title: Sex-specific hemodynamic and non-hemodynamic determinants of aortic root size in hypertensive subjects with left ventricular hypertrophy.
abstract: Aortic root (AoR) dilatation is more frequently observed in hypertensive individuals and is independently associated with left ventricular (LV) hypertrophy. Although the LV structure has sex-specific predictors, it remains unknown whether there are gender-related differences in the determinants of AoR size. We carried out a cross-sectional analysis of clinical, laboratory, anthropometric, funduscopic and echocardiographic features of 438 hypertensive patients with LV hypertrophy (266 women and 172 men). Women with enlarged AoR had higher cardiac output (P=0.0004), decreased peripheral vascular resistance (P=0.009), higher prevalence of mild aortic regurgitation (P=0.02) and increased waist circumference (P=0.04), whereas AoR-dilated men presented with a higher prevalence of concentric LV hypertrophy (P=0.0008) and mild aortic regurgitation (P=0.005) and increased log C-reactive protein levels (P=0.02), compared with sex-matched normal AoR subjects. In women, AoR dilatation associated with cardiac output, mild aortic regurgitation and waist circumference in a multivariate model including age, body surface area, height, homeostasis model assessment index, LV mass index, diastolic blood pressure, menopause status and use of antihypertensive medications as independent variables. Conversely, AoR dilatation associated with LV relative wall thickness, log C-reactive protein and mild aortic regurgitation without contributions from diastolic blood pressure, height, body surface area, LV mass index, peripheral vascular resistance and antihypertensive medications in men. Taken together, these results suggest that both volume overload and abdominal obesity are related to AoR dilatation in hypertensive women, whereas AoR enlargement is associated more with inflammatory and myocardial growth-related parameters in hypertensive men with LV hypertrophy.
authors.affiliation: Department of Internal Medicine, School of Medicine, University of Campinas, Campinas, Brazil.
authors.forename: José A A
authors.initials: JA
authors.lastname: Cipolli
authors.forename: Felipe A S
authors.initials: FA
authors.lastname: Souza
authors.forename: Maria C S
authors.initials: MC
authors.lastname: Ferreira-Sae
authors.forename: José A
authors.initials: JA
authors.lastname: Pio-Magalhães
authors.forename: Eugênio S
authors.initials: ES
authors.lastname: Figueiredo
authors.forename: Vanessa G
authors.initials: VG
authors.lastname: Vidotti
authors.forename: José R
authors.initials: JR
authors.lastname: Matos-Souza
authors.forename: Kleber G
authors.initials: KG
authors.lastname: Franchini
authors.forename: Wilson
authors.initials: W
authors.lastname: Nadruz
mesh_terms: D000368:Aged; D001011:Aorta / Q000000981:diagnostic imaging* / Q000503:physiopathology; D001022:Aortic Valve Insufficiency / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D010641:Phenotype; D012044:Regression Analysis; D012727:Sex Characteristics; D013318:Stroke Volume / Q000502:physiology; D014463:Ultrasonography; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology; D055105:Waist Circumference