Serum Soluble Tumor Necrosis Factor Receptors 1 and 2 Are Early Prognosis Markers After ST-Segment Elevation Myocardial Infarction

Abstract

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.

Levels of soluble tumor necrosis factor receptor 1 and 2 are associated with survival after ST segment elevation myocardial infarction

“…When comparing our data to theirs, our control group was younger and with more female donors, and we observed lower levels of sTNFR1 but higher levels of sTNFR2, but in both studies, the sTNFR levels in the patients were significantly higher than in the control group. However, it has to be noted that the levels of sTNFR1 reported by us and others 16 – 18 in STEMI patients are relatively similar to the ones reported in prospective studies in patients with stable CAD 7 , 8 , 20 , and also to levels reported in population-based studies in older adults 9 , 11 – 13 . Thus, the level of sTNFR1 may not be of diagnostic interest on the population level in this age group.…”

“…Thus, the level of sTNFR1 may not be of diagnostic interest on the population level in this age group. On the other hand, similar to us, both Vaglimigli et al 17 and Paccalet et al 16 report an increased risk of adverse events in STEMI patients with higher sTNFR1 levels, and Nilsson et al 18 shows associations between levels of sTNFR1 and the final infarct size. Also, the two studies with measurements at different time points 16 , 18 show the same trend as us with increasing levels of sTNFR1 between admission and 24 h, which might indicate a rapid response to the acute event and following intervention which is mirrored in the levels of sTNFR1 released.…”

“…On the other hand, similar to us, both Vaglimigli et al 17 and Paccalet et al 16 report an increased risk of adverse events in STEMI patients with higher sTNFR1 levels, and Nilsson et al 18 shows associations between levels of sTNFR1 and the final infarct size. Also, the two studies with measurements at different time points 16 , 18 show the same trend as us with increasing levels of sTNFR1 between admission and 24 h, which might indicate a rapid response to the acute event and following intervention which is mirrored in the levels of sTNFR1 released. Interestingly, the only time point where the levels of sTNFR1 showed prognostic value in our data was in the sample collected 1–3 days after PCI, if this indicates that the immediate response after the PCI procedure is the most prognostic may be an area for future studies.…”

“…Increased levels have also been found in patients with recurrent ventricular arrhythmia 14 or recurrent myocardial infarction 15 after coronary stenting. However, only a few studies so far have measured sTNFRs in patients with acute ST-segment elevation myocardial infarction (STEMI) 16 – 18 . In this study, we aimed to investigate the dynamic changes in sTNFR1 and sTNFR2 in STEMI patients at different time points, before, 1–3 days after and 3 months after a percutaneous coronary intervention (PCI) and to study whether this had any correlation to the long-term mortality of the patients.…”

The Effect of TNF-α on CHD and the Relationship between TNF-α Antagonist and CHD in Rheumatoid Arthritis: A Systematic Review

“…STEMI patients with significantly elevated levels of TNF- α are more likely to have subsequent ischemic events, HF, and all cardiovascular events [ 7 ]. Since TNF- α induces the release of soluble TNF- α receptors 1 and 2 (sTNFR1 and sTNFR2) into the circulation in STEMI patients, these patients with high circulating sTNFR1 or sTNFR2 are at high risk of adverse clinical events [ 83 ]. Furthermore, TNF- α is also involved in adverse remodeling after myocardial infarction [ 84 ].…”