This study aimed to assess the time course of circulating neutrophil and lymphocyte counts and their ratio (NLR) in ST-segment elevation myocardial infarction (STEMI) and coronavirus disease (COVID)-19 and explore their associations with clinical events and structural damage. Circulating neutrophil, lymphocyte and NLR were sequentially measured in 659 patients admitted for STEMI and in 103 COVID-19 patients. The dynamics detected in STEMI (within a few hours) were replicated in COVID-19 (within a few days). In both entities patients with events and with severe structural damage displayed higher neutrophil and lower lymphocyte counts. In both scenarios, higher maximum neutrophil and lower minimum lymphocyte counts were associated with more events and more severe organ damage. NLR was higher in STEMI and COVID-19 patients with the worst clinical and structural outcomes. A canonical deregulation of the immune response occurs in STEMI and COVID-19 patients. Boosted circulating innate (neutrophilia) and depressed circulating adaptive immunity (lymphopenia) is associated with more events and severe organ damage. A greater understanding of these critical illnesses is pivotal to explore novel alternative therapies.

Decision-making is challenging in patients with chest pain and normal high-sensitivity cardiac troponin T (hs-cTnT; <99th percentile; <14 ng/L) at hospital arrival. Most of these patients might be discharged early. We investigated clinical data and hs-cTnT concentrations for risk stratification. This is a retrospective study including 4476 consecutive patients presenting to the emergency department with chest pain and first normal hs-cTnT. The primary endpoint was one-year death or acute myocardial infarction, and the secondary endpoint added urgent revascularization. The number of primary and secondary endpoints was 173 (3.9%) and 252 (5.6%). Mean hs-cTnT concentrations were 6.9 ± 2.5 ng/L. Undetectable (<5 ng/L) hs-cTnT (n = 1847, 41%) had optimal negative predictive value (99.1%) but suboptimal sensitivity (90.2%) and discrimination accuracy (AUC = 0.664) for the primary endpoint. Multivariable analysis was used to identify the predictive clinical variables. The clinical model showed good discrimination accuracy (AUC = 0.810). The addition of undetectable hs-cTnT (≥ or <5 ng/L; HR, hazard ratio = 3.80; 95% CI, confidence interval 2.27–6.35; p = 0.00001) outperformed the clinical model alone (AUC = 0.836, p = 0.002 compared to the clinical model). Measurable hs-cTnT concentrations (between detection limit and 99th percentile; per 0.1 ng/L, HR = 1.13; CI 1.06–1.20; p = 0.0001) provided further predictive information (AUC = 0.844; p = 0.05 compared to the clinical plus undetectable hs-cTnT model). The results were reproducible for the secondary endpoint and 30-day events. Clinical assessment, undetectable hs-cTnT and measurable hs-cTnT concentrations must be considered for decision-making after a single negative hs-cTnT result in patients presenting to the emergency department with acute chest pain.

Background: Acute heart failure (AHF) is a complex syndrome associated with high mortality and hospital readmissions, characterized by volume overload and inflammation. Soluble ST2 (sST2) and antigen carbohydrate 125 (CA125) are emerging biomarkers that reflect these processes and may interact to influence long-term outcomes in AHF patients. This study aims to examine the prognostic relationship between sST2 and CA125 in predicting mortality and heart failure (HF)-related hospitalizations in patients with decompensated heart failure. Methods: In a cohort of 635 patients with AHF, we investigated whether the prognostic value of sST2 varies according to CA125 levels (≤35 vs. >35 U/mL). The endpoints were: (a) time to all-cause death, and (b) the combination of time to death or new HF admission. Results: This study of EAHFE registry data shows that the association between sST2 and long-term adverse outcomes (mortality and HF hospitalizations) in patients with AHF was differentially influenced by CA125 concentrations (p-value for interactions = 0.031 and 0.029, respectively). Higher sST2 was associated with the risk of death and the combined risk of death/HF readmission when CA125 was >35 U/mL [HR = 1.02 (CI 95%: 1.01–1.04), p = 0.006 and 1.02 (CI 95%: 1.01–1.03); p = 0.013 per increase in 10 ng/mL, respectively], but not when CA125 was ≤35 U/mL. Conclusions: This study highlights the prognostic interaction between sST2 and CA125 in AHF. Elevated sST2 predicts poor outcomes mainly in patients with high CA125 levels (>35 U/mL), suggesting CA125’s role in modulating inflammatory activity in HF. Further research is needed.

Background: Acute heart failure (AHF) is a complex syndrome associated with high mortality and hospital readmissions, characterized by volume overload and inflammation. Soluble ST2 (sST2) and antigen carbohydrate 125 (CA125) are emerging biomarkers that reflect these processes and may interact to influence long-term outcomes in AHF patients. This study aims to examine the prognostic relationship between sST2 and CA125 in predicting mortality and heart failure (HF)-related hospitalizations in patients with decompensated heart failure. Methods: In a cohort of 635 patients with AHF, we investigated whether the prognostic value of sST2 varies according to CA125 levels (≤35 vs. >35 U/ ml). The endpoints were: a) time to all-cause death, and b) the combined of time to death or new HF-admission. Results: This substudy of the EAHFE registry shows that the association between sST2 and long-term adverse outcomes (mortality and HF-hospitalizations) in patients with AHF was differentially influenced by CA125 concentrations (p-value for interactions= 0.031 and 0.029, respectively). Higher sST2 was associated with the risk of death and the composite of death/HF readmission when CA125 was >35 U/mL [HR=1.02 (CI 95%: 1.01-1.04), p=0.006 and 1.02 (CI 95%: 1.01-1.03), p=0.013 per increase in 10 ng/mL, respectively], but not when CA125 was ≤35 U/mL. Conclusions: This study highlights the prognostic interaction between sST2 and CA125 in AHF. Elevated sST2 predicts poor outcomes mainly in patients with high CA125 levels (>35 U/mL), suggesting CA125's role in modulating inflammatory activity in HF. Further research is needed.