Hoyos-Gutierrez S, Gómez-Ramírez LA, Torres-Zapata A, Mazo JA, Berrouet-Mejía MC

Language: Spanish
References: 11
Page: 117-121
PDF size: 325.65 Kb.

ABSTRACT

Introduction: cocaine is an illicit stimulant associated with acute coronary syndrome in young adults without traditional cardiovascular risk factors. Its sympathomimetic effects induce coronary vasospasm, endothelial dysfunction, platelet activation, and thrombus formation. Concomitant alcohol use leads to the formation of cocaethylene, a metabolite with greater cardiotoxicity and a prolonged half-life. During pregnancy and the postpartum period, hemodynamic adaptations may increase cardiovascular vulnerability to these effects.
Objective: to describe two distinct phenotypes of acute myocardial infarction (AMI) associated with cocaine use and highlight the importance of a pathophysiology-oriented management approach.
Cases: Case 1: a 20-year-old woman in the immediate postpartum period with a history of chronic cocaine and alcohol use presented after recent consumption of both substances and developed hemodynamic collapse. Elevated troponin levels, ischemic electrocardiographic changes, and non-obstructive coronary arteries were documented, consistent with myocardial infarction with non-obstructive coronary arteries (MINOCA). She was treated with benzodiazepines, vasodilators, and acute heart failure management, with favorable clinical recovery. Case 2: a 32-year-old man with habitual cocaine use presented with chest pain and elevated troponin levels. Coronary angiography revealed a 100% thrombotic occlusion of the distal circumflex artery and the obtuse marginal branch. Thromboaspiration and drug-eluting stent implantation were performed, resulting in complete clinical recovery.
Discussion: cocaine use may produce different mechanisms of coronary injury, including MINOCA mediated by vasospasm or microthrombosis, as well as frank coronary thrombosis. In the postpartum setting, physiological cardiovascular adaptations may further potentiate these effects. Management should focus on controlling adrenergic discharge and coronary vasospasm, or performing percutaneous coronary intervention when thrombotic occlusion is present.
Conclusions: cocaine-associated myocardial infarction should be suspected in young patients presenting with chest pain or cardiovascular collapse, even in the presence of angiographically normal coronary arteries. Identifying the underlying pathophysiological mechanism allows targeted treatment and may reduce complications.

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