Abstract
BackgroundAcute myocardial infarction (MI) following anaphylaxis is rare, especially in subjects with normal coronary arteries. The exact pathogenetic mechanism of MI in anaphylaxis remains unclear.Case presentationThe case of a 32-year-old asthmatic male with systemic anaphylaxis, due to oral intake of 500 mg amoxycillin, complicated by acute ST-elevation MI is the subject of this report. Following admission to the local Health Center and almost simultaneously with the second dose of subcutaneous epinephrine (0.2 mg), the patient developed acute myocardial injury. Coronary arteriography, performed before discharge, showed no evidence of obstructive coronary artery disease. In vivo allergological evaluation disclosed strong sensitivity to amoxycillin and the minor (allergenic) determinants of penicillin.ConclusionAcute ST-elevation MI is a rare but potential complication of anaphylactic reactions, even in young adults with normal coronary arteries. Coronary artery spasm appears to be the main causative mechanism of MI in the setting of "cardiac anaphylaxis". However, on top of the vasoactive reaction, a thrombotic occlusion, induced by mast cell-derived mediators and facilitated by prolonged hypotension, cannot be excluded as a possible contributory factor.
Highlights
Acute myocardial infarction (MI) following anaphylaxis is rare, especially in subjects with normal coronary arteries
Acute myocardial infarction (MI) complicating anaphylaxis induced by drugs or other chemicals is uncommon and only sporadic cases have been reported [1,2,3,4,5,6,7,8,9]
A 32-year-old man was admitted to the emergency room of the local Health Center because of anaphylaxis, which developed 2 hours and 15 minutes after the ingestion of amoxycillin (500 mg), prescribed by his dentist
Summary
Acute ST-elevation MI is a rare but potential complication of anaphylactic reactions, even in young adults with normal coronary arteries. It is fairly well established that that human heart can be both, the site and the target of severe anaphylaxis; in this setting cardiac mast cells – activated and releasing multiple vasoactive mediators – play an important role in pathogenesis of cardiac complications [16,17,18]. Mediator-induced coronary artery spasm was the main, but probably not the exclusive causative mechanism of anaphylaxis-related MI. The thrombotic vascular occlusion, induced by inflammatory mediators and facilitated by prolonged hypotension, cannot be excluded as a possible contributory factor. ECG = electrocardiogram; IV = intravenously; MDM = minor determinant mixute; MI = myocardial infarction; NV = normal values; PPL = penicilloyl polylysine; PST = prick skin tests; SC = subcutaneously
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