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Original Article
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Volume 330:454-459 February 17, 1994 Number 7
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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, and L. David Hillis

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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<0.001), by 12 ±4 percent after one cigarette (n = 12, P = 0.021), and by 45 ±5 percent after both cocaine use and smoking (n = 24, P<0.001). As compared with base-line measurements, the diameters of nondiseased coronary arterial segments decreased on average by 7 ±1 percent after cocaine use (P<0.001), by 7 ±1 percent after smoking (P<0.001), and by 6 ±2 percent after cocaine use and smoking (P<0.001). The diameters of diseased segments decreased by 9 ±2 percent after cocaine use (n = 18, P<0.001), by 5 ±5 percent after smoking (n = 12, P = 0.322), and by 19 ±4 percent after cocaine use and smoking (n = 12, P<0.001). The increase in the rate-pressure product and the decrease in the diameters of diseased segments caused by cocaine use and smoking together were greater (P<0.001 and P = 0.037, respectively) than the changes caused by either alone.

Conclusions The deleterious effects of cocaine on myocardial oxygen supply and demand are exacerbated by concomitant cigarette smoking. This combination substantially increases the metabolic requirement of the heart for oxygen but simultaneously decreases the diameter of diseased coronary arterial segments.


Source Information

From the Department of Internal Medicine, Cardiovascular Division, University of Texas Southwestern Medical Center, Dallas (D.J.M., J.E.W., R.A.L., B.H.N., J.D.B., D.B.G., C.L., L.D.H.), and the Department of Internal Medicine, Cardiovascular Division, University of Iowa, Iowa City (J.D.R., M.D.W.).

Address reprint requests to Dr. Hillis at Rm. CS 7.102, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-9047.

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