Vascular abnormalities associated with long-term cigarette smoking identified by arterial waveform analysis

McVeigh, Gary E.; Morgan, Dennis J.; Finkelstein, Stanley M.; Lemay, Lisa A.; Cohn, Jay N.

doi:10.1016/S0002-9343(96)00454-8

« Previous Next »The American Journal of Medicine
Volume 102, Issue 3 , Pages 227-231, March 1997

Vascular abnormalities associated with long-term cigarette smoking identified by arterial waveform analysis

Gary E. McVeigh
- From the Divisions of Internal Medicine, University of Minnesota, Minneapolis, Minnesota USA
- Requests for reprints should be addressed to Gary E. McVeigh, MD, PhD, Division of Internal Medicine, University of Minnesota, Box 741 UMHC, 416 Delaware Street S.E., Minneapolis, Minnesota 55455.
Dennis J. Morgan
- From the Cardiovascular Medicine, University of Minnesota, Minneapolis, Minnesota USA
Stanley M. Finkelstein
- From the Health Computer Sciences Division, Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota USA
Lisa A. Lemay
- From the Cardiovascular Medicine, University of Minnesota, Minneapolis, Minnesota USA
Jay N. Cohn
- From the Cardiovascular Medicine, University of Minnesota, Minneapolis, Minnesota USA

Received 18 July 1996; accepted 5 December 1996.

Purpose

Consistent changes in the arterial pulse contour are found with aging and disease states that impair the compliance characteristics of blood vessels that buffer pulsatile phenomena in the arterial tree. We assessed whether vascular adaptation in structure or tone of blood vessels associated with long-term cigarette smoking would influence steady state or pulsatile hemodynamics at a preclinical stage.

Patients and methods

We analyzed intraarterial brachial artery waveforms in 35 healthy long-term cigarette smokers and 32 nonsmoking control subjects matched for age and gender. The diastolic pressure decay was segmented into two components: an exponential decay that reflects the compliance characteristics of the large arteries and an oscillatory diastolic waveform generated principally by pulsewave reflections from small arteries and arterioles.

Results

Resting heart rate was higher in smokers than nonsmokers, mean ± SD (66 ± 9 versus 60 ± 10; P <0.05). Systolic, diastolic, and mean arterial pressures were lower in smokers compared with nonsmokers (P <0.01 for all). No differences in cardiac output, large artery compliance, or systemic vascular resistance estimates where apparent between groups. A decrease in the amplitude and duration of the diastolic wave, produced by peripheral pulsewave reflections in the arterial system, was found in smokers compared with nonsmokers (0.04 ± 0.02 versus 0.7 ± 0.03; P <0.001).

Conclusions

Quantitative changes in the arterial waveform were found in long-term smokers compared with nonsmoking control subjects. The altered arterial waveshape marks the presence of abnormal structure or tone in the peripheral vasculature that affects pulsatile arterial function. This measure of vascular injury is detectable at a preclinical stage and may relate to the subsequent risk of morbid events in chronic smokers and aid in clinical risk stratification.

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