Abstract

Swine subjected to 2weeks of repetitive pressure overload (RPO) exhibited significant myocyte loss, but leftventricular (LV) systolic function was preserved, and chamber dilatation did not occur. Instead, myocardialremodeling characterized by myocyte hypertrophy and interstitial fibrosis led to a marked reduction in LV diastolic compliance, which protected the heart from stretch-induced myocyte injury and preserved LVejection fraction without anatomic LV hypertrophy. These results support a novel paradigm that links cardiacadaptations to RPO with the pathogenesis of reduced LV diastolic compliance and may explain howLVstiffening can occur in the absence of sustained hypertension or anatomic hypertrophy.

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