Cocaine-Induced Coronary-Artery Vasoconstriction

Lange, Richard A.; Cigarroa, Ricardo G.; Yancy, Clyde W.; Willard, John E.; Popma, Jeffrey J.; Sills, Michael N.; McBride, W. T.; Kim, A. S.; Hillis, L.David

doi:10.1097/00132586-199006000-00003

Cited by 56 publications

(77 citation statements)

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“…Cocaine is also well known to cause myocardial ischemia [41] even in patients with patent coronary arteries. Cocaine can increase oxygen demand while decreasing blood flow through coronary vasoconstriction [13,[42][43], increase platelet aggregation [36,[44][45], and thrombosis [37,[46][47][48]. Although the greatest risk for cocaine-induced AMI is within the first hour following use [7,12], delayed or recurrent coronary vasoconstriction can occur concomitantly with the rise in concentrations of cocaine metabolites (benzoylecgonine and ecgonine methyl ester) more than 1 hour after cocaine use [49].…”

Section: Discussionmentioning

confidence: 99%

Coronary computerized tomography angiography for rapid discharge of low-risk patients with cocaine-associated chest pain

et al. 2009

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Background: Most patients presenting to emergency departments (EDs) with cocaine-associated chest pain are admitted for at least 12 hours and receive a "rule out acute coronary syndrome" protocol, often with noninvasive testing prior to discharge. In patients without cocaine use, coronary computerized tomography angiography (CTA) has been shown to be useful for identifying a group of patients at low risk for cardiac events who can be safely discharged. It is unclear whether a coronary CTA strategy would be efficacious in cocaine-associated chest pain, as coronary vasospasm may account for some of the ischemia. We studied whether a negative coronary CTA in patients with cocaine-associated chest pain could identify a subset safe for discharge.Methods: We prospectively evaluated the safety of coronary CTA for low-risk patients who presented to the ED with cocaineassociated chest pain (self-reported or positive urine test). Consecutive patients received either immediate coronary CTA in the ED (without serial markers) or underwent coronary CTA after a brief observation period with serial cardiac marker measurements. Patients with negative coronary CTA (maximal stenosis less than 50%) were discharged. The main outcome was 30-day cardiovascular death or myocardial infarction.Results: A total of 59 patients with cocaine-associated chest pain were evaluated. Patients had a mean age of 45.6 Ϯ 6.6 yrs and were 86% black, 66% male. Seventy-nine percent had a normal or nonspecific ECG and 85% had a TIMI score <2. Twenty patients received coronary CTA immediately in the ED, 18 of whom were discharged following CTA (90%). Thirty-nine received coronary CTA after a brief observation period, with 37 discharged home following CTA (95%). Six patients had coronary stenosis Ն50%. During the 30-day follow-up period, no patients died of a cardiovascular event (0%; 95% CI, 0-6.1%) and no patient sustained a nonfatal myocardial infarction (0%; 95% CI, 0-6.1%).Conclusions: Although cocaine-associated myocardial ischemia can result from coronary vasoconstriction, patients with cocaineassociated chest pain, a non-ischemic ECG, and a TIMI risk score <2 may be safely discharged from the ED after a negative coronary CTA with a low risk of 30-day adverse events.

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Section: Discussionmentioning

confidence: 99%

Coronary computerized tomography angiography for rapid discharge of low-risk patients with cocaine-associated chest pain

et al. 2009

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“…5,6 In addition, platelet activation and thrombosis may produce myocardial ischemia in cocaine users. 7,8,[12][13][14] Laboratory studies in animals 15,16 and humans 11,17 have demonstrated that cocaine administration produces an acute increase in coronary microvascular resistance, probably by increased stimulation of alpha-adrenergic receptors, which are plentiful in the myocardium. 6 The risk of MI has been reported to be greatly increased (more than 20-fold) within the first hour after cocaine use, 19 in part because of the relatively short half-life of cocaine (approximately 1 h after inhalation or intravenous injection, 2-3 h after nasal ingestion 5 ).…”

Section: Discussionmentioning

confidence: 99%

“…3 Proposed explanations for this include coronary artery spasm, diffuse vasoconstriction, sinus tachycardia and other tachyarrhythmias, and augmented myocardial contractility; these effects may produce a deleterious imbalance in myocardial oxygen supply and demand. 3,4 Although the systemic, myocardial, and coronary vascular effects of cocaine have been well documented, [5][6][7][8][9][10][11][12][13][14][15][16][17] the chronic effects of cocaine use on coronary microvascular function have not been studied extensively. The purpose of the present study was to assess microvascular resistance in cocaine users undergoing coronary angiography using the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (cTFC).…”

Section: Introductionmentioning

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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“…[65][66][67][68] The evidence with regard to other adrenergic and non-adrenergic vasopressors is limited. Experimentally, vasopressin leads to significantly higher coronary perfusion pressures and preliminary data in relation to return of spontaneous circulation rates may be encouraging, 69 70 but at present, no pressor agent other than adrenaline/epinephrine can be recommended.…”

Section: Vasopressorsmentioning

confidence: 99%