Abstract
A 25-year-old white woman was referred to the outpatient cardiology clinic at our institution for a second opinion regarding a newly diagnosed cardiomyopathy. She was in a normal state of excellent health, without a significant past medical history, when she began to develop exertional fatigue, dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Her primary care provider diagnosed her with pneumonia. The following day she developed severe, cramping pain in her right leg associated with pallor. She was hospitalized and diagnosed with an arterial embolization of her right femoral artery. She was managed with tissue plasminogen activator and thrombectomy, resulting in the reconstitution of her right lower extremity arterial supply. While hospitalized, the patient underwent a transthoracic echocardiogram that demonstrated a mildly dilated left ventricle (LV) with an ejection fraction (EF) of approximate to 30%, a negative microcavitation study, and no evidence of LV thrombus. N-terminal probrain natriuretic peptide was 2296 pg/mL (normal <190 pg/mL). After a standard medical regimen for heart failure, warfarin was initiated because of the arterial thromhoembolic event. Tests for Factor V Leiden mutation, protein C/S deficiency, and prothrombin gene mutation were negative. After hospital discharge she continued to experience cardiovascular symptoms. She could walk only 1 Hight of stairs without shortness of breath. She had ongoing fatigue and lost z10 pounds. She had no history of tobacco use and consumed only minimal alcohol. Her family history was remarkable for aortic dissection in her father at 49 years of age but otherwise was without cardiovascular disease. Physical examination was notable for a heart rate of 97, blood pressure of 100/70, and body mass index of 18.1. Her jugular venous pressure was estimated at 10 to 12 cm of water. She had an audible S3 gallop without murmurs and no lower extremity edema. ECG showed normal sinus rhythm with hiatrial enlargement and a QRS duration of 84 ms.