Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: Evidence for adrenergically mediated alterations in coronary artery tone

In patients with atherosclerotic coronary artery disease, cigarette smoking increases myocardial oxygen demand but may cause an inappropriate decrease in coronary blood flow and myocardial oxygen supply. This study was performed to explore the mechanism of smoking-induced coronary vasoconstriction and, specifically, to determine if smoking causes an α-adrenergically mediated increase in coronary artery tone. In 36 chronic smokers with coronary artery disease (27 men and nine women, 50 ± 9 [mean ± SD] years old), heart rate-systolic arterial pressure double product and coronary sinus blood flow (by thermodilution) were measured before and during smoking both before and after (1) normal saline (n = 5, control subjects), (2) an α-adrenergic-blocking agent, phentolamine, 5 mg (n = 15), (3) a β-adrenergic-blocking agent, propranolol, 0.1 mg/kg (n = 12), or (4) sodium nitroprusside, 0.4 to 0.8 μg/kg/min, diven in a dose sufficient to diminish systolic arterial pressure by 15% (n = 4). During the initial smoking period, rate-pressure product increased and coronary sinus blood flow was unchanged by smoking in all groups. After 30 to 75 min, saline, phentolamine, propranolol, or sodium nitroprusside was given, and measurements were repeated. In the control subjects, rate-pressure product and coronary sinus blood flow responded in a similar manner to that observed previously. In those receiving phentolamine, rate-pressure product was unchanged, but coronary sinus blood flow rose substantially with smoking (percent change + 2 ± 15% during the first smoking period [before phentolamine] and + 32 ± 17% during the second smoking period [after phentolamine]; p<.01). In the twelve patients who received propranolol, rate-pressure product was unchanged, but coronary sinus blood flow fell with smoking (percent change + 5 ± 14% during the first smoking period [before propranolol], - 12 ± 5% during the second smoking period [after propranolol]; p<.01). In those who received sodium nitroprusside, rate-pressure product fell slightly, and coronary sinus blood flow responded in a similar manner to that observed previously. Thus, smoking-induced coronary vasoconstriction is due to an α-adrenergically mediated increase in coronary artery tone.