Increased passive stiffness promotes diastolic dysfunction despite improved Ca 2+ handling during left ventricular concentric hypertrophy

ConclusionIn the hypertrophied heart with preserved systolic function,in vivo diastolic dysfunction develops as cardiac fibrosis and alterations in titin phosphorylation compromise left ventricular compliance, and despite compensatory changes in cardiomyocyte Ca2+ homeostasis.
Source: Cardiovascular Research - Category: Cardiology Source Type: research