Dj. Moliterno et al., CORONARY-ARTERY VASOCONSTRICTION INDUCED BY COCAINE, CIGARETTE-SMOKING, OR BOTH, The New England journal of medicine, 330(7), 1994, pp. 454-459
Background. In humans, the use of cocaine and cigarette smoking each i
ncreases the heart's metabolic need for oxygen but may also decrease t
he supply of oxygen. As cocaine abuse has proliferated, cocaine-associ
ated chest pain, myocardial infarction, and sudden death have occurred
, especially among smokers. We assessed the influence of intranasal co
caine 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 1
4 women; age, 34 to 79 years; 36 with angiographically demonstrable co
ronary artery disease), we measured the product of the heart rate and
systolic arterial pressure (rate-pressure product) and coronary arteri
al diameters before and after intranasal cocaine at a dose of 2 mg per
kilogram of body weight (n = 6), one cigarette (n = 12), or intranasa
l cocaine at a dose of 2 mg per kilogram followed by one cigarette (n
= 24). Results. No patient had chest pain or ischemic electrocardiogra
phic changes after cocaine use or smoking. The mean (+/-SE) rate-press
ure 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 nondisease
d coronary arterial segments decreased on average by 7+/-1 percent aft
er cocaine use (P<0.001), by 7+/-1 percent after smoking (P<0.001), an
d by 6+/-2 percent after cocaine use and smoking (P<0.001). The diamet
ers 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 di
ameters of diseased segments caused by cocaine use and smoking togethe
r were greater (P<0.001 and P = 0.037, respectively) than the changes
caused by either alone. Conclusions. The deleterious effects of cocain
e on myocardial oxygen supply and demand are exacerbated by concomitan
t cigarette smoking. This combination substantially increases the meta
bolic requirement of the heart for oxygen but simultaneously decreases
the diameter of diseased coronary arterial segments.