Key result
Pressure-overload heart failure prompts eccentric remodeling and chamber dysfunction despite preserved myocardial function.
Why the study?
The relative contributions of adverse LV chamber remodeling and decreased myocardial dysfunction to heart failure in pressure overload hypertrophy needed to be explored.
In a rat model of pressure overload hypertrophy, the development of heart failure is driven primarily by deleterious eccentric left ventricular chamber remodeling rather than intrinsic depressed myocardial function.
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May inform early HF risk assessment in hypertrophy; leaves open prospective validation before practice change.
Objectives 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 et al. (2002) studied Pressure overload hypertrophy and heart failure. Suprarenal aortic banding (pressure overload hypertrophy with vs without heart failure) vs. Pressure overload hypertrophy without heart failure (POH-NHF) and sham-operated controls was evaluated on Left ventricular chamber remodeling and myocardial systolic and diastolic function. Pressure overload hypertrophy with heart failure at 20 weeks showed eccentric LV remodeling and lower LV systolic function than non-failing hypertrophy, despite similar myocardial function.