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
Background In humans, the use of cocaine and cigarette smokingeach increases the heart's metabolic need for oxygen but mayalso decrease the supply of oxygen. As cocaine abuse has proliferated,cocaine-associated chest pain, myocardial infarction, and suddendeath have occurred, especially among smokers. We assessed theinfluence of intranasal cocaine and cigarette smoking, aloneand together, on myocardial oxygen demand and coronary arterialdimensions 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 arterialpressure (rate-pressure product) and coronary arterial diametersbefore and after intranasal cocaine at a dose of 2 mg per kilogramof body weight (n = 6), one cigarette (n = 12), or intranasalcocaine at a dose of 2 mg per kilogram followed by one cigarette(n = 24).
Results No patient had chest pain or ischemic electrocardiographicchanges after cocaine use or smoking. The mean (±SE)rate-pressure product increased by 11 ±2 percent aftercocaine use (n = 30, P<0.001), by 12 ±4 percent afterone cigarette (n = 12, P = 0.021), and by 45 ±5 percentafter both cocaine use and smoking (n = 24, P<0.001). Ascompared with base-line measurements, the diameters of nondiseasedcoronary arterial segments decreased on average by 7 ±1percent after cocaine use (P<0.001), by 7 ±1 percentafter smoking (P<0.001), and by 6 ±2 percent aftercocaine use and smoking (P<0.001). The diameters of diseasedsegments 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 cocaineuse and smoking (n = 12, P<0.001). The increase in the rate-pressureproduct and the decrease in the diameters of diseased segmentscaused by cocaine use and smoking together were greater (P<0.001and P = 0.037, respectively) than the changes caused by eitheralone.
Conclusions The deleterious effects of cocaine on myocardialoxygen supply and demand are exacerbated by concomitant cigarettesmoking. This combination substantially increases the metabolicrequirement of the heart for oxygen but simultaneously decreasesthe 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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