RESUMO
Background: Tobacco smoke is said to cause changes in the levels of catecholamines in the blood, this leads to an increase in blood pressure and heart rate. This is due to nicotine which has also been noted to cause a decrease in vasodilatory activities leading to an increase in both the blood pressure and heart rate. Aim: To determine the acute effects of tobacco smoke on haemodynamics 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 Diasys Ambulatory Blood Pressure Monitoring system (Novacor, France) was used to obtain the Systolic and Diastolic blood pressures (SBP and DBP) and the heart rate. These were obtained 15 minutes before smoking at 5 minute intervals and averaged to obtain the baseline, during the 15 minutes of smoking and on immediate cessation of smoking and thereafter every 15 minutes up to an hour after smoking. Results: There was a significant rise in SBP (mmHg) during smoking (127.9±13.80 mmHg) from baseline values (113.5±13.15 mmHg) (P < .001). It took 30 minutes for the SBP to return to baseline after cessation of smoking. DBP (mmHg) also increased from baseline (79.5±8.79 mmHg) to 85.6±10.92 mmHg during smoking (P <.01). It returned to baseline values immediately after cessation of smoking. The heart rate (bpm) was also noted to significantly increase during smoking (95.2±16.72 bpm) from the values noted before smoking (74.3±13.75 bpm) (P < .05). The mean value for heart rate returned to baseline value by the 15th minute of recovery. Conclusion: The present study demonstrates that smoking may be the cause for the acute increases in SBP, DBP and heart rate in smokers. The smoking caused significant increases in all the haemodynamic indices considered in this study within 15 minutes. Both SBP and DBP increases are indices for stroke and coronary heart disease respectively. The effect of increased SBP was noted to last for 30 minutes while DBP returned to baseline immediately after smoking. A significant increase in heart rate was also noted in the study.
RESUMO
Background: Tobacco smoke is harmful to health. In the acute phase it causes changes in the cardiovascular system that result in 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; ALAMMedical, 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 45th and 60th 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 (see Lemogoum, 2006). 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.