Author + information
- Received October 10, 1992
- Revision received February 22, 1993
- Accepted March 8, 1993
- Published online September 1, 1993.
- James E. Quillen, MD,
- James D. Rossen, MD, FACC,
- Helgi J. Oskarsson, MD,
- Robert L. Minor Jr., MD,
- J.Antonio G. Lopez, MD and
- Michael D. Winniford, MD, FACC∗
- ↵∗Address for correspondence: Michael D. Winniford, MD, Department of Internal Medicine, 4212 RCP, University of Iowa, Iowa City, Iowa 52242.
Objectives. This study was performed to determine the acute effect of cigarette smoking on proximal and distal epicardial condult and coronary resistance vessels.
Background. Cigarette smoking causes constriction of epicardial arteries and a decrease in coronary blood flow in patients with coronary artery disease, despite an increase in myocardial oxygen demand. The role of changes in resistance vessel tone in the acute coronary hemodynamic effect of smoking has not been examined.
Methods. Twenty-four long-term smokers were studied during cardiac catheterization after vasoactive medications had been discontinued. The effect of smoking one cigerette 10 to 15 mm long on proximal and distal conduit vessel segments was assessed before and immediately after smoking and at 5, 15 and 30 min after smoking (n = 8). To determine the effect of smoking on resistance vessels, coronary flow velocity was measured in a nonobstructed artery with a 3F intracoronary Doppler catheter before and for 5 min after smoking (n = 8). Eight patients were studied without smoking to control for spontaneous changes in conduit arterial diameter (n = 5) and vessel tone (n = 3).
Results. The average diameter of proximal coronary artery segments decreased from 2.56 ± 0.12 mm (mean ± SEM) before smoking to 2.41 ± 0.09 mm 5 min after amoking (−5 ± 2%, p < 0.05). Distal coronary diameter decreased from 1.51 ± 0.07 to 1.39 ± 0.06 mm (−8 ± 2%, p < 0.01). Marked focal vasoconstriction after smoking was observed in two patients. Coronary diameter returned to baseline by 30 min after smoking. There was no change in vessel diameter in control patients. Despite a significant increase in the heart rate-mean arterial pressure product, coronary flow velocity decreased by 7 ± 4% (p < 0.05) and coronary vascular increased by 21 ± 4% (p < 0.01) 5 min after smoking. There was no change in these variables in the control subjects.
Conclusions. Smoking causes immediate constrictioin of proximal and distil epicardial coronary arteries and an increase in coronay resistance vessel tone despite an increase in myocardial oxygen demand. These acute coronary hemodynamic effects may contribute to the adverse cardiovascular consequences of cigarette smoking.
☆ This study was supported in part by Ischemic SCOR Grant HL 32295 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
- Received October 10, 1992.
- Revision received February 22, 1993.
- Accepted March 8, 1993.