Cocaine Coronary Ischemia: Platelets at the Heart of the Problem
abstract & commentary
Source: Heescha CM, et al. Cocaine activates platelets and increases the formation of circulating platelet containing microaggregates in humans. Heart 2000;83:688-695.
The authors designed an experiment to determine whether there is evidence of platelet activation following in vivo cocaine administration in humans. In a randomized, double-blind crossover design, 14 healthy volunteers were studied twice, receiving cocaine (2 mg/kg intranasally) once and placebo once. Platelet-containing microaggregate formation percentage was increased at 40 minutes (from 47% to 54%, P < 0.001) and at 80 minutes (55%, P = 0.04). Bleeding time decreased marginally following cocaine, from 10 minutes to 9 minutes (P = 0.07). Individual bleeding times decreased in 10 subjects, remained unchanged in one, and increased in three following cocaine; after placebo, there was a decrease in five, no change in one subject, and an increase in eight. No changes in any of the other measured variables were noted following placebo administration. The authors conclude that cocaine exposure causes platelet activation, granule release, and platelet-containing microaggregate formation.
Comment by Richard J. Hamilton, MD, FAAEM, ABMT
There can be little doubt that cocaine is a cardiotoxic drug. It causes arrhythmias, hypertension, and coronary ischemia. The mechanism for the cardiotoxicity has been, to date, incompletely described. As a consequence, controversy still surrounds the clinical management. For example, while toxicologists would agree that beta-blockers are contraindicated in acute cocaine toxicity, many cardiologists still use beta-blockers in this population despite compelling evidence that they exacerbate coronary vasospasm.
Another area of controversy has been the etiology of cocaine-induced coronary ischemia. Some still treat cocaine ischemia as a purely vasospastic, anginal condition with few sequelae. While laboratory data thus far have been conflicting, most authorities agree that some thrombotic process accounts for many of the clinical observations to date, i.e., delay of ischemic symptoms until after the resolution of the vasoactive effects of cocaine; evidence that other organ systems are susceptible to thrombosis-related complications (e.g., bowel infarction, cerebrovascular accidents); anecdotal evidence for accelerated atherosclerosis in cocaine users, etc. This study has developed solid support for the view that cocaine, even at low recreational doses, may promote thrombosis and predispose healthy individuals to ischemic events. The value of this evidence is that it makes the early use of platelet inhibitors a clear choice in the treatment of cocaine-induced ischemia. This is welcome news, as the use of aspirin in acute coronary syndromes is a universally accepted practice with little additional risk to the patient. Based on this paper, I would encourage everyone to adopt that practice for cocaine-induced coronary ischemia as well.