Coronary-Artery Vasoconstriction Induced by Cocaine, Cigarette Smoking, or Both

Moliterno, David J.; Willard, John E.; Lange, Richard A.; Negus, Brian H.; Boehrer, James D.; Glamann, D.Brent; Landau, Charles; Rossen, James D.; Winniford, Michael D.; Hillis, L.David

doi:10.1056/nejm199402173300702

Cited by 252 publications

(108 citation statements)

References 20 publications

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“…41 Smoking appears to impair endothelial cell function in many vascular regions, and evidence supports long-term vasoconstriction and altered endothelial response 37,42,43 to various vasoactive mediators in tobacco smoke. 40,44,45 Human studies indicate abnormal choroidal vascular reactivity to carbogen (high oxygen) inhalation in chronic smokers. 30 Substances in cigarette smoke have additionally been demonstrated to induce direct oxidative damage to endothelium.…”

Section: Discussionmentioning

confidence: 99%

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

Sigler

Randolph

Calzada

et al. 2014

Eye

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Objective To compare macular choroidal thickness between cigarette smokers, those with a history of smoking, and nonsmokers in patients over 65 years of age with earlyatrophic age-related macular degeneration (AMD) and normals. Methods Prospective, consecutive, observational case series. Enhanced depth imaging spectral domain optical coherence tomography 12-line radial scans were performed and choroidal thickness manually quantified at 84 points in the central 3 mm of the macula. Data of normals, soft drusen alone, and soft drusen with additional features of early AMD were compared. A multivariate analysis of variance (MANOVA) model, controlling for age, was constructed to evaluate the effect of smoking history and AMD features on choroidal thickness. Results A history of smoking was significantly associated with a thinner choroid across all patients via logistic regression (P ¼ 0.004; O.R. ¼ 12.4). Mean macular choroidal thickness was thinner for smokers (148±63 mm) than for nonsmokers (181±65 mm) among all diagnosis categories (P ¼ 0.003). Subgroup analysis of patients with AMD features revealed a similar decreased choroidal thickness in smokers (121 ± 41 mm) compared with nonsmokers (146 ± 46 mm, P ¼ 0.006). Bivariate analysis revealed an association between increased pack-years of smoking and a thin choroid across all patients (Po0.001) and among patients with features of early AMD (Po0.001). Both the presence of features of macular degeneration (Po0.001) and a history of smoking (P ¼ 0.024) were associated with decreased choroidal thickness in a MANOVA model. ConclusionChronic cigarette smoke exposure may be associated with decreased choroidal thickness. There may be an anatomic sequelae to chronic tobacco smoke exposure that underlies previously reported AMD risk.

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Section: Discussionmentioning

confidence: 99%

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

Sigler

Randolph

Calzada

et al. 2014

Eye

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“…7 Second, within 15 minutes of intranasal administration of even low doses of cocaine, coronary vasoconstriction occurs in both stenotic and nonstenotic segments through stimulation of ␣-adrenergic receptors. 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.…”

Section: Discussionmentioning

confidence: 99%

“…For example, on the basis of the work of Moliterno et al, 8 the combination of cocaine use and cigarette smoking might be particularly harmful. Similarly, we were unable to determine whether the risk of sustaining a cocaine-associated myocardial infarction differed for frequent versus infrequent users.…”

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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“…Cocaine produces a dose-dependent increase in blood pressure and heart rate, and may therefore increase the risk of aortic dissection, especially if baseline arterial pressure is elevated (4,21,22).…”

Section: Pathophysiologymentioning

confidence: 99%

“…Cocaine also induces vasoconstriction through synaptic stimulation and endothelin release (21). Cigarette smoking has been reported to increase vasoconstriction associated with cocaine use (21).…”

Section: Pathophysiologymentioning

confidence: 99%