Extracellular vesicles in post-infarct ventricular remodelling

Post-infarct left ventricle remodelling (LVR) is defined as the structural and functional changes of the myocardium occurring after acute myocardial infarction (AMI) and leading to the loss of contractile tissue and subsequently to post-infarct heart failure (HF). LVR affects 30% of patients after AMI, deteriorating the prognosis. At present, no clinical, biochemical and imaging parameters predict which patients will develop LVR and progress to HF. Despite recent progress in pharmacological treatment, mechanical circulatory support and multidisciplinary team management, none of the available treatments entirely prevent, inhibit or reverse LVR. Thus, post-infarct LVR lacks both reliable prediction and effective treatments. Extracellular vesicles (EVs) are biological nanoparticles with a phospholipid bilayer released by probably all eukaryotic and prokaryotic cells to the extracellular environment. EVs are capable of transferring proteins, nucleic acids and signalling ligands between cells, by which they affect the recipient cells. Evidence is accumulating that EVs released from cardiac cells mediate the interplay between cardiomyocytes, fibroblasts, endothelial cells, vascular smooth muscle cells and extracellular matrix underlying LVR. Depending on the cellular origin and concentration of EVs, EVs are either cardioprotective or promote adverse LVR. Hence, EVs from cardiac cells are candidate biomarkers to predict LVR, and are potential drug vehicles of LVR therapy. Here we present the historical background of EVs, introduce EVs derived from cardiac cells, summarize the current evidence on the role of EVs in cardioprotection and adverse LVR, and present the potential clinical applications of EV-based biomarkers and therapeutics