Angela J. Woodiwiss

TL;DR: Reductions in myocardial collagen cross-linking may be an important mechanism contributing to LV dilatation in heart disease.

TL;DR: An association between alterations in LVED k and collagen solubility but not between changes in LV ED k and total collagen or phenotype ratios after antihypertensive therapy in SHRs suggests that myocardial stiffness in hypertension is the consequence of an enhanced myocardian collagen cross-linking rather than of an increase in total collagen and type I phenotype concentrations.

TL;DR: It is demonstrated that diabetes mellitus can produce a stiff myocardium before the development of myocardial fibrosis and in these circumstances is associated with the formation of collagen AGEs.

TL;DR: The two POH groups differed primarily in their remodeling process, which led to a chronically compensated state in one group and to heart failure in the other.

TL;DR: In a population sample with a high prevalence of obesity, excess adiposity promotes concentric, rather than eccentric LV geometric changes, effects which are independent of conventional, central artery or 24-h BP measured on a single occasion.