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. 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.

Keywords: Coronary artery disease; HFrEF; Heart failure; Ischemic cardiomyopathy; Myocardial infarction; Remodeling.

Fig. 1

Heart failure and ischemic cardiomyopathy. Left ventricular dysfunction in patients with coronary artery disease (i.e., ischemic cardiomyopathy) is often the consequence of an irreversible loss of viable myocardium following a large AMI occasionally in combination with loss of contractility in ischemic, but still viable, myocardium (hibernating myocardium). However, even smaller infarcts, not necessarily associated with cardiac dilatation and dysfunction at rest, may put that patient at risk of developing HF with preserved EF as result of the combination of the post-infarction inflammatory, hemodynamic and neurohormonal response, and predisposing individual risk factors (i.e., obesity, older age, hypertension, chronic kidney disease, diabetes)