Heart failure in pressure overload hypertrophy. The relative roles of ventricular remodeling and myocardial dysfunction.
OBJECTIVE
We sought to explore the relative contributions of ventricular remodeling and myocardial dysfunction to heart failure in pressure overload hypertrophy (POH).


BACKGROUND
The mechanism that underlies heart failure in POH is adverse left ventricular (LV) chamber remodeling or decreased myocardial function, or a combination of these.


METHODS
Twenty weeks after suprarenal aortic banding in rats, animals with POH were classified as those with heart failure (POH-HF) or those with no heart failure (POH-NHF). The LV chamber and myocardial systolic and diastolic functions were determined from in vivo and ex vivo experiments.


RESULTS
The LV mass was similar in both POH groups. Chamber remodeling in the POH-HF group was characterized by marked LV enlargement with a normal relative wall thickness (eccentric remodeling), whereas remodeling in the POH-NHF group was characterized by a normal chamber size and increased relative wall thickness (concentric remodeling). The LV systolic function, as determined in vivo from the end-systolic pressure-diameter relationship and ex vivo from the pressure-volume relationship, was lower in the POH-HF group than in the POH-NHF and sham-operated control groups. In contrast, myocardial function was similar in both POH groups, as determined in vivo from the stress-midwall fractional shortening relationship and myocardial systolic stiffness, and ex vivo from the slope of the LV systolic stress-strain relationship. The diastolic chamber stiffness constant was lower in the POH-HF group than in the POH-NHF group, but the myocardial stiffness constant was similar in the two POH groups.


CONCLUSIONS
The two POH groups differed primarily in their remodeling process, which led to a chronically compensated state in one group and to heart failure in the other. Hence, heart failure in POH is more closely related to deleterious LV remodeling than to depressed myocardial function.
Norton
Gavin R
GR
Laboratory of Cardiovascular Pathophysiology, Department of Physiology, University of the Witwatersrand, Johannesburg, South Africa.
Woodiwiss
Angela J
AJ
Gaasch
William H
WH
Mela
Theofanie
T
Chung
Eugene S
ES
Aurigemma
Gerard P
GP
Meyer
Theo E
TE
D000818:Animals; D009202:Cardiomyopathies / Q000150:complications* / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology; D004195:Disease Models, Animal; D006333:Heart Failure / Q000209:etiology* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013599:Systole / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*