Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
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Elsevier BV
Abstract
Swine subjected to 2 weeks of repetitive pressure overload (RPO) exhibited significant myocyte loss, but left ventricular (LV) systolic function was preserved, and chamber dilatation did not occur. Instead, myocardial remodeling 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 LV ejection fraction without anatomic LV hypertrophy. These results support a novel paradigm that links cardiac adaptations to RPO with the pathogenesis of reduced LV diastolic compliance and may explain how LV stiffening can occur in the absence of sustained hypertension or anatomic hypertrophy.
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BP, blood pressure, EDPVR, end-diastolic pressure−volume relationship, HFpEF, heart failure with preserved ejection fraction, LV, left ventricular, LVEDP, left ventricular end-diastolic pressure, LVEDV, left ventricular end-diastolic volume, PE, phenylephrine, PV, pressure−volume, RPO, repetitive pressure overload, TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, cTnI, cardiac troponin I, diastolic dysfunction, fibrosis, heart failure, myocardial stunning, stretch, ΔEDP/ΔEDV, changes in end-diastolic pressure/end-diastolic volume