Myocardial infarction cocaine abuse

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. 

Cocaine abuse is a risk factor for myocardial ischemia, infarction, and dysrhythmias, as well as pulmonary edema, ruptured aortic aneurysm, infectious endocarditis, vascular thrombosis, myocarditis, and dilated cardiomyopathy (35). 

Based on a retrospective study of 344 patients with cocaine-associated chest pain, it has been suggested that patients who do not have evidence of ischemia or cardiovascular complications over 9-12 hours in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge (59). Nevertheless, patients with cocaine-associated chest pain should be evaluated for potential acute coronary syndromes those who do not have recurrent symptoms, increased concentrations of markers of myocardial necrosis, or dysrhythmias can be safely discharged after 9-12 hours of observation. A protocol of this sort should incorporate strategies for treating substance abuse, since there is an increased likelihood of non-fatal myocardial infarction in patients who continue to use cocaine. 

Cocaine abuse is a risk factor for myocardial ischemia, infarction, and dysrhythmias, as well as pulmonary edema, ruptured aortic aneurysm, infectious endocarditis, vascular thrombosis, myocarditis, and dilated cardiomyopathy (32). Acutely, cocaine suppresses myocardial contractility, reduces coronary caliber and coronary blood flow, induces electrical abnormalities in the heart, and increases heart rate and blood pressure. These effects can lead to myocardial ischemia (33,34). However, intranasal cocaine in doses used medicinally or recreationally does not have a deleterious effect on intracardiac pressures or left ventricular performance (35). 

Cocaine is a central nervous system stimulant that inhibits the peripheral reuptake of catecholamines, leading to increased sympathomimetic activity [129]. Its abuse is associated with a variety of medical problems. These include acute myocardial infarction, cardiac arrhythmias, cerebrovascular accidents, hyperpyrexia and stimulated sympathetic activity, seizures and coma, obstetrical comphcations, intestinal ischemia and a variety of psychiatric complications [128-131]. A number of reports in the mid to late 1980 s described patients who developed rhabdomyolysis while using cocaine [132-134]. Some of these patients experienced acute kidney injury [135-139]. While the exact incidence of acute kidney injury secondary to cocaine rhabdomyolysis is unknown, in one reported series it occurred... 

Adverse effects include increased risk of seizures, myocardial infarction, rhabdomyolysis, renal failure, and stroke. Other life-threatening adverse effects include hyperthermia, hypertension, vasoconstriction, tachycardia, cardiac ischemia, and paranoia. Prolonged cocaine abuse has been shown to cause cardiomyopathy. 

Ethanol is frequently consumed with other recreational drugs. Cocaine abuse has resulted in an increase of catastrophic cardiovascular events such as myocardial infarction, ventricular arrhythmias, angina pectoris, and sudden death. Many of those so affected also consume ethanol prior to cocaine use. The drug combination of ethanol first followed by cocaine use has been shown to generate synergistic cardiovascular effects in humans and animalsJ24-27 The findings are believed to be due to the inhibition effect of ethanol on cocaine metabolism. 281... 

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