Flow-mediated dilatation of the brachial artery and left ventricular geometry in hypertensive patients

Objectives In arterial hypertension, the spectrum of geometric patterns in the left ventricle may parallel the structural alterations detected in the carotid arteries and in subcutaneous small arteries. It has been also repor ted that hypertensive left ventricular hypertrophy (LVH) may be associated with endothelial dysfunction, as evaluated by the response of coronary or f orearm vasculature to acetylcholine infusion. The aim of this study was to evaluate the flow-mediated vasodilatation (FMD) of the brachial artery, non -invasive estimate of endothelium-dependent vasodilatation according to lef t ventricular geometric adaptations in hypertensive patients. Methods and results In 16 normotensive (nine males, seven females, aged 40- 68 years) and in 78 hypertensive subjects (50 males, 28 females, aged 42-67 years), we performed an echocardiographic study for the measurement of lef t ventricular mass index (LVMI) and relative wall thickness (RWT); we measu red to a high resolution the brachial artery diameter at rest, during react ive hyperaemia (5 min of brachial artery occlusion) and after sublingual gl yceril trinitrate (GTN); brachial artery flow velocity was measured by puls ed Doppler. Twenty-six hypertensive patients had a normal LVMI (LVMI < 51 g /m(2.7)) and geometry (RWT < 0.44), five had concentric remodelling (RWT gr eater than or equal to 0.44), and concentric and eccentric LVH were observe d in 19 and 28 patients, respectively. FMD was reduced in hypertensive pati ents as compared with normotensive subjects (P < 0.01), P lo correlation wa s found between FMD and LVMI (r = -0.078) or RWT (r = 0.049); in addition, no difference in FMD was found among the left ventricular geometric pattern s in hypertensive patients. Conclusions In hypertensives, the presence of endothelial dysfunction is no t associated with the LVH or with different left ventricular geometric patt erns, suggesting that different and independent mechanisms may be responsib le for the presence of LVH and of endothelial dysfunction.