Sudden cardiac death complicating acute myocardial infarction following synthetic cannabinoid use

Abstract

Synthetic cannabinoids represent a large and heterogeneous group of agents, broadly producing psychotropic effects of a similar nature to tetrahydrocannabinol (THC), the active component of cannabis. In recent years, a variety of such preparations has become readily available, with a perception that these may represent a safe and legal alternative to cannabis use.

The advent of these synthetic cannabinoids exposes the user to as yet unrecognised adverse effects on the cardiovascular system, in addition to the established and anticipated psychotropic actions of these agents.

We report a case of sudden cardiac death in a known user of synthetic cannabinoids caused by multi-vessel myocardial infarction complicating acute thrombosis of all three main epicardial coronary arteries.

A 45-year-old man with a background of untreated hypertension presented with sudden cardiac death following an unwitnessed collapse while in the toilet. The patient's past history was characterised by a background of heavy tobacco use and alcohol ingestion. There was no history of prior coronary artery disease or reproducible exertional chest typical of myocardial ischaemia. The patient had, however, commenced using a synthetic cannabinoid, colloquially known as ‘black widow’, in the weeks preceding his demise.

During the week preceding his abrupt presentation, the patient noted nonspecific chest discomfort, believed to be musculoskeletal in origin.

On post-mortem examination, the most striking finding was thrombosis of all three major coronary arteries with associated features of acute and chronic ischaemic heart disease. The myocardium confirmed a spectrum of ischaemic changes, including cardiac dilatation (648 g), evidence of previous anterior myocardial infarction with an apical aneurysm containing mural thrombus, thinning of the anterior papillary muscle of the mitral valve, patchy fibrinoid pericarditis and evidence of recent posterior septal myocardial infarct.

The left anterior descending coronary artery had severe atherosclerosis with luminal thrombosis and recanalisation (Fig. 1a). The right coronary artery and left circumflex coronary artery demonstrated moderate atherosclerosis with intraluminal thrombus (Fig. 1b,c). The lungs had smoking-related changes, including emphysematous changes. The cranial and abdominal cavities were not examined.