During cardiac filling, the relative contribution of distension of interstitial collagen, of
distension of cytoskeletal proteins, and of low-grade diastolic cross-bridge cycling in the
generation of diastolic left ventricular (LV) pressure remains unclear. In failing myocardium,
interstitial collagen deposition and cross-linking are augmented. This increase in collagen
deposition is accompanied by expression of a stiffer isoform of titin in the cardiomyocytes.
Higher diastolic stiffness of failing myocardium is therefore not necessarily related to …