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Aortic valve endocarditis causing fatal myocardial infarction caused by ostial coronary artery obliteration
  1. M Schmitt,
  2. S Puri,
  3. N R Dalal

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A 43 year old man developed biventricular heart failure over a period of eight weeks following dental extraction. On admission he was found to have severe congestive hepatopathy with profound jaundice, pronounced ascites, and peripheral oedema. Auscultation of the heart revealed a 3/6 holosystolic and a 3/6 diastolic decrescendo murmur, both audible over all precordium. Transthoracic echocardiography (see panels) confirmed moderate to severe aortic regurgitation and the presence of a large vegetation (VEG), located apparently at the downstream side (vegetations typically arise from the upstream side of valve leaflets/cusps) of the right coronary cusp of the aortic valve (parasternal short axis and long axis views show a partly obstructive mass in the aortic root above the right coronary cusp). The patient, at the time unfit for surgical intervention, was treated medically with oral angiotensin converting enzyme inhibition, intravenous antibiotics, diuretics, subcutaneous heparin, and percutaneous ascites drainage. He made a steady recovery clinically before dying suddenly 13 days following hospital admission. Blood cultures had remained sterile throughout. Postmortem examination revealed absence of significant coronary artery disease but presence of a myocardial infarction of the posterior wall of the left ventricle. A large friable vegetation measuring 2.1 × 1.5 × 1.0 cm appeared to occlude the ostium of the left coronary artery. Acute myocardial infarction caused by coronary artery occlusion and/or embolisation is a rare but recognised complication of aortic valve endocarditis. Vegetation size (> 10 mm), extent, mobility, and consistency have been proposed as echocardiographic predictors of systemic embolic events in some but not all studies.

This case highlights the risk of acute myocardial infarction associated with very large aortic valve vegetations and emphasises that the relative risk for embolisation may not dramatically decline with time after initiation of antimicrobial treatment.

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