title: Focalized contractile impairment at hypertrophied myocardium proven in consideration of wall stress in patients with hypertrophic cardiomyopathy.
abstract: In hypertrophic cardiomyopathy (HCM) a hyperkinetic state is sometimes observed in spite of impaired systolic function in the hypertrophied myocardium. The aim of the present study was to determine the mechanism of this paradox. Seventeen patients with HCM and 10 normal subjects underwent cine magnetic resonance (MR) imaging to measure percent systolic wall thickening and percent fractional shortening. The ratio of systolic radial wall stress of the LV at the hypertrophied myocardium over that at the nonhypertrophied myocardium was evaluated to describe the focal advantageous condition for wall thickening. The ratio was 0.66 +/- 0.36 at the start of contraction and 0.78 +/- 0.31 at early-systole, indicating consistently smaller radial wall stress at the hypertrophied myocardium. Although the condition for contraction was favorable (a ratio less than 1.00), percent systolic wall thickening at the hypertrophied myocardium (23.0 +/- 11.8%) was smaller than that at the nonhypertrophied myocardium (70.5 +/- 32.3%). Smaller end-diastolic dimension (HCM group; 45.2 +/- 4.2 mm, reference group; 48.9 +/- 4.1 mm, P = 0.04) with a statistically identical value of systolic decrease in intraventricular dimension (HCM group; 19.7 +/- 3.9 mm, reference group; 18.9 +/- 3.2 mm, P = 0.60) yielded high percent fractional shortening in patients with HCM (43.5 +/- 7.6%). Although contractile impairment was proven at the hypertrophied region with low radial wall stress in the HCM group, the smaller end-diastolic dimension in this group resulted in high percent fractional shortening.
authors.affiliation: Department of Internal Medicine, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Japan.
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamazaki
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Suzuki
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Shimamoto
authors.forename: Taeko
authors.initials: T
authors.lastname: Tsuji
authors.forename: Yuki
authors.initials: Y
authors.lastname: Ohmoto
authors.forename: Teruhiko
authors.initials: T
authors.lastname: Toyo-oka
authors.forename: Masao
authors.initials: M
authors.lastname: Omata
authors.forename: Kuni
authors.initials: K
authors.lastname: Ohtomo
authors.forename: Ryozo
authors.initials: R
authors.lastname: Nagai
mesh_terms: D002312:Cardiomyopathy, Hypertrophic / Q000175:diagnosis / Q000503:physiopathology*; D004562:Electrocardiography; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D013318:Stroke Volume; D013599:Systole; D016277:Ventricular Function, Left