Physiologic or pathologic hypertrophy.
TL;DR: Comparison of LV function with myocardial structure is pathologic even in the presence of normal LV function and depressed function appears likely to be related to excessive fiber hypertrophy rather than to IF.
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Abstract: Physiologic hypertrophy occurs as the result of exercise conditioning and is characterized by normal or supranormal left ventricular (LV) contractile function and reversibility of structural alterations. Whether hypertrophy produced by chronic abnormal loading can be termed 'physiologic' is a matter of debate because in experimental pressure overload hypertrophy normal in vivo ventricular function may be associated with abnormal in vitro function of the papillary muscles. In patients with moderate LV hypertrophy from aortic valve disease (angiographic mass less than 180 g/m2) ejection fraction (EF) is preserved, but at similar levels of afterload, when mass exceeds 180 g/m2, EF is depressed. Comparison of LV function with myocardial structure (endomyocardial biopsies) has shown that in patients with compensated LV function and those with left heart failure (EF less than 57%, LVEDP greater than 20 mm Hg and/or cardiac index less than 2.5 l/min/m2) interstitial fibrosis (IF) was increased to a similar extent (16 and 18%; normal less than 5%), whereas muscle fiber diameter (MFD; normal less than or equal to 20 mu) was larger (P less than 0.05) in the patients with failure (30 mu) than in those with preserved function (27 mu). Moreover patients with depressed postoperative function had a larger (P less than 0.01) preoperative MFD (35 mu) than those with normal postoperative function (30 mu). Seventeen months after successful aortic valve replacement IF increased (P less than 0.02) and MFD decreased (P less than 0.001) but did not become normal regardless whether postoperative function was normal or depressed. Thus in secondary hypertrophy myocardial structure is pathologic even in the presence of normal LV function and depressed function appears likely to be related to excessive fiber hypertrophy rather than to IF. Massive fiber hypertrophy heralds an unfavorable postoperative LV function and fibrosis is irreversible after surgical correction of the abnormal load.
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References
Mechanical Properties of Rat Cardiac Muscle during Experimental Hypertrophy
TL;DR: The mechanical properties of trabecular muscles from the hearts of 77 rats subjected to aortic arch constriction were compared with those from 77 unoperated and sham-operated control animals at 1, 3, 7, 14, and 28 days after operation and depressed maximum velocity of shortening and maximum isometric force were observed.
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Determinants of ejection performance in aortic stenosis.
TL;DR: The observation that contractile state can be normal or impaired at normal and increased systolic wall stress is evidence for nonuniform myocardial quality in adequate as well as inadequate hypertrophy.
204
Mechanism for the Abnormal Energetics of Pressure-Induced Hypertrophy of Cat Myocardium
TL;DR: The present study suggests a mechanism for the abnormal myocardial oxygen consumption in pressure overload hypertrophy and relates it to nonphosphorylating mitochondrial respiration linked to calcium transport.
133
Left ventricular relaxation in patients with left ventricular hypertrophy secondary to aortic valve disease.
TL;DR: High-fidelity pressure and single-beam echocardiographic measurements were carried out simultaneously in patients with aortic valve disease and Relaxation was assessed from peak negative dP/dt (index of left-heart relaxation) and peak positive dS/dt(index of myocardial relaxation).
130
Normal Myocardial Function and Energetics in Volume-Overload Hypertrophy in the Cat
TL;DR: The data demonstrate that contractility and energetics are normal in volume-overload hypertrophy, although these same factors are abnormal in pressure- overload hyperTrophy, which is not a common denominator for abnormal myocardial function and ener getics.
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