Ischemic Cardiomyopathy and Heart Failure After Acute Myocardial Infarction

Abstract

Purpose of Review Ischemic cardiomyopathy refers to systolic left ventricular dysfunction in the setting of obstructive coronary artery disease and represents the most common cause of heart failure worldwide. It is often the combination of an irreversible loss of viable mass following an acute myocardial infarction (AMI) with a dysfunctional, but still viable, myocardium in the context of a chronically reduced myocardial blood flow and reduced coronary reserve. Medical treatments aiming at modulating neurohumoral response and restoring blood flow to the ischemic cardiomyocytes were shown to dramatically abate the occurrence of ventricular dysfunction and adverse remodeling in ischemic cardiomyopathy. Recent Findings Novel therapeutic approaches, such as mechanical unloading and modulation of the inflammatory response, appear to be promising. Furthermore, the understanding of the mechanisms by which, despite optimal treatment, heart failure ensues after AMI, with or without adverse remodeling and systolic dysfunction, is a critical step in the search for novel ways to tackle heart failure risk beyond preservation of left ventricular volumes and systolic function. Summary In this review article, we explore the principal pathophysiological mechanisms and pathways of heart failure in ischemic cardiomyopathy, therapeutic opportunities, and knowledge gaps in this area.

A Pharmacological Review of Tanshinones, Naturally Occurring Monomers from Salvia miltiorrhiza for the Treatment of Cardiovascular Diseases

“…The structural and biochemical changes caused by an inflammatory response directed at the injury site can lead to severe cardiac remodeling and dysfunction, which can manifest clinically as HF [ 124 ]. Therefore, resisting excessive inflammation responses emerges as a critical strategy for cardioprotection.…”

Acute myocardial infarction reparation/regeneration strategy using Wharton’s jelly multipotent stem cells as an ‘unlimited’ therapeutic agent: 3-year outcomes in a pilot cohort of the CIRCULATE-AMI trial

“…Long-term follow-up data in CIRCULATE-AMI PSC suggest that WJMSC transcoronary application in a recent large AMI in humans may be associated with inhibition of LV adverse remodeling and an improvement in LVEF that is sustained at 3 years. Although lack of a control group results in a lack of feasibility for any direct comparisons, our present results -taken in relation to the literature data on the degree of LV adverse remodeling with large infarcts [32,33,39] -suggest a potential benefit of WJMSC delivery via the IRA in the subacute phase of AMI in terms of reduction of LV adverse remodeling and improvement in contractility. This is consistent with experimental data demonstrating improvement in myocardial contractility with WJMSC administration in small-animal and large-animal models of AMI [42][43][44][45].…”

“…Left ventricle adverse remodeling is usually defined as an at least 15-20% increase in LV end-diastolic volume (LVEDV) [32,33] and it is associated with significantly poorer clinical outcomes after MI [33,34]. Both increase in LVEDV (a measure of LV dilatation) and fall of LVEF are part of post-MI left ventricular adverse remodeling, and they are powerful predictors of adverse cardiovascular events after MI [35][36][37][38][39][40]. Data from the present study suggest that even in patients with large infarcts (such as those in the CIRCULATE-AMI PSC) this degree of pathologic increase in LVEDV can be prevented with WJMSCs delivered through the IRA in the subacute phase of myocardial infarction (example in Figure 3).…”

Targeting ferroptosis as a promising therapeutic strategy to treat cardiomyopathy

“…Ischemic cardiomyopathy (ICM) principally results from long-term ischemia/hypoxia within coronary atherosclerosis; it impairs the systolic or diastolic function of the heart. ICM represents the leading cause of heart failure (HF) worldwide ( Chang et al, 2022 ; Del Buono et al, 2022 ). Further, it leads to numerous phenotypic changes, such as myocardial remodeling and HF.…”