title: Left ventricular strain and transmural distribution of structural remodeling in hypertensive heart disease.
abstract: Left ventricular (LV) systolic wall strain is a new candidate for prognostic indicator of hypertensive heart failure. It remains unclear how underlying transmural structural remodeling corresponds to LV wall systolic deformation as hypertensive hypertrophy progresses. We fed 68 Dahl salt-sensitive rats a high-salt (hypertensive group) or low-salt diet (control group) from 6 weeks old. At 10, 14, and 18 weeks, pressure-volume relation, transmural distribution of LV fibrosis, and myocyte hypertrophy were evaluated. LV global longitudinal and circumferential strain was measured with speckle tracking echocardiography. Emax was preserved throughout the study period, whereas τ and end-diastolic pressure-volume relation progressively deteriorated from 14 weeks (diastolic dysfunction stage). Lung weight increased significantly at 18 weeks (decompensated stage). Histological percentage area fibrosis and collagen type I/III, myocyte hypertrophy, and α-myosin heavy chain isoform increased in the subendocardial layer at 14 weeks and progressed into the midlayer at 18 weeks. Longitudinal strain progressively deteriorated in the hypertensive group versus control group at 14 weeks (hypertensive group: -17±3%, control: -27±4%; P<0.001), and circumferential strain decreased at 18 weeks (hypertensive group: -17±2%, control: -27±3%; P=0.002). After adjustment for systolic wall stress, subendocardial percentage area fibrosis was selected as the independent determinant of longitudinal strain. This study showed that LV wall strain alternations were accompanied by fibrosis and myocyte hypertrophy from subendocardium to epicardium, and longitudinal strain related significantly to subendocardial layer fibrosis. Longitudinal strain could be a surrogate of subendocardial fibrotic changes and may be useful for risk stratification of hypertensive heart failure.
authors.affiliation: Cardiovascular Division, Institute of Clinical Medicine, Graduate School of Comprehensive Human Science, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. yo-seo@md.tsukuba.ac.jp.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Ishizu
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Seo
authors.forename: Yuri
authors.initials: Y
authors.lastname: Kameda
authors.forename: Ryo
authors.initials: R
authors.lastname: Kawamura
authors.forename: Taizou
authors.initials: T
authors.lastname: Kimura
authors.forename: Nobutake
authors.initials: N
authors.lastname: Shimojo
authors.forename: Dongzhu
authors.initials: D
authors.lastname: Xu
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Murakoshi
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Aonuma
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D004452:Echocardiography; D006333:Heart Failure / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D006339:Heart Rate; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D006973:Hypertension / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D008297:Male; D051381:Rats; D020303:Rats, Inbred Dahl; D013318:Stroke Volume; D020257:Ventricular Remodeling
keywords: echocardiography; heart failure; hypertension; hypertrophy; myocardial contraction