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Ethnic differences in arterial stiffness and wave reflections after cigarette smoking.

Lemogoum D, Van Bortel L, Leeman M, Degaute JP, van de Borne P

Hypertension Clinic, Department of Cardiology, Erasme Hospital, Brussels, Belgium. dlems2002@yahoo.fr

BACKGROUND: Smoking increases plasma nicotine. Nicotine releases catecholamines and alters arterial distensibility. The nicotine intake per cigarette is greater and serum cotinine levels, the proximate metabolite of nicotine, are higher in Blacks than in Whites. We tested the hypothesis that cigarette smoking increases the pulse wave velocity (PWV), a marker of arterial stiffness, and the augmentation index (AI), a measure of wave reflection, more in Blacks than in Whites. METHODS: We matched Black (n = 30) and White (n = 30) smokers for age, gender, body mass index and height. We determined carotid-femoral PWV (PWVCF) and carotid-radial PWV (PWVCR) (Complior), the AI derived from the aortic pressure waveform (applanation tonometry, Sphygmocor), blood pressure, heart rate (HR) and cotinine levels before and after cigarette smoking. We also performed measurements in 16 participants after sham smoking. RESULTS: Smoking increased the AI, PWVCF and PWVCR in the whole population (all P < 0.05, n = 60). Increases in the AI and PWV were positively related to serum cotinine levels (all P < 0.05). Smoking increased serum cotinine (P = 0.01) and mean blood pressure (P = 0.03) more, but raised the HR to a lesser extent, in Blacks [+8 +/- 4 versus +13 +/- 6 beats/min in Whites (mean +/- SD), P = 0.01]. Blacks disclosed larger increases in AI adjusted for HR (Blacks, +7.2 +/- 8 versus Whites, +4.4 +/- 8%; P = 0.03), PWVCF (Blacks, +1.1 +/- 0.2 versus Whites, +0.6 +/- 0.3 m/s; P < 0.01) and PWVCR (Blacks, +1.4 +/- 0.1 versus Whites, +0.7 +/- 0.4 m/s; P < 0.01) normalized for the mean blood pressure. No changes were observed with sham smoking. CONCLUSIONS: Smoking acutely increases the PWV and AI in Blacks more than in Whites. Differences in nicotine metabolism and beta-adrenergic sensitivity could explain these findings.

Published 13 March 2006 in J Hypertens, 24(4): 683-9.
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