Key result
Elevated postoperative hs-cTnI was associated with 30-day mortality in patients with normal renal function (OR 1.028; 95% CI 1.013-1.043; P<.001), but not in those with renal impairment.
Why the study?
Cardiac troponin levels can be elevated without myocardial injury in renal impairment, but the prognostic value of elevated troponin levels after cardiac surgery in patients with renal impairment has not been well evaluated.
Does elevated postoperative hs-cTnI predict mortality in patients undergoing cardiac surgery, and does this vary by preoperative renal function?
Cohort (n=1,909)
Does elevated postoperative hs-cTnI predict mortality in patients undergoing cardiac surgery, and does this vary by preoperative renal function?
Odds Ratio: 1.028 (95% CI 1.013–1.043)
p-value: p=< .001
Postoperative hs-cTnI is a useful prognostic marker for short- and long-term mortality after cardiac surgery only in patients with normal preoperative renal function, losing its predictive value in those with renal impairment.
Postoperative hs-cTnI should not guide prognostication in renal impairment; observational data leave its utility in normal function hypothesis-generating.
Cardiac troponin levels can be elevated without myocardial injury in patients with renal impairment. However, the prognostic value of elevated troponin levels after cardiac surgery has not been well evaluated in patients with renal impairment. We evaluated the relationship between postoperative troponin levels and mortality following cardiac surgery according to preoperative renal function.Among 3661 patients underwent cardiac surgery between March 2005 and December 2015, 1909 patients were analyzed after excluding those with insufficient laboratory data, preoperative myocardial infarction, underwent Cox-Maze or redo surgery, or with a follow-up period <30 days. The primary outcome was risk of 30-day mortality according to elevated postoperative high-sensitivity cardiac troponin I (hs-cTnI) levels in varying degrees of renal function. Secondary outcomes included long-term cardiac-cause and all-cause mortality during the median follow-up of 52 months.After adjustment for risk factors, elevated peak postoperative hs-cTnI was associated with 30-day mortality [adjusted odds ratio 1.028, 95% confidence interval (CI) 1.013-1.043, P < .001], long-term cardiac-cause [adjusted hazard ratio (HR) 1.013, 95% CI 1.009-1.017, P < .001] and all-cause mortality (adjusted HR 1.013, 95% CI 1.009-1.016, P < .001), in patients with preoperative normal renal function [estimated glomerular filtration rate (eGFR) ≥60 ml/minute/1.73 m]. However, in patients with renal impairment (eGFR < 60 ml/minute/1.73 m), hs-cTnI levels were not associated with mortality following cardiac surgery.Elevated hs-cTnI levels following cardiac surgery did not predict short- and long-term mortality in patients with preoperative renal impairment.
No takes yet. Share an insight, caveat, or question.
Nam et al. (2020) conducted a cohort in Cardiac surgery (n=1,909). Elevated postoperative high-sensitivity cardiac troponin I (hs-cTnI) vs. Lower/normal hs-cTnI levels was evaluated on 30-day mortality (OR 1.028, 95% CI 1.013-1.043, p=< .001). Elevated postoperative hs-cTnI was associated with 30-day mortality in patients with normal renal function (OR 1.028; 95% CI 1.013-1.043; P<.001), but not in those with renal impairment.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: