https://doi.org/10.1007/s00392-024-02526-y
1Universitätsklinikum Heidelberg AG Backs, Abt. Innere Medizin III - Kardiologie Heidelberg, Deutschland; 2Universitätsklinikum Heidelberg Institut für experimentelle Kardiologie Heidelberg, Deutschland; 3Universitätsklinikum Heidelberg Klinik für Innere Med. III, Kardiologie, Angiologie u. Pneumologie Heidelberg, Deutschland
Background:
Out-of-hospital cardiac arrest (OHCA) continues to have a poor outcome despite advances in (pre)clinical care. Even with temperature management and coronary intervention, only around 40% of patients after OHCA achieve a return of spontaneous circulation (ROSC) and less than 11% are discharged from hospital alive. Regardless of the cause of OHCA, global ischaemia and reperfusion injury lead to a systemic inflammatory reaction similar to sepsis. This inflammatory reaction is referred to as post-cardiac arrest syndrome (PCAS) and leads to multi-organ failure, tissue damage caused by leukocytes, activation of the coagulation system and myocardial dysfunction. Elevated levels of interleukin (IL)-6, IL-8 and IL-10 and tumour necrosis factor (TNF)-α were observed as early as three hours after OHCA. Monocyte chemoattractant protein-1 (MCP-1) plays a key role in healing as well as in the development of interstitial fibrosis after myocardial infarction. Studies have also shown that patients with chronic heart failure (CHF) show elevated MCP-1 levels. Inflammatory heart failure can also occur in PCAS, which may correlate with the high mortality of this clinical syndrome.
Methods:
This prospective observational study investigates whether the protein MCP-1 can predict the future course and chances of survival after OHCA. For this purpose, 54 patients were recruited after OHCA from any cause. Blood samples were taken every other day for ten days after admission and throughout the progression of PCAS, during which MCP-1 was measured. Subsequently, MCP-1 was correlated with vital parameters and relevant laboratory values such as lactate, CRP and procalcitonin.
Results:
The results showed a correlation between elevated MCP-1 levels and increased mortality after OHCA. Using the Mann-Whitney U test, it was shown that the MCP-1 levels of survivors were significantly lower than those of non-survivors. In addition, patients with MCP-1 values in the highest quartile (Q4>4459,31pg/ml) had a significantly reduced probability of survival to the second day after OHCA compared to the lower quartiles (40% vs. 86%).
Conclusion:
MCP-1 is a promising biomarker for patients after OHCA. As a surrogate parameter, it provides valuable information on the inflammatory status, while as a prognostic marker it can provide essential information on the expected clinical course and the probability of survival. The integration of MCP-1 into clinical monitoring could lead to improved identification of patients at high risk of severe progression and help to provide these patients with more targeted care. In follow-up studies, potential therapeutic strategies could be found for patients with elevated MCP-1 levels that are associated with a targeted influence on MCP-1. As of now, the underlying signalling pathways are still insufficiently characterised and require extensive scientific evaluation. Only after thorough analysis will it become clear whether MCP-1 can be used as a therapeutic target or merely as a surrogate parameter.