title: LV systolic performance improves with development of hypertrophy after transverse aortic constriction in mice.
abstract: Transverse aortic constriction (TAC) is an effective technique for inducing left ventricular (LV) hypertrophy in mice. With the use of transthoracic echocardiography and Doppler measurements, we studied the effects of an acute increase in pressure overload on LV contractile performance and peak systolic wall stress index (WSI) at early time points after TAC and the time course of the development of LV hypertrophy in mice. The LV mass index was similar between TAC and sham-operated mice at postoperative day 1 but progressively increased in TAC mice by day 10. There was no further increase in the LV mass index between postoperative days 10 and 20. On day 1, whereas peak systolic WSI increased significantly, the LV ejection fraction (LVEF) and percent fractional shortening (%FS) decreased in TAC mice compared with sham-operated mice. By day 10, peak systolic WSI, LVEF, and %FS had recovered to baseline levels and were not significantly different between postoperative days 10 and 20. Thus LV systolic performance in mice declines immediately after TAC, associated with increased peak systolic WSI, but recovers to baseline levels with the development of compensatory LV hypertrophy over 10-20 days.
authors.affiliation: Division of Cardiology, Department of Medicine, University of California, San Francisco 94143, USA.
authors.forename: A
authors.initials: A
authors.lastname: Nakamura
authors.forename: D G
authors.initials: DG
authors.lastname: Rokosh
authors.forename: M
authors.initials: M
authors.lastname: Paccanaro
authors.forename: R R
authors.initials: RR
authors.lastname: Yee
authors.forename: P C
authors.initials: PC
authors.lastname: Simpson
authors.forename: W
authors.initials: W
authors.lastname: Grossman
authors.forename: E
authors.initials: E
authors.lastname: Foster
mesh_terms: D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D003251:Constriction, Pathologic / Q000150:complications / Q000503:physiopathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D004452:Echocardiography; D006339:Heart Rate; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009200:Myocardial Contraction; D015588:Observer Variation; D013599:Systole; D016277:Ventricular Function, Left