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Prediction, staging, and outcomes of ischaemic cardiogenic shock after STEMI: a complex clinical interplay

Despite the implementation of an early coronary reperfusion strategy with primary percutaneous coronary intervention (PCI), cardiogenic shock (CS) remains a persistent complication of ST-segment elevation myocardial infarction (STEMI), affecting a significant proportion of cases, with high in-hospital and short-term mortality. Until recently, few risk-scoring models of post-STEMI CS were available, and most had limitations such as absence of external validation, difficult to assess variables, or inclusion of causes of CS other than STEMI. Early coronary reperfusion (most frequently with PCI) and appropriate haemodynamic support remain the main treatment to avert CS complications or improve CS outcomes. A user-friendly model for CS risk stratification was introduced last year. A simple age-based stratification was associated with improved mid-term survival, as was demonstrated 18 years ago by the SHOCK trial investigators. Since then, additional pharmacological or mechanical strategies failed to improve outcomes significantly in the setting of ischaemic CS in several, mostly small sized, clinical trials. Two types of methodological bias have been raised for nearly all recent CS trials: (i) ‘sick’ patients may not be enrolled, but rather treated with maximum support for humanitarian reasons by the clinical site investigators; or (ii) on the other hand, there is no practical and objective way to screen out futile cases and therefore their inclusion may also impact the outcomes. Therefore, deriving risk factors of CS development and the recognition of different stages of CS with the understanding of their outcomes is a very relevant goal for proper clinical practice and clinical research. The extent of revascularization in CS has also been debated. Its application in non-culprit coronary lesions during the index procedure (for STEMI complicated by CS) was granted a class IIa level C recommendation by the European Society of Cardiology. However, this recommendation was recently challenged by the results of a prospective randomized trial: a culprit-lesion-only PCI strategy in CS patients was associated with lower rate of death or renal replacement at 30 days compared with immediate multivessel PCI. Additionally, routine intra-aortic balloon pump (IABP) support after PCI for STEMI with CS is no longer indicated in the absence of mechanical complications. Mechanical left ventricular assist devices correct haemodynamic parameters, but no adequately powered trials have so far demonstrated improved clinical outcomes. These devices are mainly used as a salvage strategy in the case of refractory CS. The development of a strategy to provide haemodynamic support before initiating PCI in such cases has recently stemmed from pre-clinical research. Only a small minority (<15%) of patients in a previous randomized trial were indeed given IABP support before the start of PCI, hence this proposal has never been adequately tested. A prospective randomized trial is ongoing on this subject (DanShock trial, NCT01633502) with use of a percutaneous left ventricular assist device. Regarding pharmacological therapeutics, inotropic agents such as dobutamine are used as first line-treatment in the case of low cardiac output with preserved systolic blood pressure, or norepinephrine instead of dopamine, in the case of severe hypotension. However, catecholamines are only symptomatic therapy for CS, with a lack of clear efficacy on survival. Quite complex pathophysiology is evolving in CS cases. PostSTEMI CS is the consequence of acute or subacute impairment of the entire circulatory system, driven by the initial depression of cardiac contractility and a sharp increase in intraventricular pressure, eventually leading to multiorgan dysfunction syndrome. The