Cardiovascular complications of cocaine

Isner, Jeffrey M.; Chokshi, Saurabh K.

doi:10.1016/0146-2806(91)90013-z

Cited by 88 publications

(57 citation statements)

References 51 publications

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“…In particular, the relative density of a-and fladrenoceptors and the general pharmacological profile of porcine epicardial coronary arteries are very similar to their human counterparts (Ginsburg et al, 1980;Ginsburg, 1983;Moreland & Bohr, 1984;Bradley & Morgan, 1987). Therefore, it is probably not coincidental that the only animal model of coronary hyperreactivity and vasospasm has been developed in swine (Shimokawa et al, 1983;Egashira et al, 1986;Yamamoto et al, 1987;Isner & Chokshi, 1991). The two different haemodynamic profiles seen in YS and MS in response to the administration of cocaine may be observed in human beings who abuse cocaine and present in the emergency room.…”

Section: Systemic Haemodynamicsmentioning

confidence: 99%

See 1 more Smart Citation

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Lin¹,

Núñez²,

Susulic³

et al. 1996

British J Pharmacology

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Section: Systemic Haemodynamicsmentioning

confidence: 99%

“…Epicardial vasospasm, coronary thrombosis and direct myocardial toxicity have been proposed as precipitating events in cocainemediated death (Isner & Chokshi, 1991;Rezkalla et al, 1990;Zimmerman et al, 1987). However, in experimental animals cocaine administration has been associated with a wide spectrum of systemic responses.…”

Section: Introductionmentioning

confidence: 99%

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Lin¹,

Núñez²,

Susulic³

et al. 1996

British J Pharmacology

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“…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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“…Cocaine has two primary pharmacological actions on the cardiovascular system. First, it blocks the re-uptake of catecholamines at the presynaptic level in the central and peripheral nervous systems (Ritchie & Greene, 1985;Billman, 1990;Isner & Chokshi, 1991). Second, it reduces the inward Na+ current by inhibiting the sodium channel in the sarcolemma, producing a local anaesthetic effect (Hale et al, 1989;Przywara & Dambach, 1989;Billman, 1990).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of cocaine and cocaethylene on intracellular Ca²⁴⁺ and myocardial contraction in cardiac myocytes

Qiu

Morgan

1993

British J Pharmacology

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1 Isolated cardiac myocytes of the ferret were used to investigate the influence of cocaine and cocaethylene on the intracellular Ca2`transient indicated by the indo-l 405/480 nm ratio signal, and peak cell shortening.2 Both cocaine and cocaethylene produced significant decreases in peak intracellular Ca2`and peak cell shortening in a dose-dependent manner. Of interest, (1) the minimally effective dose of cocaethylene was ten fold lower (10-8 M versus 10-M) than that of cocaine; (2) the log EC, of cocaethylene was -5.99 ± 0.13 (1.0 x 10-6M), which was about ten fold lower than that of cocaine (-5.02 ± 0.11, 9.6 X 10-6 M); and (3) 1 x 10-4 M cocaethylene decreased the contraction amplitude by 71 ± 7%, while the same concentration of cocaine decreased the amplitude only by 55 ± 5%, indicating that cocaethylene is more potent than cocaine. 3 The negative inotropic effects of either cocaine or cocaethylene could be overcome by noradrenaline (5 gM) or calcium.4 In contrast to cocaine, cocaethylene shifted the peak [Ca2+]i-peak shortening relationship downward, indicating that cocaethylene decreased myofilament Ca2+-responsiveness. 5 These data indicate that both cocaine and cocaethylene act directly on cardiac myocytes to produce a negative inotropic effect that is due to decreased Ca2+ availability. In contrast to cocaine, cocaethylene produces more potent inhibition by an additional action to decrease myofilament Ca2+-responsiveness.

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Cardiovascular complications of cocaine

Cited by 88 publications

References 51 publications

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

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

Differential effects of cocaine and cocaethylene on intracellular Ca²⁴⁺ and myocardial contraction in cardiac myocytes

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Cardiovascular complications of cocaine

Cited by 88 publications

References 51 publications

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

Cocaine‐induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine

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

Differential effects of cocaine and cocaethylene on intracellular Ca24+ and myocardial contraction in cardiac myocytes

Contact Info

Product

Resources

About

Differential effects of cocaine and cocaethylene on intracellular Ca²⁴⁺ and myocardial contraction in cardiac myocytes