Cardiovascular Effects of Cocaine
- Havakuk O, Rezkalla SH, Kloner RA.
- The Cardiovascular Effects of Cocaine. J Am Coll Cardiol 2017;70:101-113.
The following are key points to remember about the cardiovascular effects of cocaine:
- Cocaine (chemically: benzoylmethylecgonine; structurally: 2-β-carbomethoxy-3-β-benzoxytropane) is a naturally occurring alkaloid extracted from the leaves of Erythroxylum coca.
- Cocaine is the leading cause for drug–abuse-related visits to emergency departments, most of which are due to cardiovascular complaints. Through its diverse pathophysiological mechanisms, cocaine exerts various adverse effects on the cardiovascular system, many times with grave results.
- Cocaine potentiates acute sympathetic effects on the cardiovascular system, with consequent increased inotropic and chronotropic effects, and increased peripheral vasoconstriction causing hypertension.
- Cocaine has been shown to induce vascular smooth muscle cell apoptosis and cystic medial necrosis, with consequent vessel wall weakening, a pathological finding that may explain cocaine-related aortic, coronary, and carotid artery dissections.
- The mechanism behind cocaine-induced myocardial ischemia includes increased myocardial oxygen demand as a result of an increased inotropic and chronotropic effect, which is inappropriately accompanied by coronary vasoconstriction and a prothrombotic state.
- Patients who present with cocaine-related chest pain should be first evaluated by history, physical examination, and vital signs, followed by an electrocardiogram (ECG) and cardiac troponin.
- Patients who continue to have ST-segment elevation on their ECGs should be directly referred for coronary angiography with possible angioplasty and stent implantation.
- The 2012 ACC/AHA guidelines state that nonselective β-blockers might be considered in persistently hypertensive or tachycardic patients after cocaine use, provided that they were treated with a vasodilator.
- Cocaine has been shown to induce myocarditis, either through elevated levels of catecholamines, creating myocardial necrosis and local immune reaction, or from the induction of eosinophilic myocarditis.
- Both the increased prevalence of cigarette smoking and the inhaled crack might predispose cocaine users to chronic lung injury, with subsequent increased risk for pulmonary hypertension.
- The mechanisms involved in cocaine-related stroke include acute hypertension, endothelial dysfunction and vascular injury, a prothrombotic state, impaired cerebral blood flow, and cerebral artery vasoconstriction induced by cocaine’s sodium-blocking effect.
- Given the discouraging reports on the contemporary prevalence of cocaine abuse in teenagers, and even in children, there is a need to increase awareness of the deleterious effects of this perilous agent.
Clinical Topics: Acute Coronary Syndromes, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Prevention, Pulmonary Hypertension and Venous Thromboembolism, Vascular Medicine, Novel Agents, Acute Heart Failure, Pulmonary Hypertension, Interventions and ACS, Interventions and Vascular Medicine, Hypertension, Smoking
Keywords: Acute Coronary Syndrome, Adrenergic beta-Antagonists, Angioplasty, Apoptosis, Catecholamines, Cerebrovascular Circulation, Chest Pain, Coca, Cocaine, Cocaine-Related Disorders, Drug Users, Electrocardiography, Emergency Service, Hospital, Heart Failure, Hypertension, Hypertension, Pulmonary, Lung Injury, Muscle, Smooth, Vascular, Myocardial Infarction, Myocarditis, Smoking, Stents, Stroke, Troponin, Vascular Diseases, Vascular System Injuries, Vasoconstriction, Vasodilator Agents
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