Coronary-artery vasoconstriction induced by cocaine, cigarette smoking, or both

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

Research output: Contribution to journalArticlepeer-review

Abstract

Background. In humans, the use of cocaine and cigarette smoking each increases the heart's metabolic need for oxygen but may also decrease the supply of oxygen. As cocaine abuse has proliferated, cocaine-associated chest pain, myocardial infarction, and sudden death have occurred, especially among smokers. We assessed the influence of intranasal cocaine and cigarette smoking, alone and together, on myocardial oxygen demand and coronary arterial dimensions in subjects with and subjects without coronary atherosclerosis. Methods. In 42 smokers (28 men and 14 women; age, 34 to 79 years; 36 with angiographically demonstrable coronary artery disease), we measured the product of the heart rate and systolic arterial pressure (rate- pressure product) and coronary arterial diameters before and after intranasal cocaine at a dose of 2 mg per kilogram of body weight (n = 6), one cigarette (n = 12), or intranasal cocaine at a dose of 2 mg per kilogram followed by one cigarette (n = 24). Results. No patient had chest pain or ischemic electrocardiographic changes after cocaine use or smoking. The mean (±SE) rate-pressure product increased by 11±2 percent after cocaine use (n = 30, P

Original languageEnglish (US)
Pages (from-to)454-459
Number of pages6
JournalNew England Journal of Medicine
Volume330
Issue number7
DOIs
StatePublished - Feb 17 1994
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)

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