The aorta acts as both a conduit and an elastic buffering chamber that modulates left ventricular function and coronary blood flow. Previous studies have shown that active smoking has unfavorable effects on aortic elasticity. To study the association between passive smoking and the elastic properties of the human aorta. Comparison of nonsmokers during passive smoking studies and smokers during active smoking or sham smoking studies. Academic medical center. 16 male nonsmokers were assigned to passive smoking studies, and 32 current, long-term, male smokers were randomly assigned to either active smoking (16 patients) or sham smoking (16 patients) studies. All participants underwent diagnostic catheterization. In the passive smoking group, environmental tobacco smoke was vented into an exposure chamber for 5 minutes (mean carbon monoxide level, 30 parts per million). Each participant in the active smoking group smoked one filtered cigarette (1.0 mg of nicotine) under standardized conditions within 5 minutes; each participant in the sham smoking group performed a similar pattern of inhalation with one unlit cigarette. Aortic elastic properties were studied by measuring the aortic pressure-diameter relation before and for 20 minutes after passive, active, or sham smoking. Instantaneous diameter of the thoracic aorta was measured with a high-fidelity ultrasonic dimension catheter. Instantaneous aortic pressure and diameter were measured at the same site. Both passive and active smoking were associated with changes in the aortic pressure-diameter relation (change in mean distensibility in the passive smoking group, from 2.02 to 1.59 × 10⁻⁶ cm² · dyne⁻¹ [for comparisons of time course between passive and sham smoking groups, P < 0.001]; change in mean distensibility in the active smoking group, from 2.08 to 1.51 × 10⁻⁶ cm² · dyne (⁻¹) [for comparisons of time course between active and sham smoking groups, P < 0.001]). These changes represent decreases of 21% and 27%, respectively. No changes in aortic elasticity were seen in the sham smoking group. Both passive and active smoking are associated with an acute deterioration in the elastic properties of the aorta. This association between exposure to tobacco smoke and aortic elasticity indicates that aortic function deteriorates during passive or active smoking.

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Erectile dysfunction is a predictor of cardiovascular risk with high prevalence in hypertensive men. We investigated whether erectile dysfunction is related to arterial structure and function in hypertensive patients. We evaluated arterial structural and functional characteristics and measured systemic endothelial/inflammatory markers in 52 hypertensive men with vasculogenic erectile dysfunction and in 34 hypertensive men with normal erectile function, matched for age, blood pressure, risk factors and treatment. Hypertensive patients with erectile dysfunction had higher common carotid intima-media thickness (0.95 ± 0.19 vs. 0.83 ± 0.18 mm, P = 0.003) and carotid–femoral pulse-wave velocity (8.89 ± 1.38 vs. 8.11 ± 1.10 m/s, P = 0.007), lower flow-mediated dilation of the brachial artery (absolute values of 2.96 ± 1.64 vs. 4.07 ± 1.68%, P = 0.003) and a higher level of the systemic endothelial dysfunction marker asymmetric dimethylarginine (0.67 ± 0.13 vs. 0.57 ± 0.16 μmol/l, P = 0.003), and the inflammatory markers high-sensitivity C-reactive protein [2.03 (1.16–2.89) vs. 1.23 (0.67–1.90) mg/l, P = 0.029] and interleukin-6 (4.13 ± 2.38 vs. 2.77 ± 1.92 pg/ml, P = 0.011). Multivariable analysis adjusting for age, mean pressure, other risk factors and treatment showed independent associations between erectile dysfunction and parameters of arterial structure and function. In the erectile dysfunction group, there were no significant relationships between the severity of erectile dysfunction (as expressed by the Sexual Health Inventory for Men score) and the above arterial indices and level of circulating markers (all P = NS). In hypertensive men, the presence but not the severity of vasculogenic erectile dysfunction is associated with subclinical atherosclerosis, impairment of arterial function and systemic endothelial and inflammatory activation.

Endothelial dysfunction is a key early event in the process of atherosclerosis and a risk factor for cardiovascular events. Sildenafil, an effective oral treatment for patients with erectile dysfunction, inhibits cGMP degradation by specific type 5 phosphodiesterase (PDE) inhibition. Sildenafil has been shown to improve vascular function, however, the effect of type 5 PDE inhibition on acute smoking-induced endothelial dysfunction is unknown. We studied the effect of 50 mg of sildenafil on acute smoking-induced endothelial dysfunction in 14 male smokers according to a randomized, placebo-controlled, cross-over design. Endothelial function was evaluated with flow-mediated dilatation (FMD) of the brachial artery using high-resolution ultrasonography. Sildenafil abolishes the decrease in FMD of the brachial artery that is induced acutely by smoking (placebo/smoking session: from 4.56% +/- 0.60% to 2.80% +/- 0.43%, sildenafil/smoking session: from 3.83% +/- 0.64% to 4.33% +/- 0.47%, ie, improvement of 51%, P < .05). This was associated with no reversal effect of sildenafil on smoking-induced decrease in resting brachial artery diameter and with a partial reversal of the smoking-induced decrease in hyperemic brachial artery diameter (placebo/smoking session: from 4.68 +/- 0.13 mm to 4.53 +/- 0.15 mm, sildenafil/smoking session: from 4.72 +/- 0.12 mm to 4.64 +/- 0.13 mm, ie, improvement of 1.5%, P < .005). The present study shows, for the first time, that type 5 PDE inhibition with sildenafil abrogates the smoking-induced acute decrease in FMD of the brachial artery. These findings may have clinical implications given the detrimental consequences of smoking and the strategic role of normal endothelial function.

While studies have shown that red wine improves endothelial function, the effect of pure alcohol, the common denominator of all alcoholic beverages, on endothelial function has not been defined. The effect of oral intake of alcohol (one ounce - a dose corresponding to two drink equivalents) on flow-mediated dilatation of the brachial artery was studied in 12 healthy subjects using high-resolution ultrasonography according to a randomized, sham procedure-controlled, single-blind protocol. Alcohol produced a significant vasodilatation of the brachial artery at resting conditions. Furthermore, it led to a significant increase of the brachial artery diameter at reactive hyperemia; however, the percentage flow-mediated dilatation did not change. This study shows, for the first time, that acute moderate intake of alcohol has a potent dilating effect on large arteries both at resting and at reactive hyperemic conditions, without affecting flow-mediated dilatation as a percentage. This may be useful for explaining the divergent effect of different alcoholic beverages on endothelial function and provides valuable insight into the mechanisms involved in the vascular effects of alcohol.