P2.08: Endothelial Function and Renal Vasodilation, but Not Arterial Stiffness, are Impaired in Lean, Normotensive Patients with Obstructive Sleep-Apnea

Abstract

Background

Patients with obstructive sleep apnea (OSA), a condition with a strong comorbidity with hypertension and obesity, exhibit an accelerated vascular aging and renal damage. The aim of the study was to evaluate endothelial function, arterial stiffness, and renal vasodilating response to glyceryl trinitrate (GTN), a new parameter of renal vascular damage, in lean, normotensive patients with OSA.

Methods

17 lean normotensive patients with moderate-severe OSA (AHI 31 ±19), and 21 matched healthy controls were recruited. Renal resistive index (RI) was obtained by Duplex ultrasound at baseline and after sublingual GTN (25 µg), evaluating renal vasodilation as percent RI change. Endothelium-dependent (flow-mediated-dilation, FMD) and -independent (response to GTN) vasodilation in the brachial artery was assessed by computerized edge detection system. Arterial stiffness was assessed as carotid-femoral pulse wave velocity (PWV).

Results

OSAS patients and controls presented similar RI (0.61 vs 0.59, p = ns), but impaired renal vasodilation to GTN (-5.7±6.2% vs -10.3±4.6%, p<0.05). FMD was reduced (4.1±2.5% vs 6.2±3.1%, p<0.05), while endothelial-independent brachial artery vasodilation was preserved. PWV was not different between OSAS and controls (7.9±1.5 vs 7.7±1.4 m/s, p = ns). Conclusions: Even in the absence of hypertension and obesity, OSAS is characterized by endothelial dysfunction and impaired renal vasodilating capacity. Thus, OSAS could predispose per se to vascular and renal damage.