Effects of Smoking on Arterial Stiffness in Male Adolescents in Lusaka, Zambia.

BACKGROUND

Tobacco smoke is harmful to health. In the acute phase it causes changes in the cardiovascular system that result in an increase in blood pressure (BP). An increase in arterial stiffness due to arteriolar endothelial dysfunction has been cited among the causes. Pulse Wave Velocity (PWV) and Arterial Stiffness Index (ASI) are used as measures of arterial stiffness in the adult population.

AIM

To determine the acute effects of tobacco smoke on arterial stiffness in black male adolescents in Lusaka, Zambia.

STUDY DESIGN

This was an observational study done at the University of Zambia School of Medicine Cardiovascular Research Laboratory in the month of December 2014.

METHODOLOGY

Twenty-two (22) black, male-adolescent (age range 19-25 years), active-smokers, consented to participate in the study. The Complior Analyse Unit (V1.9 Beta Version 2013; ALAM-Medical, France) protocol was used to obtain the carotid-femoral PWV (cfPWV) and carotid-femoral ASI (cfASI) starting 15 minutes before smoking, on immediate cessation of smoking and thereafter every 15 minutes up to an hour after smoking. ASI was a surrogate measure of the loss of elasticity in the arteries.

RESULTS

The mean baseline cfPWV was 7.9±1.94 m/s and cfASI was 26.1±6.0 m/s. Smoking two tobacco cigarettes (2.8 mg Nicotine) in 15 minutes caused an increase in mean cfPWV and cfASI from their baseline values to cfPWV of 8.5±1.87 m/s and cfASI of 28.6±6.19 m/s respectively. These values reverted to baseline within 15 minutes post-smoking cessation. There was further reduction in both cfPWV and cfASI to more stable values at 45 and 60 minutes which were statistically significantly lower than the peak values recorded.

CONCLUSION

The mean baseline cfPWV and cfASI in these late adolescents were comparatively higher than those recorded in non-smoking black adolescents and smoking white men and women. These recordings were also much higher than the values recorded 60 minutes after cessation of smoking. Compared to these values, we conclude that tobacco smoke may be the cause of the significant acute increase in cfPWV and cfASI in African male adolescents presumably signifying an increase in arterial stiffness probably due to endothelial dysfunction in elastic arteries. These alterations in vascular compliance may predispose these individuals to developing hypertension and other cardiovascular complications. There is need for further investigation of this phenomenon.