title: Functional differences of left ventricular hypertrophy induced by either arterial hypertension or aortic valve stenosis.
abstract: The aim of this study was to reveal functional differences of left ventricular (LV) hypertrophy induced by either aortic stenosis (AS) or arterial hypertension (AH) assessed by strain-rate imaging. Twenty patients with AS and 19 patients with AH were enrolled. In the 2 groups, coronary artery disease was ruled out invasively. All subjects underwent echocardiographic studies, including strain-rate imaging studies of LV long- and short-axis function. Eight patients underwent follow-up examinations after aortic valve replacement, and 20 healthy volunteers served as a control group. LV end-diastolic posterior wall thickness was not different between the 2 patient groups (12.7 +/- 2.5 mm in AS vs 12.8 +/- 1.6 mm in AH) but was significantly increased compared with the control group (8.5 +/- 1.1 mm). The LV ejection fraction was within normal limits in all groups but significantly lower in the patient groups (54 +/- 9% in AS, 55 +/- 6% in AH) compared with the control group (66 +/- 3%). Radial and longitudinal systolic strain rates were depressed in patients with AS compared with those with AH and controls (radial 1.6 +/- 0.6 vs 2.6 +/- 0.6 and 3.8 +/- 0.6 s(-1), respectively, p <0.005). After valve replacement, longitudinal strain rate remained unchanged, but radial strain rate gradually increased (1.6 +/- 0.6 vs 2.1 +/- 0.8 s(-1), p = NS). In parallel, the ejection fraction gradually improved and LV hypertrophy gradually diminished. In conclusion, despite the same degree of LV wall thickness, AS and AH have different impacts on the rate of LV deformation.
authors.affiliation: Clinic of Internal Medicine I/Center of Cardiovascular Disease, University of Würzburg, Würzburg, Germany.
authors.forename: Jörg M
authors.initials: JM
authors.lastname: Strotmann
authors.forename: Björn
authors.initials: B
authors.lastname: Lengenfelder
authors.forename: Jacques
authors.initials: J
authors.lastname: Blondelot
authors.forename: Wolfram
authors.initials: W
authors.lastname: Voelker
authors.forename: Sebastian
authors.initials: S
authors.lastname: Herrmann
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Frank
authors.initials: F
authors.lastname: Weidemann
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D018450:Disease Progression; D018619:Echocardiography, Doppler, Pulsed / Q000379:methods; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*