Key result
High circulating sTNFR1 concentrations above the median value significantly increased the risk of major adverse cardiovascular events within 24 months after STEMI (HR 8.8).
Why the study?
Because inflammation following STEMI is both beneficial and deleterious, new biomarkers of STEMI severity are needed to predict clinical outcomes.
Do elevated circulating concentrations of sTNFR1 and sTNFR2 predict adverse clinical events in STEMI patients undergoing percutaneous coronary intervention?
Cohort (n=251)
No
Do elevated circulating concentrations of sTNFR1 and sTNFR2 predict adverse clinical events in STEMI patients undergoing percutaneous coronary intervention?
Hazard Ratio: 8.8 (95% CI 4.2–18.6)
p-value: p=<0.0001
Elevated serum levels of sTNFR1 and sTNFR2 are early independent predictors of morphological injury and adverse clinical outcomes in patients with STEMI.
sTNFR1/2 levels may mark post-STEMI injury severity; leaves open their value as prognostic biomarkers pending prospective validation.
Background: As inflammation following ST-segment elevation myocardial infarction (STEMI) is both beneficial and deleterious, there is a need to find new biomarkers of STEMI severity. Objective: We hypothesized that the circulating concentration of the soluble tumor necrosis factor α receptors 1 and 2 (sTNFR1 and sTNFR2) might predict clinical outcomes in STEMI patients. Methods: We enrolled into a prospective cohort 251 consecutive STEMI patients referred to our hospital for percutaneous coronary intervention revascularization. Blood samples were collected at five time points: admission and 4, 24, 48 h, and 1 month after admission to assess sTNFR1 and sTNFR2 serum concentrations. Patients underwent cardiac magnetic resonance imaging at 1 month. Results: sTNFR1 concentration increased at 24 h with a median of 580.5 pg/ml [95% confidence interval (CI): 534.4–645.6]. sTNFR2 increased at 48 h with a median of 2,244.0 pg/ml [95% CI: 2090.0–2,399.0]. Both sTNFR1 and sTNFR2 peak levels were correlated with infarct size and left ventricular end-diastolic volume and inversely correlated with left ventricular ejection fraction. Patients with sTNFR1 or sTNFR2 concentration above the median value were more likely to experience an adverse clinical event within 24 months after STEMI [hazards ratio (HR): 8.8, 95% CI: 4.2–18.6, p < 0.0001 for sTNFR1; HR: 6.1, 95% CI: 2.5 –10.5, p = 0.0003 for sTNFR2]. Soluble TNFR1 was an independent predictor of major adverse cardiovascular events and was more powerful than troponin I ( p = 0.04 as compared to the troponin AUC). Conclusion: The circulating sTNFR1 and sTNFR2 are inflammatory markers of morphological and functional injury after STEMI. sTNFR1 appears as an early independent predictor of clinical outcomes in STEMI patients.
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Paccalet et al. (2021) conducted a cohort in ST-Segment Elevation Myocardial Infarction (STEMI) (n=251). High circulating sTNFR1 concentration (above median) vs. Low circulating sTNFR1 concentration (below median) was evaluated on Composite of all-cause death, rehospitalization for heart failure, recurrent infarction, and stroke within 24 months (HR 8.8, 95% CI 4.2-18.6, p=<0.0001). High circulating sTNFR1 concentrations above the median value significantly increased the risk of major adverse cardiovascular events within 24 months after STEMI (HR 8.8).