Troponin elevation in septic shock: prognostic value and association with myocardial dysfunction

Troponin elevation is common in septic shock and often attributed to type 2 myocardial infarction (T2MI) from supply–demand mismatch. However, growing evidence suggests that in sepsis, troponin release frequently reflects sepsis-induced cardiomyopathy (SICM)—a transient, non-ischemic myocardial dysfunction driven by inflammatory and metabolic mechanisms. Differentiating ischemic from sepsis-related myocardial injury remains a major diagnostic challenge.

To evaluate whether troponin elevation predicts in-hospital mortality and correlates with cardiac dysfunction in patients with septic shock, and to assess the incidence of coronary artery disease (CAD) or myocardial ischemia at one-year follow-up among survivors.

We conducted a single-centre retrospective study including 70 patients admitted to the ICU with septic shock in 2024. Admission biomarkers included NT-proBNP, CRP, procalcitonin, lactate, and creatinine; peak troponin values during ICU stay were recorded. All biomarkers were log-transformed before analysis. Echocardiography was available in 37 patients. Associations were tested with Spearman’s correlation and multivariable logistic regression including biomarkers, LVEF, and SOFA/SAPS II scores. Discriminative ability for mortality was assessed by ROC curves. Survivors were screened within one year for myocardial ischemia or CAD.

Patients had a mean age of 71.9 ± 11.7 years; 61.4% were male. In-hospital mortality was 47%. Non-survivors were more often male and had higher SAPS II (66.8 vs. 44.8) and SOFA scores (11.9 vs. 6.6; both p<0.05). Comorbidities and inflammatory biomarkers were comparable between groups. Median admission and peak troponin were markedly elevated (201 and 243 ng/L, respectively) but did not differ significantly between survivors and non-survivors (p>0.1). In 37 echocardiograms, reduced LVEF (<50%) occurred in 35%, without significant mortality difference (p=0.114). Troponin moderately correlated with NT-proBNP (ρ=0.497, p<0.001) but not with LVEF or outcomes. In multivariable analysis, only SOFA score independently predicted mortality (OR 1.94, 95% CI 1.23–3.05, p=0.005). ROC analysis showed good discrimination for SOFA (AUC=0.891) and SAPS II (AUC=0.825), while troponin and NT-proBNP performed poorly (AUC≈0.56–0.59). At one-year follow-up, four survivors underwent ischemia evaluation: none showed significant obstructive CAD.

Troponin elevation in septic shock was frequent but not independently associated with mortality, systolic dysfunction, or coronary disease. Although correlated with NT-proBNP and illness severity, troponin lacked prognostic value compared with SOFA and SAPS II scores. These findings support SICM as a reversible, non-ischemic myocardial dysfunction distinct from T2MI. Clinically, troponin elevation in sepsis should be interpreted within the full clinical and imaging context, rather than as an isolated marker of ischemia or prognosis.