This study examined the impact of symptom duration on prognosis in AMICS patients undergoing PCI. Prolonged symptom duration before hospital presentation was significantly associated with increased 30-day mortality. In the population treated with MCS, symptom duration > 24 h was also associated with higher mortality and was an independent predictor in a multivariate analysis for 30-day mortality.

With over 1,300 patients included, our study provides real-world data on AMICS care in the Netherlands. Our observed 30-day mortality falls within the lower range of rates documented in previous studies [1, 2, 5, 14, 15]. We observed a significant increase in 30-day mortality as prehospital symptom duration prolonged, consistent with the subgroup analysis conducted in the SHOCK trial [6]. In this trial, early revascularisation did not lead to a significant reduction in the primary endpoint, 30-day mortality. However, a subgroup analysis focusing on patients randomised within 6 h of symptom onset (approximately one quarter of the study population, n = 73) did reveal a significant decrease in 30-day mortality [16]. Furthermore, the long-term evaluation in the SHOCK trial showed higher 1‑year mortality rates (although not significant) associated with increasing time intervals from myocardial infarction to revascularisation, ranging from 0 to 8 h (< 4 h, 36%; 4 to < 6 h, 55%; 6 to < 8 h, 82%) [17].

We excluded patients with OHCA to enhance the homogeneity of our study cohort. It is noteworthy that mortality in these excluded patients differed significantly from that in our non-OHCA AMICS population (47% vs 34%, p < 0.001). In the OHCA population, no significant correlation was identified between symptom duration and mortality. OHCA patients constitute a distinctive subgroup within AMICS, often present within a short time frame with severe shock, due to cardiac dysfunction and systemic effects of whole-body ischaemia-reperfusion injury [18]. Mortality is high and often driven by anoxic brain injury and multiorgan failure, a condition that limits the potential for improving prognosis through interventions such as MCS, even if myocardial recovery is successful. Important prehospital prognostic factors for OHCA patients include time to first cardiopulmonary resuscitation and time until return of spontaneous circulation [19, 20], aspects that have not been included in our assessment. By excluding OHCA patients, we aimed to provide accurate outcomes of AMICS regarding symptom duration.

In our subgroup analysis, we compared patients receiving MCS with those who did not. Within the MCS group, vasoactive agents were administered more frequently, heart rates were higher, and higher levels of lactate, troponin and CK-MB were observed, indicating substantial disparity in shock severity. Patients receiving MCS appeared to be in a more critical condition, necessitating support. Consequently, the use of MCS in our study is likely biased towards those with more advanced shock severity, impacting the observed mortality differences.

No significant correlation was found between symptom duration and the MCS device selected. However, a trend towards significance emerged concerning patients receiving IABP after 24 h, demonstrating higher mortality rates compared to initiation before 24 h (55% vs 38%, p = 0.061). These findings support the view that IABP, considered a less potent device, might be less effective in later stages of CS [21], emphasising the importance of a personalised MCS strategy, tailored to individual patient characteristics.

Comparing our MCS subgroup with the IABP group in the IABP-SHOCK II trial [22], our mortality rates are higher (50% vs 40%). This finding might be a result of selective patient enrollment, as the IAPB-SHOCK II trial excluded patients with onset of shock > 12 h, potentially having a favourable effect on outcomes.

The mortality observed in our MCS population corresponds to those reported in the recently published ECLS-SHOCK trial (50% vs 48%) [11]. Notably, this trial did not exclude OHCA patients, who constituted 78% of the ECLS population. In contrast to our study, subanalysis within the ECLS cohort revealed no significant mortality differences between patients presenting with or without OHCA.

Multivariate logistic regression analysis identified > 24 h symptom duration as an independent predictor for 30-day mortality in the AMICS population receiving MCS. As the duration of shock increases, a cascade of progressive systemic inflammation and multiorgan failure is initiated. Once cardiometabolic shock is established, therapeutic interventions may fail to reverse the downward spiral and improve survival. Hence, early shock recognition and treatment, including timely usage of MCS, might improve prognosis. In practical terms, this necessitates early referral and accurate recognition of shock, which could shorten the time to MCS implantation and may enhance survival. Furthermore, patient selection could impact the effectiveness of MCS regarding clinical outcomes. In cases of severe cardiometabolic shock, therapeutic interventions have a limited impact on prognosis, whereas patients with deteriorating early-stage shock might derive greater benefit from timely intervention. Additionally, as previously discussed, a personalised MCS strategy could potentially enhance prognosis.

There are some important potential limitations associated with our study. Firstly, the retrospective design of this study makes it more susceptible to selection bias, impacting the reliability of our findings. Secondly, missing data could have hindered identifying significant prognostic variables, particularly within the MCS population where some variables (e.g. haemodynamic parameters, laboratory results and TIMI flow post-PCI) were excluded from the multivariate analysis. Variables with respective percentages of missing data are provided in Supplementary Table S4 (Electronic Supplementary Material). Thirdly, 17% of the population underwent multivessel PCI, which was associated with higher 30-day mortality rates and contradicts the established standard of care highlighted by the CULPRIT-SHOCK trial [23].