A 65‐year‐old man with a medical history significant for hypertrophic cardiomyopathy presented with a 3‐week history of mid‐sternal chest pain, fevers, and sweats. His primary care physician sent him to the emergency department after outpatient blood cultures returned positive for S. viridans. He denied recent dental procedures, surgeries, or cough. Physical exam revealed a temperature of 38.5 degrees Celsius, diaphoresis, and a crescendo decrescendo mid‐to‐late peaking systolic murmur heard best at the apex and left lower sternal border. There was no evidence of vascular phenomena. EKG showed sinus tachycardia with left ventricular hypertrophy. TEE demonstrated a thickened ventricular septum measuring 3.4 centimeters in diastole, left atrial enlargement, and a mobile vegetation on the anterior mitral valve leaflet. On TTE, the resting peak systolic gradient of the left ventricular outflow tract was elevated at 65 mmHg. There was mild to moderate mitral regurgitation without prolapse of the mitral valve. During his hospital course, he defervesced and was discharged with intravenous ceftriaxone on hospital day 5.
Hypertrophic cardiomyopathy (HCM) is a relatively common disease, occurring in about 1 of every 500 people. It is typically characterized by ventricular septal hypertrophy and can uncommonly manifest as sudden death, primarily as a result of ventricular arrhythmias1. However, other complications may occur, which include atrial fibrillation, heart failure, and less commonly infective endocarditis (IE). Although IE is uncommon in the HCM population (1.4 per 1000 person‐years)2, the incidence is greater than community‐acquired native‐valve IE (1.7‐6.2 per 100,000 person‐years)3, and its morbidity and mortality risk is high. The literature on IE in HCM is scant, but all cases have occurred when the left ventricular outflow is obstructed under resting conditions2 (≥ 30 mmHg), as was the case in this patient. Some theorize that obstructive HCM carries an increased risk of IE because high velocity and turbulent blood flow during systole, as well as contact between the anterior mitral valve leaflet and septum, damage the valve endocardium. The damaged valve serves as a nidus for bacterial adherence. Although there is controversy4, the American Heart Association guidelines5 do not recommend antibiotic prophylaxis for most individuals with HCM prior to dental procedures. However, now that this patient has developed IE, he is a candidate for future antibiotic prophylaxis.
Hospitalists should be aware of the risk of IE in patients with HCM, particularly when left ventricular outflow tract obstruction is present.
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