title: Flow-mediated dilatation of the brachial artery and left ventricular geometry in hypertensive patients.
abstract: OBJECTIVE
  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 reported that hypertensive left ventricular hypertrophy (LVH) may be associated with endothelial dysfunction, as evaluated by the response of coronary or forearm 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 left ventricular geometric adaptations in hypertensive patients.
  
  
  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 left ventricular mass index (LVMI) and relative wall thickness (RWT); we measured to a high resolution the brachial artery diameter at rest, during reactive hyperaemia (5 min of brachial artery occlusion) and after sublingual glyceril trinitrate (GTN); brachial artery flow velocity was measured by pulsed Doppler. Twenty-six hypertensive patients had a normal LVMI (LVMI < 51 g/ m2.7) and geometry (RWT < 0.44), five had concentric remodelling (RWT > or = 0.44), and concentric and eccentric LVH were observed in 19 and 28 patients, respectively. FMD was reduced in hypertensive patients as compared with normotensive subjects (P< 0.01). No correlation was 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 patterns in hypertensive patients.
  
  
  CONCLUSIONS
  In hypertensives, the presence of endothelial dysfunction is not associated with the LVH or with different left ventricular geometric patterns, suggesting that different and independent mechanisms may be responsible for the presence of LVH and of endothelial dysfunction.
authors.affiliation: Department of Medical and Surgical Sciences, Internal Medicine, University of Brescia, Italy. muiesan@master.cci.unibs.it
authors.forename: M L
authors.initials: ML
authors.lastname: Muiesan
authors.forename: M
authors.initials: M
authors.lastname: Salvetti
authors.forename: C
authors.initials: C
authors.lastname: Monteduro
authors.forename: C
authors.initials: C
authors.lastname: Corbellini
authors.forename: D
authors.initials: D
authors.lastname: Guelfi
authors.forename: D
authors.initials: D
authors.lastname: Rizzoni
authors.forename: M
authors.initials: M
authors.lastname: Castellano
authors.forename: E
authors.initials: E
authors.lastname: Agabiti-Rosei
mesh_terms: D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity / Q000502:physiology; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D012039:Regional Blood Flow / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*