediastinal lymphadenopathy with increased interstitial lung markings. Pulmonary function tests revealed a mild restrictive disease pattern. From these findings, we were able to arrive at a diagnosis of cardiac sarcoidosis. The patient was treated with oral steroids. Five months later, repeat 2-dimensional echocardiography showed improvement in left ventricular systolic function (LV ejection fraction, 0.40).




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