Cocaine-induced myocardial injury seen as multiple mid-wall foci of late enhancement by contrast-enhanced cardiac magnetic resonance imaging

A previously well 26-year-old man presented with severe retrosternal chest pain. There were no associated symptoms, and no relationship of the pain to inspiration, exertion, or posture. He was a frequent user of cocaine, most recently 48 h prior to presentation. Initial cardiac enzymes were substantially elevated [creatine kinase level 710 U/L (normal range 40–300 U/L) and troponin I 10.3 µg/L (normal value <0.14 µg/L)] but rapidly returned to normal values. Twelve-lead electrocardiogram showed biphasic T-waves in the inferolateral leads. Computed tomography of the coronary and pulmonary arteries was normal. Cardiac magnetic resonance (CMR) imaging performed the day after presentation demonstrated normal left ventricular function with no evidence of regional wall motion abnormality, pericardial effusion, or pericardial enhancement on late gadolinium imaging. However, there were multiple foci of mid-wall and subepicardial late enhancement (LE) in the apical septum and apical lateral wall consistent with myocardial infarction or fibrosis. Cocaine-associated cardiovascular complications such as arrhythmia, myocardial infarction, and sudden death are usually linked to catecholamine excess caused by presynaptic reuptake blockade of dopamine and its subsequent biosynthesis to noradrenaline and adrenaline. Adrenergic hyperstimulation increases myocardial oxygen demand through tachycardia, arterial hypertension, and hyperdynamic left ventricular contractility. Additionally, cocaine administration increases endothelin-1 (a potent vasoconstrictor) and thromboxane production. Therefore, myocardial injury can be caused by any combination of a variety of different mechanisms such as increased oxygen demand or decreased supply, e.g. through epicardial coronary spasm, atherosclerotic plaque rupture, or de novo thrombus formation in otherwise non-stenotic coronary arteries. There is also a direct toxic effect of excess catecholamines on cardiac myocytes. Myocardial LE detected by CMR imaging represents irreversible myocardial damage. This is most commonly secondary to coronary artery disease and related infarction, where the pattern of enhancement is subendocardial in the distribution of the specific coronary artery territory. In contrast, the multiple, well-defined mid-wall foci seen in this case are not restricted to a single coronary artery territory and likely reflect infarction secondary to cocaine-induced vasoconstriction of coronary arterioles. Although this has long been considered a likely mechanism of cocaine-induced myocardial injury, we believe that this is the first CMR imaging evidence in support of this phenomenon. The authors would like to acknowledge James House and Anne Bright from North Shore Radiology for their assistance in the acquisition of the CMR images. Supported by grants from the North Shore Heart Research Foundation and the Medical Foundation, University of Sydney, Australia. Panels A–D. Late gadolinium enhancement imaging identifying multiple mid-wall and subepicardial foci (four-chamber view: Panel A, end-diastole, and Panel B, end-systole, white arrows) of myocardial injury 8 min after administration of 0.2 mmol/kg body weight of gadolinium-DTPA (Magnevist, Schering). Corresponding four-chamber b-SSFP cine images displaying normal biventricular function at end-diastole (Panel C) and end-systole (Panel D; 1.5 T General Electric MRI scanner).