European Heart Journal Management of Cardiogenic Shock Complicating Myocardial Infarction An Update 2019 Holger Thiele; E. Magnus Ohman; Suzanne deWaha-Thiele; Uwe Zeymer; Steffen Desch DISCLOSURES Eur Heart J. 2019;40(32):2671-2683. Cardiogenic shock (CS) remains the most common cause of death in patients admitted with acute myocardial infarction (AMI) and mortality remained nearly unchanged in the range of 40–50% during the last two decades. Early revascularization, vasopressors and inotropes, fluids, mechanical circulatory support, and general intensive care measures are widely used for CS management. However, there is only limited evidence for any of the above treatment strategies except for revascularization and the relative ineffectiveness of intra-aortic balloon pumping. This updated review will outline the management of CS complicating AMI with major focus on state-of-the art treatment. Ventricular failure subsequent to acute myocardial infarction (AMI) remains the most frequent cause of cardiogenic shock (CS) accounting for more than 80% of cases. Mechanical complications of AMI represent less frequent causes of CS [ventricular septal rupture (4%), free wall rupture (2%), and acute severe mitral regurgitation (7%)].[1] Non-infarct-related CS may be caused by different diseases such as decompensated chronic heart failure, valvular heart disease, acute myocarditis, Takotsubo syndrome, or arrhythmias with heterogeneous treatment targets.[2] The incidence of CS complicating AMI is still in the range of 3–13%.[3–6] Recent registries showed contradictory data with a decreased, stable, or even increased incidence of CS.[3–6] Based on these data, approximately 40 000–50 000 CS patients per year are treated in the USA and approximately 60 000–70 000 in Europe.[7] Despite a more widespread implementation of early revascularization with subsequent mortality reduction to 40–50%, CS remains a leading cause of death in AMI.[3,4,6,8,9] Some recent registries even reported an increase in mortality rates which may be explained by an ageing population and increasing risk profiles of CS patients.[6,10,11] The underlying causes, pathophysiology, treatment of CS complicating AMI have been reviewed previously.[2,12] This 2019 update will focus on evidence-based therapeutic management of CS complicating AMI with major emphasis on current guideline recommendations, revascularization strategies, intensive care unit (ICU) treatment, adjunctive medication, and mechanical circulatory support (MCS) devices. Furthermore, research areas and gaps in evidence will be elucidated. Definition of cardiogenic shock. In general, CS is defined as a state of critical endorgan hypoperfusion and hypoxia due to primary cardiac disorders.[2] Pragmatically, the diagnosis of CS can be made on the basis of clinical criteria such as persistent hypotension without adequate response to volume replacement and accompanied clinical features of endorgan hypoperfusion such as cold extremities, oliguria, or altered mental status. In addition, biochemical manifestations of inadequate tissue perfusion such as elevated arterial lactate are usually present. Although not mandatory in clinical practice, objective haemodynamic parameters such as reduced cardiac index and elevated pulmonary capillary wedge pressure are helpful for diagnosis confirmation, enabling comparisons across CS cohorts and randomized clinical trials and are essential for defining right ventricular (RV) function in CS. Definitions applied in European guidelines and selected major randomized trials are shown in Table 1. Recent efforts of the Society for Cardiovascular Angiography and Interventions (SCAI) is directed towards a more uniform CS definition and a classification scheme similar to the INTERMACS heart failure classification.[16] Based on this new definition, there are five categories of at risk, pre-shock to extreme CS labelled as A–E (Figure 1). This new classification system of different shock states will also help to make different trials of CS better comparable and may also trigger new randomized trials on the pre-shock state.
