Heart failure in pressure overload hypertrophy
The relative roles of ventricularremodeling and myocardial dysfunction
Gavin R. Norton, MB, BCh, PhD ,
Angela J. Woodiwiss, PhD ,
William H. Gaasch, MD, FACC ,
Theofanie Mela, MD*,
Eugene S. Chung, MD, FACC*,
Gerard P. Aurigemma, MD, FACC* and
Theo E. Meyer, MD, DPhil*,*
* Division of Cardiology, Department of Medicine, University of Massachusetts, Worcester, Massachusetts, USA
Laboratory of Cardiovascular Pathophysiology, Department of Physiology, University of the Witwatersrand, Johannesburg, South Africa
Lahey Clinic, Burlington, Massachusetts, USA

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Figure 3 Left ventricular and myocardial diastolic function in rats with POH. A reduced diastolic chamber stiffness is noted for the POH-HF group (A), although there is a trend (p > 0.25) for myocardial stiffness to increase in the same group, as compared with the control and POH-NHF groups (B). LVED(P) or (V) = left ventricular end-diastolic (pressure) or (volume). Abbreviations as in Figure 1.
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Figure 4 Myocardial systolic function in rats with POH. The in vivo stress ( )shortening (FSmw) relationship exhibits a trend toward depression in both POH groups (top). However, at a common stress of 75 g·cm2, shortening in both POH groups was similar to that of the control group (bottom). Thus, myocardial function in the POH-HF and POH-NHF groups was similar. Abbreviations as in Figure 1.
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Figure 5 Myocardial systolic function in rats with pressure overload hypertrophy (POH). The in vivo left ventricular end-systolic (LVES) stressstrain (systolic stiffness) relationship was similar in both POH groups and was not different from that of the control group. ESD = end-systolic diameter; other abbreviations as in Figure 1.
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