Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w

Association of systemic inflammation with shock severity, 30-day mortality and therapy response in patients with cardiogenic shock
A. Dettling1, J. Weimann1, J. Sundermeyer1, B. Beer1, L. Besch1, P. M. Becher1, F. J. Brunner1, S. Kluge2, P. Kirchhof1, S. Blankenberg1, D. Westermann3, B. Schrage1
1Klinik und Poliklinik für Kardiologie, Universitäres Herz- und Gefäßzentrum Hamburg, Hamburg; 2Klinik für Intensivmedizin, Universitätsklinikum Hamburg-Eppendorf, Hamburg; 3Innere Medizin III, Kardiologie und Angiologie, Universitäts-Herzzentrum Freiburg - Bad Krozingen, Freiburg im Breisgau;

Background: Cardiogenic shock (CS) remains a clinical challenge with a high mortality. It is often complicated by systemic inflammation, however the exact role of systemic inflammation in the pathogenesis of cardiogenic shock remains unclear. The aim of this study was to explore the association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with CS.

 

Methods: From a registry of 1338 CS patients, unselected for its etiology, those with available plasma CRP concentrations, as a surrogate for systemic inflammation, were selected. The association between plasma CRP concentrations and CS severity (SCAI stage, reference SCAI B) was analyzed using logistic regression models, adjusted for relevant confounders. The association between plasma CRP concentrations and 30-day mortality was analyzed using adjusted Cox regression models; and the interaction between plasma CRP concentrations and treatment response was assessed by fitting an interaction term between plasma CRP concentrations and mechanical circulatory support (MCS) use in the above described Cox regression models. 

 

Results: A total of 1116 patients were analyzed, median age was 70 years [interquartile range 58-78.6 years], 71.3% were male, 47.7% presented with CS due to acute myocardial infarction and 51.5% with prior cardiac arrest. The median plasma CRP concentration in the study population was 17 mg/dl [interquartile range 5.0-71.0 mg/dl]. With higher CS severity (higher SCAI stage), plasma CRP concentrations appeared to decrease [SCAI C: Odds ratio (OR) 0.53, 95% confidence interval (CI) (0.26-1.03); SCAI D: OR 0.83, 95% CI (0.41-1.65); SCAI E: OR 0.44, 95% CI (0.21-0.92)]; although higher plasma CRP concentrations were strongly associated with a higher risk of 30-day mortality, irrespective of CS severity [8% relative risk increase per 50 mg/dl increase in plasma CRP, range 3-13%]. Higher plasma CRP concentrations were only associated with higher mortality in patients not treated with MCS, but not in those treated with MCS [p-interaction = 0.01].

 

Conclusion: Increased concentrations of plasma CRP are associated with a higher 30-day mortality regardless of shock severity; and are consistent with prior studies associating increased inflammatory markers with a poor prognosis. Furthermore, our results indicate that MCS use might mitigate the negative impact of systemic inflammation, potentially by providing sufficient end-organ perfusion, and call for further research on this topic. 

Figure 1: Association between plasma CRP concentrations and 30-day mortality



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