Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock

Angela Dettling; Jessica Weimann; Jonas Sundermeyer; Benedikt N. Beer; Lisa Besch; Peter M. Becher; Fabian J. Brunner; Stefan Kluge; Paulus Kirchhof; Stefan Blankenberg; Dirk Westermann; Benedikt Schrage

doi:10.1007/s00392-023-02336-8

Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock

Angela Dettling, Jessica Weimann, Jonas Sundermeyer, Benedikt N. Beer, Lisa Besch, Peter M. Becher, Fabian J. Brunner, Stefan Kluge, Paulus Kirchhof, Stefan Blankenberg, Dirk Westermann, Benedikt Schrage^*

^*Corresponding author for this work

Cardiovascular Sciences

Research output: Contribution to journal › Article › peer-review

13 Downloads (Pure)

Abstract

Background: Mortality in cardiogenic shock (CS) remains high even when mechanical circulatory support (MCS) restores adequate circulation. To detect a potential contribution of systemic inflammation to shock severity, this study determined associations between C-reactive protein (CRP) concentrations and outcomes in patients with CS.

Methods: Unselected, consecutive patients with CS and CRP measurements treated at a single large cardiovascular center between 2009 and 2019 were analyzed. Adjusted regression models were fitted to evaluate the association of CRP with shock severity, 30-day in-hospital mortality and treatment response to MCS.

Results: The analysis included 1116 patients [median age: 70 (IQR 58–79) years, 795 (71.3%) male, lactate 4.6 (IQR 2.2–9.5) mmol/l, CRP 17 (IQR 5–71) mg/l]. The cause of CS was acute myocardial infarction in 530 (48%) patients, 648 (58%) patients presented with cardiac arrest. Plasma CRP concentrations were equally distributed across shock severities (SCAI stage B–E). Higher CRP concentrations were associated with 30-day in-hospital mortality (8% relative risk increase per 50 mg/l increase in CRP, range 3–13%; p < 0.001), even after adjustment for CS severity and other potential confounders. Higher CRP concentrations were only associated with higher mortality in patients not treated with MCS [hazard ratio (HR) for CRP > median 1.50; 95%-CI 1.21–1.86; p < 0.001], but not in those treated with MCS (HR for CRP > median 0.92; 95%-CI 0.67–1.26; p = 0.59; p-interaction = 0.01).

Conclusion: Elevated CRP concentrations are associated with increased 30-day in-hospital mortality in unselected patients with cardiogenic shock. The use of mechanical circulatory support attenuates this association.

Original language	English
Pages (from-to)	324-335
Number of pages	12
Journal	Clinical Research in Cardiology
Volume	113
Issue number	2
Early online date	20 Nov 2023
DOIs	https://doi.org/10.1007/s00392-023-02336-8
Publication status	Published - Feb 2024

Bibliographical note

Open Access funding enabled and organized by Projekt DEAL

Conflict of interest:
BS received speaker fees from Abiomed, AstraZeneca and Abbott; and research support from Abiomed, the German Research Foundation and the Else Kröner-Fresenius-Stiftung. PK was partially supported by European Union AFFECT-AF (grant agreement 847770), and MAESTRIA (grant agreement 965286), British Heart Foundation (PG/17/30/32961; PG/20/22/35093; AA/18/2/34218), German Centre for Cardiovascular Research supported by the German Ministry of Education and Research (DZHK), Deutsche Forschungsgemeinschaft (Ki 509167694), and Leducq Foundation. PK receives research support for basic, translational, and clinical research projects from European Union, British Heart Foundation, Leducq Foundation, Medical Research Council (UK), and German Centre for Cardiovascular Research, from several drug and device companies active in atrial fibrillation, and has received honoraria from several such companies in the past, but not in the last three years. PK is listed as inventor on two issued patents held by University of Hamburg (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). FJB reports grants from Daiichi Sankyo, Novartis, Pfizer, and Sanofi, non-financial support from Abbott, ASAHI INTECC, and Inari Medical, personal fees from Amgen and Novartis outside of the submitted work. The other authors have no conflicts of interest to declare.

Keywords

Cardiogenic shock
Mechanical circulatory support
Systemic inflammation
Mortality

Access to Document

10.1007/s00392-023-02336-8Licence: Creative Commons: Attribution (CC BY)

DettlingA2023AssociationFinal published version, 1.06 MBLicence: Creative Commons: Attribution (CC BY)

Cite this

Dettling, A., Weimann, J., Sundermeyer, J., Beer, B. N., Besch, L., Becher, P. M., Brunner, F. J., Kluge, S., Kirchhof, P., Blankenberg, S., Westermann, D., & Schrage, B. (2024). Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock. Clinical Research in Cardiology, 113(2), 324-335. https://doi.org/10.1007/s00392-023-02336-8

