Approximately 2 decades ago, or more, some laboratory animals were experimented for the effect of atrial and ventricular arrhythmias, myocardial ischemia with coronary vasoconstriction, and direct depression in myocyte function. In 1980, some cases were reported with high grade ventricular arrhythmias, myocardial infarction, and sudden deaths because of cocaine use. It has been observed that even mild or recreational use of cocaine can cause myocardial infarction. The research surprised everyone with the finding that cocaine even if used as medicine for treatment is not safe. Cocaine has also been causing other heart-related disorders such as cardiomyopathy, hypertension, aortic aneurysm, and non-cardiac chest pain.
Myocardial Infarction generally results from cocaine use, and is found mostly in patients from 18 to 45 years of age. It does not get detected in angiographies of coronary artery disease, not even in acute cases. It has been found that cocaine and platelet activation together, may create coronary artery occlusion. Generally primary coronary intervention by expert physician is the preferred revascularization modality, but in the absence of it, thromobolytic therapy can also be of help. The second preventive measure in cocaine-related myocardial infarction is to prevent cocaine abuse.
There is no clear scale to which myocardial infarction associated with cocaine use can be monitored. However, it has been reported to be on the higher side in most of the patients.
Pathophysiology of myocardial infarction is generally aligned with the development of atherosclerotic coronary artery disease. The research conducted on animals showed a strong link between cocaine administration and atherosclerotic change, hence it is assumed that cocaine may cause coronary artery disease. 42% of the cocaine users who underwent angiography, were found with positive signs of coronary artery disease. It has also been noted that the risk is higher in patients with concomitant tobacco abuse and hypertension. However, it has been established that the cocaine users are more prone to develop myocardial infarction, and extensive coronary atherosclerosis, mostly without plaque rupture incidences.
Cocaine has also been found to be responsible for activation of platelets which may lead to increased adhesiveness and aggregation causing coronary thrombi and myocardial infarction.
Thus the researches conducted so far show that cute use of the drug , coronary spasm, decrease in blood flow, and activation of platelets may be considered as the possible causes for development of coronary thrombosis and myocardial infarction in patients. This situation reduces oxygen supply to the myocardium and results in hypertension and tachycardia. The diagnosis of cocaine-induced myocardial infarction requires a careful study of the patient’s history and current condition through appropriate laboratory tests, cardiac enzyme study, and classic electrocardiographic findings. Some patients will not accept that they use cocaine and it calls for direct inquiry about drug abuse through blood and urine (for presence of benzoylecgonine and ecgonine) tests.
