Relation of acute myocardial infarction to cocaine abuse

Cregler, Louis L.; Mark, Herbert

doi:10.1016/0002-9149(85)91140-3

Cited by 132 publications

(23 citation statements)

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“…The underlying process still remains unclear. There are numerous studies concerning only the influence of cocaine [1][2][3][4][5][7][8][9][10][11][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28]. The present study includes 21 cases of death induced by primarily morphine and/or adulterants in drug abusers, but only in 2 cases, cocaine was involved.…”

Section: Discussionmentioning

confidence: 99%

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Heroin-associated myocardial damages—Conventional and immunohistochemical investigations

Dettmeyer

Friedrich

Schmidt

et al. 2009

Forensic Science International

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Section: Discussionmentioning

confidence: 99%

“…The effects of drugs, especially cocaine, on the cardiovascular system have been extensively documented in animal models and in humans, respectively [1][2][3][4][5][6][7][8][9][10][11][12]. There are reports of transitory cocaine-induced ischemic attacks (TIAs) and clinically silent cerebrovascular accidents (CVAs) [13].…”

Section: Introductionmentioning

confidence: 99%

Heroin-associated myocardial damages—Conventional and immunohistochemical investigations

Dettmeyer

Friedrich

Schmidt

et al. 2009

Forensic Science International

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“…The effects of cocaine on the heart have been popularized by the sudden deaths of sports figures who used the drug and a series of case studies showing a temporal relation between the use of cocaine and cardiac illness. [1][2][3][4][5][6][7][8] Although there had been widespread belief among users that cocaine is safe and nonaddicting, it is now clear that its cardiotoxic effects in any given individual are unpredictable.…”

Section: U Clinical Progress Seriesmentioning

confidence: 99%

“…A large variety of cardiovascular diseases have been associated with cocaine use, including acute myocardial ischemia and infarction," [4][5][6][7][8][9][10][11][12] arrhythmias and sudden death,l-3 contraction bands,13 myocarditis,1415 cardiomyopathy,'6-18 hypertension,19 ruptured aorta,20 cerebrovascular aneurysm,2' accelerated atherosclerosis522 and endocarditis. 23 The purpose of the following review is to clarify the effects of an acute cocaine dose on the heart both in experimental animals and in humans and to compare this with the effects the drug may have when used chronically.…”

Section: U Clinical Progress Seriesmentioning

confidence: 99%

The effects of acute and chronic cocaine use on the heart.

et al. 1992

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It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.

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“…The effects of cocaine on the cardiovascular system have been extensively documented in animal models and in humans, respectively [1][2][3][4][5][6][7][8][9][10]. There are reports of transitory cocaine-induced ischaemic attacks (TIAs) and clinically silent cerebrovascular accidents (CVA) [11].…”

Section: Introductionmentioning

confidence: 99%