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

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.

Kinetics and prognostic value of soluble VCAM-1 in ST-segment elevation myocardial infarction patients.

BACKGROUND: Soluble vascular cell adhesion molecule-1 (sVCAM-1) is a biomarker of endothelial activation and inflammation. There is still controversy as to whether it can predict clinical outcome after ST-elevation myocardial infarction (STEMI). Our aim was to assess the sVCAM-1 kinetics and to evaluate its prognostic predictive value. METHOD: We prospectively enrolled 251 consecutive STEMI patients who underwent coronary revascularization in our university hospital. Blood samples were collected at admission, 4, 24, 48 h and 1 month after admission. sVCAM-1 serum level was assessed using ELISA assay. All patients had cardiac magnetic resonance imaging at 1-month for infarct size (IS) and left ventricular ejection fraction (LVEF) assessment. Clinical outcomes were recorded over 12 months after STEMI. RESULTS: sVCAM-1 levels significantly increased from admission up to 1 month and were significantly correlated with IS, LVEF, and LV end-systolic and diastolic volume. (H48 area under curve (AUC) ≥ H48 median) were associated with an increased risk of adverse clinical events during the 12-month follow-up period with a hazard ratio (HR) = 2.6 (95% confidence interval [CI] of ratio = 1.2-5.6, p = .02). The ability of H48 AUC for sVCAM-1 to discriminate between patients with or without the composite endpoint was evaluated using receiver operating characteristics with an AUC at 0.67 (0.57-0.78, p = .004). This ability was significantly superior to H48 AUC creatine kinase (p = .03). CONCLUSIONS: In STEMI patients, high sVCAM-1 levels are associated with a poor clinical outcome. sVCAM-1 is an early postmyocardial infarction biomarker and might be an interesting target for the development of future therapeutic strategies.

Bioelectrical impedance analysis for heart failure diagnosis in the ED.

INTRODUCTION: The aim of this study was to evaluate bioimpedance vector analysis (BIVA) for the diagnosis of acute heart failure (AHF) in patients presenting with acute dyspnea to the emergency department (ED). METHODS: Patients with acute dyspnea presenting to the ED were prospectively enrolled. Four parameters were assessed: resistance (R), reactance (Ra), total body water (TBW), and extracellular body water (EBW). Brain natriuretic peptide (BNP) measures and cardiac ultrasound studies were performed in all patients at admission. Patients were classified into AHF and non-AHF groups retrospectively by expert cardiologists. RESULTS: Seventy-seven patients (39 men; age, 68±14years; weight, 79.8±20.6 kg) were included. Of the 4 BIVA parameters, Ra was significantly lower in the AHF compared to non-AHF group (32.7±14.3 vs 45.4±19.7; P<.001). Brain natriuretic peptide levels were significantly higher in the AHF group (1050.3±989 vs 148.7±181.1ng/L; P<.001). Reactance levels were significantly correlated to BNP levels (r=-0.5; P<.001). Patients with different mitral valve Doppler profiles (E/e'≤8, E/e' ≥9 and <15, and E/e'≥15) had significant differences in Ra values (47.9±19.9, 34.7±19.4, and 31.2±11.7, respectively; P=.003). Overall, the sensitivity of BIVA for AHF diagnosis with a Ra cutoff at 39Ω was 67% with a specificity of 76% and an area under the curve at 0.76. However, Ra did not significantly improve the area under the curve of BNP for the diagnosis of AHF (P=not significant). CONCLUSION: In a population of patients presenting to the ED with dyspnea, BIVA was significantly related to the AHF status but did not improve the diagnostic performance for AHF in addition to BNP alone.