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.

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.

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).

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.