@article{6ef290a00ffc4d36afe607f4a558e1f5,

title = "Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock",

abstract = "Background: Mortality in cardiogenic shock (CS) remains high even when mechanical circulatory support (MCS) restores adequate circulation. To detect a potential contribution of systemic inflammation to shock severity, this study determined associations between C-reactive protein (CRP) concentrations and outcomes in patients with CS. Methods: Unselected, consecutive patients with CS and CRP measurements treated at a single large cardiovascular center between 2009 and 2019 were analyzed. Adjusted regression models were fitted to evaluate the association of CRP with shock severity, 30-day in-hospital mortality and treatment response to MCS. Results: The analysis included 1116 patients [median age: 70 (IQR 58–79) years, 795 (71.3%) male, lactate 4.6 (IQR 2.2–9.5) mmol/l, CRP 17 (IQR 5–71) mg/l]. The cause of CS was acute myocardial infarction in 530 (48%) patients, 648 (58%) patients presented with cardiac arrest. Plasma CRP concentrations were equally distributed across shock severities (SCAI stage B–E). Higher CRP concentrations were associated with 30-day in-hospital mortality (8% relative risk increase per 50 mg/l increase in CRP, range 3–13%; p < 0.001), even after adjustment for CS severity and other potential confounders. Higher CRP concentrations were only associated with higher mortality in patients not treated with MCS [hazard ratio (HR) for CRP > median 1.50; 95%-CI 1.21–1.86; p < 0.001], but not in those treated with MCS (HR for CRP > median 0.92; 95%-CI 0.67–1.26; p = 0.59; p-interaction = 0.01). Conclusion: Elevated CRP concentrations are associated with increased 30-day in-hospital mortality in unselected patients with cardiogenic shock. The use of mechanical circulatory support attenuates this association.",

keywords = "Cardiogenic shock, Mechanical circulatory support, Systemic inflammation, Mortality",

author = "Angela Dettling and Jessica Weimann and Jonas Sundermeyer and Beer, {Benedikt N.} and Lisa Besch and Becher, {Peter M.} and Brunner, {Fabian J.} and Stefan Kluge and Paulus Kirchhof and Stefan Blankenberg and Dirk Westermann and Benedikt Schrage",

note = "Open Access funding enabled and organized by Projekt DEAL Conflict of interest: BS received speaker fees from Abiomed, AstraZeneca and Abbott; and research support from Abiomed, the German Research Foundation and the Else Kr{\"o}ner-Fresenius-Stiftung. PK was partially supported by European Union AFFECT-AF (grant agreement 847770), and MAESTRIA (grant agreement 965286), British Heart Foundation (PG/17/30/32961; PG/20/22/35093; AA/18/2/34218), German Centre for Cardiovascular Research supported by the German Ministry of Education and Research (DZHK), Deutsche Forschungsgemeinschaft (Ki 509167694), and Leducq Foundation. PK receives research support for basic, translational, and clinical research projects from European Union, British Heart Foundation, Leducq Foundation, Medical Research Council (UK), and German Centre for Cardiovascular Research, from several drug and device companies active in atrial fibrillation, and has received honoraria from several such companies in the past, but not in the last three years. PK is listed as inventor on two issued patents held by University of Hamburg (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). FJB reports grants from Daiichi Sankyo, Novartis, Pfizer, and Sanofi, non-financial support from Abbott, ASAHI INTECC, and Inari Medical, personal fees from Amgen and Novartis outside of the submitted work. The other authors have no conflicts of interest to declare.",

year = "2024",

month = feb,

doi = "10.1007/s00392-023-02336-8",

language = "English",

volume = "113",

pages = "324--335",

journal = "Clinical Research in Cardiology",

issn = "1861-0684",

publisher = "Springer",

number = "2",

}

Dettling, A, Weimann, J, Sundermeyer, J, Beer, BN, Besch, L, Becher, PM, Brunner, FJ, Kluge, S, Kirchhof, P, Blankenberg, S, Westermann, D & Schrage, B 2024, 'Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock', Clinical Research in Cardiology, vol. 113, no. 2, pp. 324-335. https://doi.org/10.1007/s00392-023-02336-8

TY - JOUR

T1 - Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock

AU - Dettling, Angela

AU - Weimann, Jessica

AU - Sundermeyer, Jonas

AU - Beer, Benedikt N.

AU - Besch, Lisa

AU - Becher, Peter M.

AU - Brunner, Fabian J.

