Original Article
Coronary-Artery Vasoconstriction Induced by Cocaine, Cigarette Smoking, or Both
N Engl J Med 1994; 330:454-459February 17, 1994
- 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.
Media in This Article
Figure 1
Rate-Pressure Product at Base Line, after Cocaine Use, and after Smoking One Cigarette in the 12 Subjects in Group 2 with Coronary Arterial Stenosis.Figure 2
Diameters of Nondiseased (Panel A) and Diseased (Panel B) Segments of Coronary Arteries at Base Line, after Cocaine Use, and after Smoking One Cigarette in the 12 Subjects in Group 2 with Coronary Arterial Stenosis.Article Activity
- Article
Over the past decade, cocaine abuse has become widespread, with over 30 million Americans estimated to have used it1. As its use has escalated, cocaine-associated catastrophic cardiac events, such as acute myocardial infarction and sudden death, have been reported occasionally. Although even small amounts of intranasal cocaine increase the metabolic requirement of the heart for oxygen and decrease the supply of oxygen,2 the mechanisms whereby cocaine abuse sometimes causes cardiac catastrophes are poorly understood.
Previous studies have shown that cigarette smoking also causes a slight increase in myocardial oxygen demand and a concomitant reduction in supply3-8. Other reports have noted that many subjects with cocaine-associated myocardial infarction are cigarette smokers who admit to smoking while using cocaine9. We investigated the hypothesis that the deleterious effects of cocaine and cigarette smoking together might be greater than the effect of either one alone.
Methods
Patient Population
The data were obtained in 42 smokers (28 men and 14 women, 34 to 79 years of age) undergoing elective cardiac catheterization for the evaluation of chest pain. None had an unstable cardiac condition, recent myocardial infarction, or other acute medical illness, and none admitted to previous cocaine use. Of the 42 subjects, 6 had angiographically normal coronary arteries, 15 had coronary artery disease affecting a single vessel ( ≥ 70 percent narrowing of the luminal diameter of a major epicardial coronary artery), 14 had disease involving two vessels, and 7 had disease involving three vessels. The protocols were approved by the Human Subjects Review committees of the University of Texas Southwestern Medical Center and the University of Iowa Hospitals, and all subjects gave written, informed consent. We have administered intranasal cocaine, at a dose of 2 mg per kilogram of body weight, to more than 100 study patients,2,10-14 and none have had adverse sequelae. Antianginal medications (beta-blockers, calcium-channel blockers, and long-acting nitrates) were discontinued 24 hours before the study. All subjects were studied between 8 a.m. and 10 a.m. after an overnight fast and received 5 mg of oral diazepam approximately 60 minutes before the procedure. All subjects refrained from smoking for more than 12 hours before the study.
Experimental Protocol
A 9-French arterial sheath was inserted percutaneously into the femoral artery, through which an 8-French Judkins catheter was advanced to the ostium of the left coronary artery. Systemic arterial pressure was monitored through the sheath's side-port extension, and the heart rate was determined electrocardiographically. All coronary angiography was performed with non-ionic contrast material, with 9 to 10 ml given over a period of three seconds. Cineangiography of the left coronary artery was performed to exclude disease of the left main segment and was followed by cineangiography of the left anterior descending or circumflex coronary artery in the right anterior oblique projection with cranial or caudal angulation, respectively. In each patient, the artery that was optimally opacified and rendered free of foreshortening and overlapping adjacent vessels was selected.
