Cardiovascular disease caused by smoking is related to the pathophysiological burden placed on the vascular endothelium [1,2]. We studied the effect of chronic cigarette smoking on arterial wave reflection in age- and sex-matched smokers and non-smokers (study 1). A second study was performed to investigate the effect of smoking cessation on pulse wave analysis as a surrogate for endothelial dysfunction (study 2).

One hundred healthy volunteers participated in study 1. Fifty were current smokers and 50 age- and sex-matched non-smokers. Study 2 recruited 20 volunteers from the stop smoking clinic at the Royal Hallamshire Hospital, Sheffield, UK. Both studies had local ethics committee approval. Arterial wave reflection was measured supine by applanation tonometry using the SphygmoCor system version 6.31 (AtCor Medical, Sydney, Australia). The central aortic pressure waveform was calculated using a validated general transform function [3] to derive augmentation index (AIx). Carotid-femoral pulse wave velocity (PWV) was also determined using the SphygmoCor system. Data for cardiovascular risk assessment was collected at screening in study 1. Brachial BP (Omron 705-CP-E, Omron Corporation, Tokyo, Japan), AIx and PWV were recorded at a single visit in study 1. Study 2 measured these variables on ‘quit day’ and 4 weeks later.

In study 1, subjects were aged 37.9 ± 11.4 years and had a BMI of 25.8 ± 3.9 kg m^-2 (mean ± SD). Brachial systolic BP of the study population was 112.5 ± 14.3 mmHg, diastolic BP 69.6 ± 8.7 mmHg and total : HDL cholesterol ratio was 3.9 ± 1.3. The smokers reported smoking 16.2 ± 5.1 cigarettes per day over the previous year. AIx was significantly higher in smokers than non-smokers (median 17.25 vs 11.75%, p = 0.004). Multiple regression analysis showed a significant correlation between AIx and age, diastolic BP, smoking status ( p < 0.001) and weight ( p = 0.03). Predicted 10-year Framingham CHD risk was found to be associated with AIx ( p < 0.001). In study 2, six subjects did not attend the 4-week study visit and were withdrawn from the study. The study population was aged 59.6 ± 8.4 years, had a brachial systolic BP of 127.9 ± 17.1 mmHg, diastolic BP 75.6 ± 10.2 mmHg and smoked 20.2 ± 8.6 cigarettes per day when enrolling in the clinic. AIx significantly reduced after 4 weeks of abstinence in successful quitters (n = 10) compared with relapsed smokers (n = 4) (median 5.0 vs -9.5; p = 0.013). PWV did not reach significance in either study.

These studies show that chronic tobacco smoking is associated with endothelial dysfunction and increased AIx in subjects of a wide age range free from additional cardiovascular risk factors. Further studies are required to confirm our initial findings that the effect of chronic smoking on AIx may be partially reversed after 4 weeks of smoking cessation.

1. Barua RS, et al. J Am Coll Cardiol 2002; 39: 1758.
2. Gottlieb SO. Heart Dis Stroke 1992; 1: 173.
3. O’Rourke MF, et al. Br J Clin Pharmacol 2001; 51: 507.