American journal of hypertension · 2009
Association of passive smoking with masked hypertension in clinically normotensive nonsmokers.
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Makris Thomas K, Thomopoulos Costas, Papadopoulos Dimitris P, Bratsas Athanassios, Papazachou Ourania, Massias Spiros, Michalopoulou Elena, Tsioufis Costas, Stefanadis Christodoulos
Аннотация
BACKGROUND: We investigated ambulatory blood pressure (BP) levels among clinically normotensive nonsmokers exposed (PS) and not exposed (SF) to passive smoking aiming to evaluate the relative prevalence of masked hypertension (MH).
METHODS: From 790 consecutive never-treated subjects who were self-referred to an outpatient hypertensive clinic, we excluded active smokers and those having a mean clinic BP >140/90 mm Hg. In the remaining population, echocardiography and routine biochemical profile assessment was performed, whereas by the implementation of additional exclusion criteria, all clinically normotensive subjects eligible to participate (i.e., 154 PS and 100 SF) underwent to ambulatory BP monitoring.
RESULTS: PS with respect to SF subjects were younger, followed a less hygienic diet and consumed more alcohol (all P < 0.05). Moreover, PS in comparison with SF showed higher 24-h systolic BP, standing diastolic BP, and clinic heart rate (126 +/- 6 mm Hg vs. 122 +/- 5 mm Hg, 89 +/- 4 mm Hg vs. 84 +/- 4 mm Hg and 79 +/- 5 beats/min vs. 73 +/- 4 beats/min, respectively, P < 0.05 for all) and higher prevalence of MH (23% vs. 8%, P < 0.01). After adjustment for confounders determinants of MH remained passive smoking, weekly duration and intensity of passive smoke exposure, younger age, clinic heart rate, low physical activity score, and standing/sitting difference of diastolic BP and heart rate (P < 0.05 for all).
CONCLUSIONS: MH is associated with passive smoking in a dose-related manner and low physical activity, increased heart rate and postural hemodynamic reaction may represent potential accelerators of that phenomenon.
METHODS: From 790 consecutive never-treated subjects who were self-referred to an outpatient hypertensive clinic, we excluded active smokers and those having a mean clinic BP >140/90 mm Hg. In the remaining population, echocardiography and routine biochemical profile assessment was performed, whereas by the implementation of additional exclusion criteria, all clinically normotensive subjects eligible to participate (i.e., 154 PS and 100 SF) underwent to ambulatory BP monitoring.
RESULTS: PS with respect to SF subjects were younger, followed a less hygienic diet and consumed more alcohol (all P < 0.05). Moreover, PS in comparison with SF showed higher 24-h systolic BP, standing diastolic BP, and clinic heart rate (126 +/- 6 mm Hg vs. 122 +/- 5 mm Hg, 89 +/- 4 mm Hg vs. 84 +/- 4 mm Hg and 79 +/- 5 beats/min vs. 73 +/- 4 beats/min, respectively, P < 0.05 for all) and higher prevalence of MH (23% vs. 8%, P < 0.01). After adjustment for confounders determinants of MH remained passive smoking, weekly duration and intensity of passive smoke exposure, younger age, clinic heart rate, low physical activity score, and standing/sitting difference of diastolic BP and heart rate (P < 0.05 for all).
CONCLUSIONS: MH is associated with passive smoking in a dose-related manner and low physical activity, increased heart rate and postural hemodynamic reaction may represent potential accelerators of that phenomenon.