The inflammatory response in myocardial injury, repair, and remodelling

Abstract

In the infarcted myocardium, cardiomyocyte death and degradation of the cardiac extracellular matrix releases signals that activate innate immune pathways and trigger an intense inflammatory reaction The role of postinfarction inflammation in extending ischaemic cardiomyocyte injury is controversial; however, inflammatory mediators are implicated in dilative remodelling and in the pathogenesis of postinfarction heart failure Early stimulation of inflammatory signalling is important for clearance of dead cells from the infarcted area and for tissue repair Timely repression of proinflammatory mediators protects the heart from excessive inflammatory injury Patients who survive a large myocardial infarction exhibit pathophysiological heterogeneity, as subpopulations with progressive dilative remodelling or predominant diastolic dysfunction are identified Biomarker-based approaches are needed to identify patients with overactive proinflammatory signalling or excessive fibrosis who might benefit from targeted therapies