AU - Kluge, Stefan

AU - Kirchhof, Paulus

AU - Blankenberg, Stefan

AU - Westermann, Dirk

AU - Schrage, Benedikt

N1 - Open Access funding enabled and organized by Projekt DEAL Conflict of interest: BS received speaker fees from Abiomed, AstraZeneca and Abbott; and research support from Abiomed, the German Research Foundation and the Else Kröner-Fresenius-Stiftung. PK was partially supported by European Union AFFECT-AF (grant agreement 847770), and MAESTRIA (grant agreement 965286), British Heart Foundation (PG/17/30/32961; PG/20/22/35093; AA/18/2/34218), German Centre for Cardiovascular Research supported by the German Ministry of Education and Research (DZHK), Deutsche Forschungsgemeinschaft (Ki 509167694), and Leducq Foundation. PK receives research support for basic, translational, and clinical research projects from European Union, British Heart Foundation, Leducq Foundation, Medical Research Council (UK), and German Centre for Cardiovascular Research, from several drug and device companies active in atrial fibrillation, and has received honoraria from several such companies in the past, but not in the last three years. PK is listed as inventor on two issued patents held by University of Hamburg (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). FJB reports grants from Daiichi Sankyo, Novartis, Pfizer, and Sanofi, non-financial support from Abbott, ASAHI INTECC, and Inari Medical, personal fees from Amgen and Novartis outside of the submitted work. The other authors have no conflicts of interest to declare.

PY - 2024/2

Y1 - 2024/2

N2 - Background: Mortality in cardiogenic shock (CS) remains high even when mechanical circulatory support (MCS) restores adequate circulation. To detect a potential contribution of systemic inflammation to shock severity, this study determined associations between C-reactive protein (CRP) concentrations and outcomes in patients with CS. Methods: Unselected, consecutive patients with CS and CRP measurements treated at a single large cardiovascular center between 2009 and 2019 were analyzed. Adjusted regression models were fitted to evaluate the association of CRP with shock severity, 30-day in-hospital mortality and treatment response to MCS. Results: The analysis included 1116 patients [median age: 70 (IQR 58–79) years, 795 (71.3%) male, lactate 4.6 (IQR 2.2–9.5) mmol/l, CRP 17 (IQR 5–71) mg/l]. The cause of CS was acute myocardial infarction in 530 (48%) patients, 648 (58%) patients presented with cardiac arrest. Plasma CRP concentrations were equally distributed across shock severities (SCAI stage B–E). Higher CRP concentrations were associated with 30-day in-hospital mortality (8% relative risk increase per 50 mg/l increase in CRP, range 3–13%; p < 0.001), even after adjustment for CS severity and other potential confounders. Higher CRP concentrations were only associated with higher mortality in patients not treated with MCS [hazard ratio (HR) for CRP > median 1.50; 95%-CI 1.21–1.86; p < 0.001], but not in those treated with MCS (HR for CRP > median 0.92; 95%-CI 0.67–1.26; p = 0.59; p-interaction = 0.01). Conclusion: Elevated CRP concentrations are associated with increased 30-day in-hospital mortality in unselected patients with cardiogenic shock. The use of mechanical circulatory support attenuates this association.

AB - Background: Mortality in cardiogenic shock (CS) remains high even when mechanical circulatory support (MCS) restores adequate circulation. To detect a potential contribution of systemic inflammation to shock severity, this study determined associations between C-reactive protein (CRP) concentrations and outcomes in patients with CS. Methods: Unselected, consecutive patients with CS and CRP measurements treated at a single large cardiovascular center between 2009 and 2019 were analyzed. Adjusted regression models were fitted to evaluate the association of CRP with shock severity, 30-day in-hospital mortality and treatment response to MCS. Results: The analysis included 1116 patients [median age: 70 (IQR 58–79) years, 795 (71.3%) male, lactate 4.6 (IQR 2.2–9.5) mmol/l, CRP 17 (IQR 5–71) mg/l]. The cause of CS was acute myocardial infarction in 530 (48%) patients, 648 (58%) patients presented with cardiac arrest. Plasma CRP concentrations were equally distributed across shock severities (SCAI stage B–E). Higher CRP concentrations were associated with 30-day in-hospital mortality (8% relative risk increase per 50 mg/l increase in CRP, range 3–13%; p < 0.001), even after adjustment for CS severity and other potential confounders. Higher CRP concentrations were only associated with higher mortality in patients not treated with MCS [hazard ratio (HR) for CRP > median 1.50; 95%-CI 1.21–1.86; p < 0.001], but not in those treated with MCS (HR for CRP > median 0.92; 95%-CI 0.67–1.26; p = 0.59; p-interaction = 0.01). Conclusion: Elevated CRP concentrations are associated with increased 30-day in-hospital mortality in unselected patients with cardiogenic shock. The use of mechanical circulatory support attenuates this association.

KW - Cardiogenic shock

KW - Mechanical circulatory support

KW - Systemic inflammation

KW - Mortality

U2 - 10.1007/s00392-023-02336-8

DO - 10.1007/s00392-023-02336-8

M3 - Article

SN - 1861-0684

VL - 113

SP - 324

EP - 335

JO - Clinical Research in Cardiology

JF - Clinical Research in Cardiology

IS - 2

ER -

Association of systemic inflammation with shock severity, 30-day mortality, and therapy response in patients with cardiogenic shock

Abstract

Bibliographical note

Keywords

Access to Document

Fingerprint

Cite this