Troponin in cardiogenic shock not caused by acute myocardial infarction, a predictor of mortality
Authors: Beer B N , Sundermeyer J , Dettling A , Besch L , Skurk C , Thiele H , Bertoldi L , Dauw J , Proudfoot A , Orban M , Pazdernik M , Graf T , Kirchhof P , Blankenberg S , Schrage B 
Published: November 2023

Background

Cardiogenic shock is associated with a high mortality and morbidity due to organ damage and multi-organ failure including direct damage to the myocardium.

Purpose

This study aimed to assess troponin as a marker of myocardial damage in patients with cardiogenic shock outside of a myocardial infarction (e.g., non-ischaemic cardiogenic shock).

Methods

Data from unselected patients with cardiogenic shock not caused by myocardial infarction were anonymised and combined in a multicentre cohort study from 15 centres in 5 European countries (2011-2020). Cardiogenic shock was defined by clinical signs and symptoms, elevated lactate concentrations (arterial &gt;2.0 mmol/l, venous &gt;2.5 mmol/l), and hypotension (systolic &lt;90 mmHg or need for vasopressors). Patients with need for urgent coronary revascularisation, predominant right heart failure, eCPR or cardiogenic shock after cardiotomy were excluded. Baseline was defined to reflect the worst clinical status within 6 hours before/after admission (for patients not treated with mechanical circulatory support) or after device implantation (for patients treated with mechanical circulatory support). Troponin concentrations at baseline as well as after 24 hours were quantified using the Elecsys® Troponin T high-sensitive assay by Roche (99th percentile 14 ng/l). Baseline troponin (displayed per 250 ng/l) and its increase within 24 hours were associated with 30-day mortality by fitting Cox regression models adjusted for age, sex, baseline creatinine, baseline lactate, baseline pH, prior cardiac arrest, duration of CPR, acute-on-chronic or de novo heart failure, and mechanical ventilation.

Results

Overall, 477 patients were analysed [mean age 62 (±15) years, 144 women (30.2%), acute-on-chronic heart failure in 255 (53.6%)]. Median LVEF was 20% (IQR 15-30%), CPR was performed in 196 cases (41.1%), median lactate at baseline was 7.3 mmol/l (IQR 4.2-10.8 mmol/l) and median baseline troponin T was 164 ng/l (IQR 77-678 ng/l). Patients with a higher troponin T at baseline (e.g., ≥median) more frequently presented with de novo heart failure (54.8 vs. 37.9%, p&lt;0.01) or after prior CPR (47.7 vs. 34.3%, p&lt;0.01) although other parameters reflecting cardiogenic shock severity (e.g., blood pressure, baseline lactate or LVEF) were not significantly different. Finally, troponin T at baseline showed a significant association with 30-day mortality (HR 1.006, 95% CI: 1.0-1.011, p = 0.041) while the relative troponin T increase within 24 hours did not (HR 1.005, 95% CI: 0.997-1.013, p = 0.212) (Figure 1).

Conclusion

Cardiac organ damage in cardiogenic shock outside of a myocardial infarction (e.g., non-ischaemic cardiogenic shock) is associated with increased risk of death within 30 days. Elevated troponin levels could identify a group of patients with cardiogenic shock in need for cardioprotective therapies.Figure 1