Vericiguat for Post-Myocardial Infarction Heart Failure Prevention: From Molecular Mechanisms to Clinical Translation

Abstract Myocardial infarction (MI) remains a major cause of morbidity and mortality, largely due to the development of heart failure (HF). More molecular mechanisms should be investigated concerning the pathophysiology of HF after MI since current therapies for reperfusion and clinical guidelines in medicine cannot solve the problem. The regulation of the signalling pathway involving nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate is responsible for the stability of the cardiovascular system. This pathway works properly in healthy individuals but gets disrupted in MI, causing adverse consequences. Vericiguat acts as an orally administered soluble guanylate cyclase stimulator that restores the levels of cyclic guanosine monophosphate to counteract pathological events leading to HF. Numerous pre-clinical and clinical investigations into vericiguat have shown the capacity of early administration to prevent HF following MI, especially in patients who are at risk of having continued myocardial stress. Moreover, combination approaches using vericiguat alongside current cardioprotective modalities have proven to be promising in yielding better outcomes. The current review is therefore designed to give an insight into various aspects relating to heart with special attention being paid to the role of vericiguat as a disease-modifying agent for prevention of post-MI myocardial HF.