In the initial 30 patients (18 men and 12 women, 34 to 66 years of age), base-line hemodynamic recordings were obtained and cineangiography was performed, after which each received intranasal cocaine hydrochloride (10 percent solution, Roxane Laboratories, Columbus, Ohio) at a dose of 2 mg per kilogram, according to methods described previously2. This dose is smaller than that consumed during most illicit use14. Fifteen minutes later, hemodynamic measurements and cineangiography were repeated, and a blood sample was collected in an iced tube containing sodium fluoride for the measurement of the cocaine concentration. During the subsequent five minutes, 24 of these 30 subjects were assigned by a random drawing to smoke one cigarette (group 2), whereas the other 6 were assigned randomly to wait without smoking (group 1, the controls). Then, hemodynamic measurements and cineangiography were repeated. In these 30 subjects, therefore, myocardial oxygen demand and the dimensions of epicardial coronary arteries were assessed at base line, 15 minutes after intranasal cocaine, and immediately after one cigarette had been smoked (20 minutes after cocaine use) or no cigarettes had been smoked. We have previously observed that smoking-induced vasoconstriction of the epicardial coronary arteries is short-lived, since it is maximal 5 minutes after smoking and resolves within 15 minutes15. On the basis of these data, we thought the subjects should not smoke before receiving intranasal cocaine, since the influence of the former would have resolved by the time the latter began to exert its vasoconstrictive effect.
After the initial 30 subjects were studied as described above, 12 additional subjects (10 men and 2 women, 42 to 79 years of age) (group 3) with a stenosis of the left anterior descending (n = 7) or circumflex (n = 5) coronary artery were enrolled consecutively. In these 12, heart rate, systemic arterial pressure, and coronary arterial diameter were measured at base line and immediately after one cigarette had been smoked.
Variables Assessed
In each subject, heart rate as well as systolic and mean arterial pressures were measured at each time noted. In all 42 subjects, a segment of the proximal, middle, and distal left anterior descending or circumflex coronary artery that appeared free of atherosclerotic narrowing was identified for quantitative analysis, as described below. In the 30 subjects with atherosclerotic narrowing of the left anterior descending or circumflex coronary artery (6 from group 1, 12 from group 2, and 12 from group 3), the dimensions of each stenosis were analyzed in a similar fashion. We performed all quantitative coronary analyses without knowledge of the subject's group assignment. Cine frames were selected at comparable points in the cardiac cycle, and computer-assisted analysis (Cardiovascular Angiography Analysis System, Pie Medical, Maastricht, the Netherlands) was performed according to methods described previously2,10-13,16. Arterial segments were digitized from the 35-mm cine film and optically magnified. The contours of the selected vessel regions were detected automatically by the computer on the basis of the weighted sums of the first and second derivative functions applied to the digitized image. Contour data were corrected for pincushion distortion, and the absolute dimensions of the vessel were determined with the use of the coronary catheter for calibration. The luminal diameter of each nondiseased and diseased arterial segment was determined. We have had extensive experience with quantitative coronary arteriography2,10-13,15; the variability of this analysis in our laboratories is similar to that previously reported16.
Statistical Analysis
All data are reported as the means ±1 SE. The changes in the product of the heart rate and systolic arterial pressure (the rate-pressure product) and in the diameters of the coronary arteries among the three groups were compared by analysis of variance. We performed hemodynamic and arteriographic analyses without knowledge of the subject's group assignment. For the 30 subjects who received cocaine (groups 1 and 2), the effect of cocaine on the heart rate, systemic arterial pressure, the rate-pressure product, and coronary arterial diameter was assessed with a paired t-test17. For the 12 subjects who smoked one cigarette (group 3), the effect of smoking on these variables was also assessed with a paired t-test17. To test the influence of smoking in the 24 subjects in group 2 who received cocaine, a paired t-test was used to compare each variable after cocaine use and after smoking. The effect of not smoking was assessed in a similar manner for the six subjects in group 1. For all analyses, a two-tailed P value of less than 0.05 was considered to indicate statistical significance.
