Cocaine Increases the Endothelial Release of Immunoreactive Endothelin and Its Concentrations in Human Plasma and Urine

Wilbert-Lampen, Ute; Seliger, Christian; Zilker, Thomas; Arendt, R

doi:10.1161/01.cir.98.5.385

Cited by 163 publications

(90 citation statements)

References 46 publications

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“…8,9 In addition, cocaine has been shown to increase the endothelial release of endothelin, probably through stimulation of -receptors. 39 Animal models indicate that cocaine administration leads to a rapid rise in intracellular free Ca 2ϩ 40,41 and a concomitant loss of intracellular Mg 2ϩ 42,43 in vascular smooth muscle cells. These fluxes in divalent cations may directly contribute to vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Triggering of Myocardial Infarction by Cocaine

et al. 1999

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Background-Cocaine has been implicated as a trigger of acute myocardial infarction in patients with and those without underlying coronary atherosclerosis. However, the magnitude of the increase in risk of acute myocardial infarction immediately after cocaine use remains unknown. Methods and Results-In the Determinants of Myocardial Infarction Onset Study, we interviewed 3946 patients (1282 women) with acute myocardial infarction an average of 4 days after infarction onset. Data were collected on the use of cocaine and other potential triggers of myocardial infarction. We compared the reported use of cocaine in the hour preceding the onset of myocardial infarction symptoms with its expected frequency by using self-matched control data based on the case-crossover study design. Of the 3946 patients interviewed, 38 (1%) reported cocaine use in the prior year and 9 reported use within the 60 minutes preceding the onset of infarction symptoms. Compared with nonusers, cocaine users were more likely to be male (87% vs 67%, Pϭ0.01), current cigarette smokers (84% vs 32%, PϽ0.001), younger (44Ϯ8 vs 61Ϯ13 years, PϽ0.001), and minority group members (63% vs 11%, PϽ0.001). The risk of myocardial infarction onset was elevated 23.7 times over baseline (95% CI 8.5 to 66.3) in the 60 minutes after cocaine use. The elevated risk rapidly decreased thereafter. Conclusions-Cocaine use is associated with a large abrupt and transient increase in the risk of acute myocardial infarction in patients who are otherwise at relatively low risk. This finding suggests that studying the pathophysiological changes produced by cocaine may provide insights into the mechanisms by which myocardial infarction is triggered by other stressors. (Circulation. 1999;99:2737-2741.)

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Section: Discussionmentioning

confidence: 99%

Triggering of Myocardial Infarction by Cocaine

et al. 1999

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“…20 Vasoconstriction in the setting of cocaine use is most likely secondary to stimulation of the ␣-adrenergic receptors in smooth muscle cells in the coronary arteries, as pure ␣-adrenergic antagonists reduce coronary vasoconstriction in cocaine users. 20 In addition to ␣-adrenergic stimulation, cocaine has been shown to increase levels of endothelin-1, which is a powerful vasoconstrictor, 21 and to decrease production of nitric oxide, which is a vasodilator. 22 Thus, cocaine decreases oxygen supply and induces myocardial ischemia through a variety of mechanisms.…”

Section: Pathophysiologymentioning

confidence: 99%

Management of Cocaine-Associated Chest Pain and Myocardial Infarction

McCord¹,

Jneid²,

Hollander³

et al. 2008

Circulation

365

131

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“…Other potential explanations, not assessed in the present study, include upregulation of adrenergic receptors, chronic catecholamine depletion, effects on mast cells, and stimulation of endothelin release. 21,22,31,32 …”

Section: Discussionmentioning

confidence: 99%

Increased TIMI frame counts in cocaine users: A case for increased microvascular resistance in the absence of epicardial coronary disease or spasm

Kelly

Sompalli

Sattar

et al. 2003

Clinical Cardiology

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SummaryBackground: Cocaine produces adverse cardiovascular effects, some of which cannot be explained by epicardial coronary artery disease (CAD) or spasm.Hypothesis: The hypothesis of this study was that cocaine users would have increased coronary microvascular resistance, even in the absence of recent myocardial infarction (MI), CAD, or spasm.Methods: Microvascular resistance was assessed by the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (cTFC) method in a consecutive series of 59 cocaine users without acute or recent MI or angiographically significant epicardial stenosis (> 50%) or spasm. The cTFCs in these patients were compared with 21 normal controls and with published normal cTFC values.Results: The cTFC was significantly elevated (by 26-54%) in cocaine users. The cTFCs in the left anterior descending (LAD), circumflex (LCx), and right coronary (RCA) arteries in cocaine users were 30.0 ± 10.9, 34.1 ± 11.5, and 28.6 ± 11.8, respectively, compared with values in normal controls of 21.3 ± 4.3 (p = 0.001), 24.4 ± 7.2 (p = 0.001), and 22.7 ± 5.1 (p = 0.04), respectively, and published normal cTFC values (all p < 0.01). An abnormally high cTFC was present in 61% of patients in the LAD, 69% in the LCx, and 47% in the RCA.

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Cocaine Increases the Endothelial Release of Immunoreactive Endothelin and Its Concentrations in Human Plasma and Urine

Cited by 163 publications

References 46 publications

Triggering of Myocardial Infarction by Cocaine

Triggering of Myocardial Infarction by Cocaine

Management of Cocaine-Associated Chest Pain and Myocardial Infarction

Increased TIMI frame counts in cocaine users: A case for increased microvascular resistance in the absence of epicardial coronary disease or spasm

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