Cocaine-induced myocardial infarction: not your average acute coronary syndrome

Abstract

A 31-year-old woman presented to accident and emergency at 03.20 hrs complaining of central chest pain since the preceding evening. She denied any significant medical history or family history and initially denied taking any medication or drugs of abuse. On examination her pulse was 110 beats per minute and her blood pressure 126/82 mmHg but there were no other abnormal physical findings. Her initial electrocardiogram showed multiple ventricular ectopics with periods of idioventricular rhythm but no acute ST segment elevation that met thrombolysis criteria (Figure 1). She was initially treated with aspirin, low molecular weight heparin and intravenous nitrates. Although her symptoms of pain resolved overnight, the electrocardiogram evolved Q waves suggesting a significant anterior myocardial infarction (Figure 2). This was confirmed by a raised cardiac troponin T level at 12 hours. It was not until some 15 hours after admission, and only after direct questioning, that she admitted to being a regular cocaine user, often using up to 3 g per week. She had smoked a pipe containing crack cocaine the preceding evening, and then immediately afterwards injected cocaine into a femoral vein. She described a euphoric rush followed by a non-resolving severe chest pain. She underwent coronary angiography 36 hours after presentation which revealed a thrombus in the proximal left anterior descending artery (Figure 3). The coronary arteries were angiographically normal, with no evidence of angiographic atheromatous disease. She was treated with intravenous heparin and abciximab, and thereafter remained pain free and haemodynamically stable. An echocardiogram showed severe left ventricular impairment (ejection fraction 30%) with gross apical dyskinesis. She was discharged on aspirin and an angiotensin-converting enzyme inhibitor and given strong advice to cease using cocaine. She failed to return for pre-arranged follow up, was not registered with the GP she indicated and could not be traced through the NHS database.

Peripheral blood microRNA levels in females with cocaine use disorder

“…Interestingly, the systemic pathophysiology of CUD includes several metabolic alterations. For instance, chronic cocaine use is associated with increased prevalence of hypertension (Brecklin, Gopaniuk-Folga, Kravetz et al, 1998) and myocardial infarction (Behar, Lindsay & McEwan, 2009), which are hallmark features of metabolic syndrome (Virmani, Binienda, Ali et al, 2007). In addition, we and others have found elevated blood levels of adiponectin, a protein hormone that modulates a number of metabolic processes such as glucose uptake and fatty acid oxidation, among individuals with CUD during early abstinence (Levandowski, Viola, Tractenberg et al, 2013;You, Wang, Gardner et al, 2019).…”