Key result
In rat and canine models of severe pressure overload, 88% of apoptotic cells were nonmyocytes, and the extent of apoptosis correlated with LV hypertrophy but not LV function.
In severe pressure overload-induced LVH, apoptosis occurs predominantly in nonmyocytes and correlates with hypertrophy but not with LV dysfunction.
Nonmyocyte apoptosis may contribute to pressure-overload LVH in animals; leaves open its role in human dysfunction and requires translational validation.
It is widely held that myocyte apoptosis in left ventricular hypertrophy (LVH) contributes to left ventricle (LV) dysfunction and heart failure. The main goal of this investigation was to determine if there is a statistical relationship among LV hypertrophy, apoptosis and LV function, and importantly whether the apoptosis occurs in myocytes or nonmyocytes in the heart. We used both rat and canine models of severe LVH induced by chronic thoracic aortic banding with resultant LV-aortic pressure gradients 145-155 mmHg and increases in LV/body weight of 58 and 70%. These models also provided the ability to examine transmural apoptosis in LVH. In both models, the overwhelming majority (88%) of apoptotic cells were nonmyocytes. The regressions for apoptosis vs. LVH were stronger for nonmyocytes than myocytes and also stronger in the subendocardium than the subepicardium. Importantly, LV systolic and diastolic wall stresses were normal, indicating that the apoptosis could not be attributed to LV stretch or heart failure. In addition, there was no relationship between the extent of apoptosis and LV ejection fraction, which actually increased (P < 0.05), in the face of elevated LV systolic pressure, indicating that greater apoptosis did not result in a decrease in LV function. Thus, in response to chronic, severe pressure overload, LVH in the absence of LV dilation, and elevated LV wall stress, apoptosis occurred predominantly in nonmyocytes in the myocardial interstitium, more in the subendocardium than the subepicardium. The extent of apoptosis was linearly related to the amount of LV hypertrophy, but not to LV function.
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Gelpi et al. (2010) studied Severe left ventricular hypertrophy (LVH). Chronic thoracic aortic banding was evaluated on Proportion of apoptotic cells that were nonmyocytes. In rat and canine models of severe pressure overload, 88% of apoptotic cells were nonmyocytes, and the extent of apoptosis correlated with LV hypertrophy but not LV function.
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