Contemporary Management of Cardiogenic Shock Complicating Acute Myocardial Infarction

Abstract

Despite an improvement in pharmacological therapies and mechanical reperfusion, the outcome of patients with acute myocardial infarction (AMI) is still suboptimal, especially in patients with cardiogenic shock (CS). The incidence of CS accounts for 3–15% of AMI cases, with mortality rates of 40% to 50%. In contrast to a large number of trials conducted in patients with AMI without CS, there is limited evidence-based scientific knowledge in the CS setting. Therefore, recommendations and actual treatments are often based on registry data. Similarly, knowledge of the available options in terms of temporary mechanical circulatory support (MCS) devices is not equally widespread, leading to an underutilisation or even overutilisation in different regions/countries of these treatment options and nonuniformity in the management of CS. The aim of this article is to provide a critical overview of the available literature on the management of CS as a complication of AMI, summarising the most recent evidence on revascularisation strategies, pharmacological treatments and MCS use.

Macrophage-enriched Sectm1a promotes efficient efferocytosis to attenuate ischemia/reperfusion-induced cardiac injury

“…Over the past decades, tremendous effort has been spent on how to regenerate de novo CMs, how to reduce CM apoptosis and fibrosis, as well as how to increase cardiac angiogenesis for the repair of cardiac I/R injury (2)(3)(4). However, less attention has been paid to efficient clearance of massive cardiac cell death produced during myocardial I/R.…”

“…Acute myocardial infarction (MI) is a leading cause of death worldwide (1). Currently, it is well appreciated that timely reperfusion via thrombolytic agents or primary percutaneous coronary intervention represents the most effective remedy for patients with MI (2)(3)(4). However, the reperfusion of ischemic heart can trigger additional damage, such as extensive cardiomyocyte death and subsequent cardiac inflammation (5)(6)(7).…”