Article

Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification

Department of Pharmacology and Therapeutics, Trinity College Dublin, and the Hypertension Clinic, St James's Hospital, Dublin, Ireland.
Hypertension (Impact Factor: 7.63). 01/2003; 41(1):183-7. DOI: 10.1161/01.HYP.0000047464.66901.60
Source: PubMed

ABSTRACT The brachial artery pressure waveform is abnormal in smokers, but the effect of smoking on the aortic pressure waveform in both smokers and nonsmokers, particularly in the younger population, is unknown. We compared the acute and chronic effects of smoking on large-artery properties in 185 healthy young smokers and nonsmokers (mean+/-SD, 22+/-5 years). We matched 41 chronic smokers for age, height, weight, and gender with 116 nonsmokers. The augmentation index, a measure of arterial wave reflection in the aorta, was measured by applanation tonometry (Sphygmocor). We also compared augmentation index, aortic pulse wave velocity (Complior), and blood pressure in 28 subjects (11 chronic smokers) before and for 15 minutes after smoking 1 cigarette (nicotine content, 1.2 mg). Although brachial blood pressure was not different, the aortic systolic blood pressure (101+/-8 versus 97+/-9 mm Hg) and augmentation index (0.7+/-13 versus -5.7+/-14) were higher (P<0.01) in chronic smokers than in nonsmokers, whereas aortic-brachial pulse pressure amplification was reduced (13.7+/-8 versus 17.7+/-5 mm Hg, P<0.01). These effects were seen in both male and female subjects. Acutely in both groups, smoking significantly increased (P<0.01) both brachial and aortic blood pressure, augmentation index, and pulse wave velocity. No changes were seen after sham smoking. This study shows an acute increase in arterial stiffness after smoking 1 cigarette in chronic smokers and nonsmokers. Higher aortic systolic blood pressure and greater arterial stiffness, in part due to reduced pulse pressure amplification and increased arterial wave reflection, suggest that the adverse hemodynamic effects have hitherto been underestimated in young chronic smokers.

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    • "autonomic) mechanisms were implicated in these vascular changes. Previous studies reported arterial rigidity (Kool et al., 1993; Mahmud & Feely, 2003) attributed to reduced nitric oxide bioavailability (Nuttall et al., 2002; Tsuchiya et al., 2002), endothelium dysfunction (Karatzi et al., 2007a) and compromised vasodilatory capacity (Karatzi et al., 2007b; Winniford et al., 1986) immediately after smoking a cigarette. "
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    ABSTRACT: Background: Tobacco cigarette smoking is a global health problem that kills millions each year. Recently, tobacco smoking using a waterpipe (WP) has become popular worldwide. However, unlike cigarettes, the cardiovascular (CV) risks associated with WP smoking are uncertain. In this study, the immediate effects of WP smoking on central and peripheral CV indices were evaluated in 53 young healthy smokers. Materials and methods: Strain-gauge plethysmography was used to measure forearm blood flow (Bf), vascular resistance (Vr), and venous capacitance (Vc) and outflow (Vf) at rest (R) and after occlusion (Oc), whereas heart rate (HR) and blood pressure (BP) were measured using standard automated auscultatory methods immediately before and after a 30-min WP smoking session. Results: Smoking resulted in HR, diastolic BP, mean arterial BP, rate pressure product and OcVr increases (p < 0.05) 6.6, 3.6, 2.5, 8.0 and 16%, respectively, whereas OcBf and OcVf decreased (p < 0.05) 8.8 and 14.3%, respectively. Additionally, smoking-induced changes in the central CV components correlated (p < 0.05) with changes in the periphery. Conclusion: These results demonstrated changes in the CV central and peripheral components immediately after WP smoking. The correlations between the changes in these components suggest that the periphery is controlled, at least partially, by the same mechanism(s) affecting the central CV components during WP smoking.
    Inhalation Toxicology 08/2014; 26(10). DOI:10.3109/08958378.2014.936572 · 2.34 Impact Factor
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    • "Smoking behaviour exhibits both chronic and acute effects on the vasculature. Specifically, vascular stiffening has been observed in chronic smokers (Failla et al. 1997; Kim et al. 2005; Kool et al. 1993; Lekakis et al. 1997; Mahmud and Feely 2003; Rehill et al. 2006) and immediately following 1 cigarette (Failla et al. 1997; Kim et al. 2005; Kool et al. 1993; Kubozono et al. 2011; Wiesmann et al. 2004). The transition from acute changes in vascular stiffness to vascular pathology has not been determined. "
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    Applied Physiology Nutrition and Metabolism 05/2014; 39(5):572-80. DOI:10.1139/apnm-2013-0272 · 2.01 Impact Factor
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    • "Smoking behaviour exhibits both chronic and acute effects on the vasculature. Specifically, vascular stiffening has been observed in chronic smokers (Failla et al. 1997; Kim et al. 2005; Kool et al. 1993; Lekakis et al. 1997; Mahmud and Feely 2003; Rehill et al. 2006) and immediately following 1 cigarette (Failla et al. 1997; Kim et al. 2005; Kool et al. 1993; Kubozono et al. 2011; Wiesmann et al. 2004). The transition from acute changes in vascular stiffness to vascular pathology has not been determined. "
    [Show abstract] [Hide abstract]
    ABSTRACT: We tested the hypotheses that smoking-induced changes in vascular mechanics would be detected earlier in the lumped properties of peripheral vascular beds, which include the properties of microvasculature, than in the local properties of central conduits, and that such changes are reversible with lifestyle changes that include smoking cessation and exercise. Vascular measures were made in 53 young (18-40 years) female smokers and 25 age-matched non-smokers. Twenty-two of the smokers were tested before and after a 14-week smoking cessation program and, of these, 13 were tested again after 52 weeks of smoking cessation. Compared with non-smokers, lumped forearm vascular bed compliance (C: mL/mm Hg) was lower, while lumped viscoelasticity (K: mm Hg/(mL·min)) and resistance (R: mm Hg/(mL·min)) were higher in the smoker group. Neither the carotid-to-toe pulse wave velocity nor local carotid artery elasticity indices were different between groups. Compared with non-smokers, brachial artery distensibility was less, and other markers of stiffness higher, in the smoker group. At 14 and 52 weeks of smoking cessation, forearm vascular R was reduced and C was increased while K was unchanged. The changes in C and R occurred while maintaining a constant R×C value, which represents a dynamic time constant. Thus, early changes in K were observed in the forearm vascular bed of smokers, which were not reflected in the local properties of central conduit vessels. Forearm C, but not K, was reversed following smoking cessation, a finding that may represent a persistent effect of smoking on the intercellular matrix of the vessel wall.
    Applied Physiology Nutrition and Metabolism 01/2014; 39(5):572-80. · 2.23 Impact Factor
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