title: Left ventricular contractile performance in the early stage of hypertension in humans.
abstract: The aim of the present study was to assess how cardiac structural changes contribute to increasing left ventricular pump function during exercise in subjects with mild hypertension. In 23 young male subjects with mild hypertension and 12 male normotensive control subjects, left ventricular function was measured echocardiographically using the fractional shortening/ meridional stress relationship at rest and during longlasting exercise at the anaerobic threshold. Mean exercise duration and intensity were 61 (SEM 1.7) min and 71.3 (SEM 2.5)% VO2max (maximal oxygen uptake), respectively, in the hypertensive subjects, and 63 (SEM 1.5) min and 75.7 (SEM 2.2)% VO2max, respectively, in the normotensive subjects (all differences= n.s.). Left ventricular fractional shortening was measured both at the endocardium and at the midwall. In the hypertensive subjects the endocardial fractional shortening, predicted on the basis of the shortening/stress relationship in the normotensive controls, overestimated midwall fractional shortening throughout rest (P=0.04) and exercise (P=0.004). To study how an increase in left ventricular wall thickness contributed to increasing ejection performance during exercise, the hypertensive subjects were divided according to whether their relative wall thickness was less than 0.35 or equal to or greater than 0.35. Subjects with relative wall thicknesses equal to or greater than 0.35 had a depressed myocardial contractility at rest (P=0.0001). During exercise they increased their stroke volume and cardiac output adequately through an increase in ejection performance, while myocardial contractility remained subnormal (P < 0.0001). In conclusion, the present results indicated that in mildly hypertensive subjects an increased left ventricular wall thickness is crucial in preserving left ventricular pump function during exercise.
authors.affiliation: Department of Clinical and Experimental Medicine, Clinica Medica 4, University of Padua, Italy. palatini@ux1.unipd.it
authors.forename: P
authors.initials: P
authors.lastname: Palatini
authors.forename: G
authors.initials: G
authors.lastname: Frigo
authors.forename: P
authors.initials: P
authors.lastname: Visentin
authors.forename: L
authors.initials: L
authors.lastname: Mario
authors.forename: P
authors.initials: P
authors.lastname: Mormino
authors.forename: A C
authors.initials: AC
authors.lastname: Pessina
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D004452:Echocardiography; D015444:Exercise / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000503:physiopathology; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*