Results
None of the subjects had chest pain or electrocardiographic changes consistent with the occurrence of myocardial ischemia after cocaine ingestion or cigarette smoking. In the 30 subjects who received cocaine (groups 1 and 2), the serum cocaine concentration averaged 0.12 ±0.01 mg per liter (range, 0.03 to 0.27). In these subjects, the rate-pressure product -- a reflection of myocardial oxygen demand -- increased 11 ±2 percent with cocaine use (P<0.001) (Table 1Table 1
Hemodynamic Data on the Three Groups of Smokers.). There was no further change in the rate-pressure product in the six subjects who did not smoke within 20 minutes after cocaine use (group 1). In contrast, the rate-pressure product increased markedly in the 24 subjects who smoked after cocaine administration (group 2), so that it was 45 ±5 percent above base line (Table 1). This increase was significantly greater (P<0.001) than that produced by cocaine use alone (group 1) or smoking alone (group 3) (Table 1 and Figure 1Figure 1Rate-Pressure Product at Base Line, after Cocaine Use, and after Smoking One Cigarette in the 12 Subjects in Group 2 with Coronary Arterial Stenosis.).In the 30 subjects who received intranasal cocaine (groups 1 and 2), cocaine caused a 7 ±1 percent decrease in the diameter of nondiseased segments of the left anterior descending or circumflex coronary arteries (P<0.001). The data on all nondiseased segments are shown in Table 2Table 2
Dimensions of Nondiseased Segments of Coronary Arteries.. These dimensions were not further altered by a five-minute wait in group 1 or by smoking one cigarette in group 2 (Table 2 and Figure 2AFigure 2Diameters of Nondiseased (Panel A) and Diseased (Panel B) Segments of Coronary Arteries at Base Line, after Cocaine Use, and after Smoking One Cigarette in the 12 Subjects in Group 2 with Coronary Arterial Stenosis.). In contrast, smoking produced a further vasoconstrictive effect in addition to that induced by cocaine in coronary arterial segments narrowed by atherosclerosis. As the data in Table 3Table 3
Dimensions of Diseased Segments of Coronary Arteries. indicate, cocaine induced a 9 ±2 percent decline in coronary arterial diameter (groups 1 and 2). This dimension was unchanged after a five-minute wait in group 1, but it was decreased further after one cigarette in group 2, so that the combination of cocaine use and smoking produced a 19 ±4 percent decline in the diameter of diseased segments of coronary arteries (Table 3 and Figure 2B and Figure 3Figure 3
Arteriograms of the Left Circumflex Coronary Artery in the Right Anterior Oblique Projection at Base Line (Panel A), after Intranasal Cocaine (Panel B), and after One Cigarette (Panel C).). This decrease was greater (P = 0.037) than that observed in diseased segments in response to cocaine use alone (group 1) or smoking alone (group 3) (Table 3).Discussion
As cocaine abuse has proliferated, the incidence of catastrophic cardiovascular events related to cocaine use has increased. Most patients in whom myocardial infarction or sudden death occur are young or middle-aged men who are smokers and who smoke while using cocaine, and the majority have angiographic or postmortem evidence of coronary artery disease9. Cocaine produces adrenergic stimulation by blocking the presynaptic reuptake of norepinephrine and dopamine, leading to an excessive amount of these substances at postsynaptic receptor sites. This adrenergic stimulation increases the heart rate, blood pressure, and left ventricular contractility, so that the metabolic requirement of the heart for oxygen increases14. Concomitantly, myocardial oxygen supply declines because of cocaine-induced vasoconstriction of the coronary arteries2,10-13. Similarly, within minutes of cigarette smoking, nicotinic receptors in the adrenal medulla are stimulated, triggering the release of epinephrine and norepinephrine18. As a result, heart rate and left ventricular contractility increase, leading to an increase in the requirement of the myocardium for oxygen3-5. Despite this increase in the need for oxygen, smoking -- like cocaine use -- has been shown to cause vasoconstriction of angiographically normal and diseased segments of coronary arteries7,15. In short, cocaine use and cigarette smoking each increase myocardial oxygen demand and simultaneously reduce oxygen supply. Since cocaine abusers often smoke while they are ingesting cocaine, this study was performed to assess the influence of the combination of intranasal cocaine and cigarette smoking on myocardial oxygen supply and demand.
