Περίληψη:
Background: 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.
Methods: 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.
Results: 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).
Conclusions: 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. (C) 2004 American Journal
of Hypertension, Ltd.
Συγγραφείς:
Vlachopoulos, C
Tsekoura, D
Alexopoulos, N
Panagiotakos, D
and Aznaouridis, K
Stefanadis, C
