LAUSR

Cardiogenic shock is the only remaining complication of acute myocardial infarction (AMI) still related to very high mortality rates despite huge investment of medical resources. The explanation is quite simple: cardiogenic shock develops when the ischaemic damage to the heart reaches a critical limit. In 1984–1988, we described echocardiographic findings in cardiogenic shock and demonstrated that not only the extent of AMI but also hypokinesis of non-infarcted myocardium (caused either by scar after previous MI or by multivessel disease leading to ischaemia of non-infarcted areas) is necessary for the development of cardiogenic shock. It thus seems natural that the only therapeutic measure with proven efficacy is immediate reversal of the ongoing ischaemia to prevent irreversible loss of cardiac function. This was clearly demonstrated by the success of primary percutaneous coronary interventions (p-PCIs): the introduction of routine p-PCI into the treatment of AMI decreased the mortality from cardiogenic shock from 80–90% (pre-reperfusion era) to 40–50%. Clinicians and researchers worldwide are trying to improve this still high mortality by mechanistic approaches aimed to stabilize the circulation. Can this approach be successful? Our centre stopped using intra-aortic balloon pumps (IABPs) for AMI complicated by cardiogenic shock >10 years prior to the publication of the IABP-SHOCK II trial. Thus, we were not surprised by the trial results and we are sceptical also about the capability of newer mechanical circulatory support devices to improve long-term outcomes. Data from the National Cardiovascular Data Registry CathPCI demonstrated a decrease in the use of IABPs, with extreme differences between hospitals (8–85%) and a low (7.1%) rate of newer mechanical support devices. Cheng et al. demonstrated that IABP insertion prior to p-PCI increased infarct size (possibly by prolonging the time delay to reperfusion), and the mortality of those in whom an IABP was inserted after p-PCI tended to be lower. The key to improving survival in these critically ill patients is ultrafast opening of the infarct-related artery before shock enters the irreversible phase. In other words, patients with a large AMI and haemodynamic instability enter a ‘slippery slope’ leading to death within minutes or hours (Figure 1). Only those patients successfully reperfused during the initial phase of this descending slope can be saved. Whatever is done later (including mechanical circulatory support) cannot save the patient’s life (due to irreversible loss of cardiac function)—it can only temporarily stabilize arterial pressure or other haemodynamic parameters. This is further supported by the meta-analysis by Thiele et al. published in this issue of the journal. This paper summarized outcomes of patients treated either with a TandemHeart device or with the ImpellaR device compared with patients treated with an IABP device. The results are discouraging: no clinical benefit from mechanical support devices was seen, but only clinical harm (more bleeding and more leg ischaemia). All four randomized trials included in the meta-analysis were designed prior to the publication of the negative IABP-SHOCK II trial, and thus we lack any randomized comparison of mechanical circulatory support devices vs. no device in cardiogenic shock. I strongly believe that potential outcomes of such a trial will be even worse for mechanical support devices due to even greater difference in complication rates favouring the control group. A critical view on mechanical support devices is summarized in Table 1. The potential limitation of the present meta-analysis is that it could not include data about the most sophisticated support device—extracorporeal membrane oxygenation (ECMO)—because no randomized data exist. There is a need for a randomized study comparing ECMO plus p-PCI vs. p-PCI alone (without any mechanical support). Most probably the results of such a study will not differ from the results of the present meta-analysis due to the