Key result
Each doubling of postoperative hs-cTn ratio is linked to ~8% higher long-term mortality.
Why the study?
Postoperative hs-cTn elevation within 72 hours of non-cardiac surgery is prognostically relevant, but impaired renal function may confound hs-cTn interpretation and potentially modify its association with long-term mortality.
Does impaired renal function (creatinine) modify the prognostic association of postoperative high-sensitivity troponin elevation with long-term all-cause mortality in patients admitted to a postoperative ICU after non-cardiac surgery?
Cohort (n=2,376)
No
Does impaired renal function (creatinine) modify the prognostic association of postoperative high-sensitivity troponin elevation with long-term all-cause mortality in patients admitted to a postoperative ICU after non-cardiac surgery?
Renal dysfunction correlates with postoperative hs-cTn levels but does not modify the long-term mortality risk associated with postoperative troponin elevation after non-cardiac surgery.
Answers are grounded in this paper and cite their sources.
Troponin elevation after non-cardiac surgery signals mortality risk irrespective of creatinine; extends prognostic data but leaves open whether troponin-guided interventions improve outcomes.
Background Postoperative high-sensitivity cardiac troponin (hs-cTn) elevation within 72 hours is common after non-cardiac surgery and is prognostically relevant even when non-ischemic. However, impaired renal function may confound hs-cTn interpretation and potentially modify its association with mortality. Purpose To evaluate (1) the correlation between creatinine and peak postoperative hs-cTn and (2) whether renal function modifies the prognostic impact of hs-cTn on long-term all-cause mortality. Methods We studied consecutive patients admitted to a postoperative ICU after non-cardiac surgery with systematic hs-cTn measurement within 3 postoperative days. Peak hs-cTn was normalized by the assay-specific 99th percentile upper reference limit (URL), generating a troponin-to-URL ratio. Creatinine was obtained from the same calendar day as the troponin peak. Chronic kidney disease (CKD) included any stage (dialysis or non-dialysis). Correlation between creatinine and troponin-to-URL ratio was assessed with Spearman’s rho. The primary endpoint was all-cause mortality (time zero: surgery date). Cox proportional hazards models tested an interaction term log(troponin-to-URL) x log(creatinine), adjusting for age, sex, SAPS3, CKD, and surgery category. Results Cox analyses included 2,376 patients (median follow-up 6.7 years, IQR ~5.0–8.3); 25.0% died (n=594). Postoperative myocardial injury (MINS) occurred in 10.2% and CKD in 4.2%. Creatinine correlated moderately with troponin-to-URL ratio (rho=0.35, p<0.001). In adjusted models, each doubling of troponin-to-URL ratio was associated with higher mortality (at creatinine 0.7, HR 1.08, 95% CI 1.04–1.11). The troponin x creatinine interaction was not significant (p=0.68), indicating a broadly consistent troponin–mortality association across renal function. CKD remained independently associated with mortality (HR 1.80, 95% CI 1.32–2.44). Conclusion Although creatinine and postoperative hs-cTn are correlated, renal dysfunction did not materially modify the long-term prognostic impact of postoperative hs-cTn elevation. A troponin-to-URL approach appears robust for long-term risk stratification after non-cardiac surgery.
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Gomes et al. (2026) conducted a cohort in Postoperative ICU admission after non-cardiac surgery (n=2,376). Peak postoperative hs-cTn-to-URL ratio and creatinine interaction was evaluated on All-cause mortality (HR 1.08, 95% CI 1.04-1.11, p=0.68 for interaction). Each doubling of the postoperative hs-cTn-to-URL ratio increased long-term mortality (HR 1.08; 95% CI 1.04-1.11), without significant modification by creatinine (p=0.68 for interaction).
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