The present article focuses on the pathophysiology of myocardial extracellular matrix (ECM) remodelling in chronic heart failure (CHF). The trigger mechanisms for ECM remodelling include acute loss of contractile elements as a consequence of myocardial ischaemia, mechanical tension, oxidative stress and neurohumoral activation. The ECM phenotype changes as a result of the expression of fetal remodelling genes with the aim of accomplishing reparatory changes. This leads to a change in the composition of the ECM, rearrangement of the existing structures and an alteration of the proportion of individual components. While the ECM represents the target structure, at the same time, individual ECM components participate to various degrees directly in myocardial remodelling as modulators of a number of signalling pathways. Matricellular proteins are expressed in reaction to pathological stimuli. These have no structural function but modulate interactions between ECM components, nonmyocyte cells and cardiomyocytes. The principal consequence of ECM remodelling is an increase in the fibrous tissue content of the heart. Pharmacological intervention affecting the process of ECM remodelling could improve the prognosis of patients with CHF.
