Myocardial ischemia and infarction can occur secondary to cocaine insufflation, smoking, intravenous use, and possibly withdrawal. Serum levels or route of administration does not play a role in the likelihood of developing ischemia.
Patients with cocaine-associated acute coronary syndromes frequently have atypical chest pain or chest pain delayed for hours to days after their most recent use of cocaine. AMI can occur after use of only small amounts of cocaine. Approximately 6 percent of patients with cocaine associated chest pain syndromes sustain AMI. 25 An additional 20 to 60 percent suffer from transient myocardial ischemia. Most infarctions occur within 24 h of cocaine use; however, reports of cocaine use leading to AMI several weeks after last use exist.
Cocaine causes myocardial ischemia through a complex pathophysiology resulting from its acute and chronic effects. 24 Acutely, cocaine results in coronary artery vasoconstriction, tachycardia, systemic arterial hypertension, increased myocardial oxygen demand, platelet aggregation, and in situ thrombus formation. Chronic cocaine users develop accelerated atherosclerosis and left ventricular hypertrophy, which can further exacerbate the O 2 supply-demand mismatch. Myocardial ischemia and infarction have occurred in patients without any underlying atherosclerotic disease or other evidence of preexisting heart disease. Q-wave and non-Q-wave infarctions occurred with equal frequency. Although cocaine can cause myocardial ischemia in patients without coronary artery disease, the majority of patients with cocaine-associated AMI have atherosclerotic coronary artery disease. Patients with cocaine-associated myocardial infarction should receive an evaluation for underlying coronary artery disease.
Risk stratification of patients with cocaine-associated acute coronary syndromes has been difficult. Clinical criteria have not been useful. ECGs reveal abnormalities consisting of ST-segment elevation and T-wave inversions that often persist during hospitalization; however, the ECG is less sensitive and less specific for myocardial infarction in patients who have recently used cocaine. CK-MB assays have diminished specificity for AMI in cocaine users. Cardiac troponin I appears to be more useful. On the other hand, risk stratification of patients with cocaine-associated acute coronary syndromes may be less important, since even patients with cocaine-associated myocardial infarction have a favorable short-term prognosis. The 1-year mortality in patients with cocaine-associated acute coronary syndromes is largely related to comorbid conditions and continued cocaine use.
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