Objective: It is well known that smoking and obesity are cardiovascular risk factors. However, many smokers fear to stop, thinking that following increase in weight will counterbalance the positive effect of smoking cessation. Our aim was to analyze the effect of smoking and obesity on early arterial damage in hypertensive men.

Methods: Hypertensive men without cardiovascular disease were included into the study (n=88, age 48.8±4.1). All patients underwent detailed assessment of cardiovascular risk. Carotid ultrasound (Art Lab System V.2.0), measurements of arterial stiffness and aortic blood pressure by applanation tonometry (Sphygmocor v.7.01) and sphygmomanometry (Vasera VS-1000) were performed in order to evaluate early arterial damage.

Results: Smokers (n=30) were younger as compared to non-smokers (n=58) – 48.5±3.91 vs. 49.28±5.0 years, p<0.05. Non-smokers had higher body mass index (31.5±3.6 vs 29.6±4.0, p<0.05), heart rate (69.1±10.2 vs. 60.7±11.0, p<0.05), and aortic mean blood pressure (101±14.5 vs.108±12.11), but not aortic pulse pressure (37.9±7.4 vs. 37.3±10.7, ns). However, the aortic augmentation index AIx/HR (22.5±9.7% vs. 15.6±8.9%, p<0.001), heart-ankle stiffness index adjusted for blood pressure (CAVI-right 7.9±0.0.9 vs. 7.3±1.3, CAVI-left 7.8±0.9 vs. 7.2±1.2, p<0.01) and intima media thickness (0.65±0.17 mm vs. 0.56±0.13 mm, p<0.05) were significantly higher in smokers as compared to non-smokers. Smokers also had higher prevalence of the carotid plaques (p<0.05). Carotid-radial and carotid-femoral pulse wave velocity (Sphygmocor) didn’t differ significantly (respectively, 9.2±1.5 vs. 9.25±1.1 m/s; 8.6±1.6 vs. 8.54±1.3 m/s, ns).

Conclusion: Although non-smoking hypertensive patients tend to be older and more obese, the smokers have worse arterial parameters in our study group.