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Background <p>Impaired renal function can increase cardiac troponin levels due to reduced elimination, potentially affecting its diagnostic utility. Limited data exist on high-sensitivity cardiac troponin I (hs-cTnI) kinetics after cardiac surgery relative to renal function. This study evaluates how impaired renal function influences hs-cTnI kinetics following cardiac surgery, distinguishing between patients with and without postoperative myocardial infarction (PMI).</p> Methods <p>We conducted a retrospective analysis of adult patients who underwent elective cardiac surgery at our hospital from January 2013 to May 2019. Serial hs-cTnI measurements were taken from baseline up to 48&#xa0;h post-surgery. Renal function was assessed using the MDRD formula, defining impaired renal function as a GFR &lt; 60&#xa0;ml/min. Acute kidney injury (AKI) was based on postoperative creatinine levels, and PMI was defined by ARC-2 criteria. Predictors of long-term all-cause mortality were analyzed using Cox regression.</p> Results <p>Out of 14,355 patients (51.4% CABG, 39.4% valvular procedures, 9.2% thoracic aortic procedures), 139 (1.0%) had PMI. Hs-cTnI levels were higher in patients with impaired renal function across the cohort and in those without PMI. However, in patients with PMI, hs-cTnI levels did not vary significantly with renal function. Elevated hs-cTnI ≥ 213 times the upper limit of normal was a significant predictor of long-term mortality regardless of renal function (hazard ratio: 1.28, 95% CI: 1.17–1.40, p &lt; 0.001), but early postoperative hs-cTnI measures held poor discriminatory yield to predict PMI with an AUC of 0.55 (95% confidence intervals: 0.54–0.56).</p> Conclusion <p>Renal function and acute kidney injury affect hs-cTnI kinetics post-surgery only in patients without PMI. Elevated hs-cTnI remains a strong predictor of long-term mortality, independent of renal function, but early postoperative detection of PMI requires additional metrics, including ECG, transthoracic echocardiography (TTE), and signs of hemodynamic instability.</p> Graphical Abstract <p> Impact of impaired renal function on kinetics of high-sensitive cardiac troponin following cardiac surgery. Legend: Postopereparative myocardial infarction (PMI) was defined in accordance with the ARC-2 criteria, as: &gt; 35x elevation of high-sensitivity cardiac troponin I (hs-cTnI) above the upper limit of normal (ULN) of 26 pg/ml and either of 1) new pathological Q waves or equivalent, 2) flow-limiting angiographic complication, or 3) new “substantial” loss of myocardium on imaging. Normal or impaired renal function at baseline was discriminated by estimated glomerular filtration rate (GFR) with a cut-off of 60 ml/ml. ECG = electrocardiogram, TTE = transthoracic echocardiography. </p>

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Impact of impaired renal function on kinetics of high-sensitive cardiac troponin following cardiac surgery

  • 期刊论文

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  • 发表日期：

    2025年1月29日

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  • Felix Rudolph,
  • Marcus-André Deutsch,
  • Kai Peter Friedrichs,
  • André Renner,
  • Werner Scholtz,
  • Muhammed Gerçek,
  • Johannes Kirchner,
  • Mohamed Ayoub,
  • Tanja Katharina Rudolph,
  • René Schramm,
  • Jan Gummert,
  • Volker Rudolph,
  • Hazem Omran

摘要

Background

Impaired renal function can increase cardiac troponin levels due to reduced elimination, potentially affecting its diagnostic utility. Limited data exist on high-sensitivity cardiac troponin I (hs-cTnI) kinetics after cardiac surgery relative to renal function. This study evaluates how impaired renal function influences hs-cTnI kinetics following cardiac surgery, distinguishing between patients with and without postoperative myocardial infarction (PMI).

Methods

We conducted a retrospective analysis of adult patients who underwent elective cardiac surgery at our hospital from January 2013 to May 2019. Serial hs-cTnI measurements were taken from baseline up to 48 h post-surgery. Renal function was assessed using the MDRD formula, defining impaired renal function as a GFR < 60 ml/min. Acute kidney injury (AKI) was based on postoperative creatinine levels, and PMI was defined by ARC-2 criteria. Predictors of long-term all-cause mortality were analyzed using Cox regression.

Results

Out of 14,355 patients (51.4% CABG, 39.4% valvular procedures, 9.2% thoracic aortic procedures), 139 (1.0%) had PMI. Hs-cTnI levels were higher in patients with impaired renal function across the cohort and in those without PMI. However, in patients with PMI, hs-cTnI levels did not vary significantly with renal function. Elevated hs-cTnI ≥ 213 times the upper limit of normal was a significant predictor of long-term mortality regardless of renal function (hazard ratio: 1.28, 95% CI: 1.17–1.40, p < 0.001), but early postoperative hs-cTnI measures held poor discriminatory yield to predict PMI with an AUC of 0.55 (95% confidence intervals: 0.54–0.56).

Conclusion

Renal function and acute kidney injury affect hs-cTnI kinetics post-surgery only in patients without PMI. Elevated hs-cTnI remains a strong predictor of long-term mortality, independent of renal function, but early postoperative detection of PMI requires additional metrics, including ECG, transthoracic echocardiography (TTE), and signs of hemodynamic instability.

Graphical Abstract

Impact of impaired renal function on kinetics of high-sensitive cardiac troponin following cardiac surgery. Legend: Postopereparative myocardial infarction (PMI) was defined in accordance with the ARC-2 criteria, as: > 35x elevation of high-sensitivity cardiac troponin I (hs-cTnI) above the upper limit of normal (ULN) of 26 pg/ml and either of 1) new pathological Q waves or equivalent, 2) flow-limiting angiographic complication, or 3) new “substantial” loss of myocardium on imaging. Normal or impaired renal function at baseline was discriminated by estimated glomerular filtration rate (GFR) with a cut-off of 60 ml/ml. ECG = electrocardiogram, TTE = transthoracic echocardiography.