Our data, obtained in 42 smokers studied during cardiac catheterization, show that myocardial oxygen demand (measured as the product of the heart rate and systolic arterial pressure) increased with cocaine use or smoking. However, oxygen demand increased much more with the combination of cocaine ingestion and smoking than with either one alone. As we have shown previously,2,10-13,15 each of these factors induced slight vasoconstriction in angiographically normal segments of coronary arteries, and smoking did not influence the magnitude of vasoconstriction in these segments in the 24 subjects who received cocaine (group 2). In contrast, diseased segments of coronary arteries narrowed 9 ±2 percent with cocaine use, and smoking induced a further decline in the diameter of coronary arteries. The magnitude of the reduction in the diameter caused by cocaine use and smoking (19 ±4 percent) was greater than that caused by either cocaine use or smoking alone.
Although little is known about the effect of cocaine use or smoking on vascular endothelium, their vasoconstrictive effect is mediated, at least in part, by alpha-adrenergic stimulation, since it is alleviated by phentolamine, an alpha-adrenergic-blocking agent2,19. The integrity of the coronary arterial endothelium may influence the vasomotor response that occurs with cocaine use, cigarette smoking, and their combination. Smoking has been shown to injure endothelial cells20 and reduce prostacyclin production21,22. Each has been shown to induce vasoconstriction in angiographically normal and diseased segments of coronary arteries; at the same time, each causes more intense vasoconstriction in diseased than nondiseased segments, suggesting that the presence of functioning endothelium may attenuate cocaine-induced or smoking-induced vasoconstriction. In the 72 nondiseased segments of coronary arteries in our 24 subjects who smoked after cocaine use (group 2), cocaine-induced vasoconstriction was not consistently worsened by smoking, although the diameter of the coronary arteries decreased by more than 10 percent in a total of six segments in 5 of these subjects. In contrast, smoking produced an additional vasoconstrictive effect in the 12 diseased segments from the same subjects.
Our study has limitations. First, we assessed the effect of a dose of only 2 mg of intranasal cocaine per kilogram followed by only one cigarette. Although the effect of cocaine when given by other routes (i.e., inhalation or intravenous injection) may be different, most reported cases of cocaine-associated myocardial infarction have occurred after its intranasal administration. The dose of cocaine that we used is smaller than that usually consumed during illicit use, and the exact amount of smoke inhaled from only one cigarette was not measured. Perhaps the combined effect of larger amounts of cocaine and cigarette smoke would produce an even greater increase in myocardial oxygen demand and a larger decrease in coronary arterial dimensions. Furthermore, it is conceivable that larger amounts of cocaine and cigarette smoke may induce vasoconstriction in nondiseased segments of coronary arteries in an occasional subject. As noted previously, smoking caused an additional decrease of more than 10 percent in the diameter of six nondiseased coronary arterial segments from five subjects in group 2. Second, we examined the effects of cocaine use and smoking 20 minutes after the former and immediately after the latter; therefore, we have no data regarding their effects on the rate-pressure product and coronary arterial dimensions at other times. Third, all 24 subjects in group 2 first received intranasal cocaine and then smoked a cigarette. No patient smoked a cigarette and then ingested cocaine. Since vasoconstriction of epicardial coronary arteries is maximal five minutes after smoking,15 its influence would have waned by the time intranasal cocaine exerted its vasoconstrictive effect.
With these caveats in mind, we conclude that intranasal cocaine in combination with cigarette smoking causes a substantial increase in myocardial oxygen demand and a decrease in the diameter of coronary arterial segments narrowed by atherosclerosis. We suggest that in an occasional subject, a larger amount of cocaine in combination with smoking might induce an even greater increase in myocardial oxygen demand and a larger decrease in coronary arterial dimensions, culminating in myocardial ischemia, infarction, or sudden cardiac death.
We are indebted to Sheila De Paola, Kelly Heathman, Jacqui Jones, Jeanette Kissee, Marsha Pecena, Karen Scherger, and Nancy Smith for technical assistance and to Shelly K. Sapp for statistical assistance.
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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