Soluble (s)ST2 has been proposed as a useful biomarker for heart failure (HF) patient management. Myocardial damage or mechanical stress stimulate sST2 release. ST2 competes with a membrane bound receptor (ST2 ligand, or ST2L) for interleukin-33 (IL-33) binding, inhibiting the effects induced by the ST2L/IL-33 interaction so that excessive sST2 may contribute to myocardial fibrosis and ventricular remodeling. Compared to natriuretic peptides (NPs), sST2 concentration is not substantially affected by age, sex, body mass index, kidney function, atrial fibrillation, anemia, or HF etiology, and has low intra-individual variation. Its prognostic role as an independent marker is well reported in the literature. However, there is a gap on its use in combination with NPs, currently the only biomarkers recommended by European and American guidelines for HF management. Reflecting the activation of two distinct biological systems, a benefit from the use of sST2 and NP in combination is advocated. The aim of this review is to report the current scientific knowledge on sST2 in the acute and chronic HF settings with a particular attention to its additive role to natriuretic peptides (NPs).

Background: Plasma omega‐3 polyunsaturated fatty acids (ω3‐PUFAs) have been shown to be inversely correlated with the risk of cardiovascular death in primary prevention. The risk relationship in the setting of an acute coronary syndrome is less well established. Methods and Results: Baseline plasma ω3‐PUFA composition (α‐linolenic acid, eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid) was assessed through gas chromatography with flame ionization detection in a case‐cohort study involving 203 patients with cardiovascular death, 325 with myocardial infarction, 271 with ventricular tachycardia, and 161 with atrial fibrillation, and a random sample of 1612 event‐free subjects as controls from MERLIN‐TIMI 36 (Metabolic Efficiency With Ranolazine for Less Ischemia in Non–ST‐Elevation‐Acute Coronary Syndrome–Thrombolysis in Myocardial Infarction 36), a trial of patients hospitalized with non–ST‐segment–elevation ‐acute coronary syndrome. After inverse‐probability‐weighted multivariable adjustment including all traditional risk factors, a higher relative proportion of long‐chain ω3‐PUFAs (eicosapentaenoic acid, docosapentaenoic acid, docosahexaenoic acid) were associated with 18% lower odds of cardiovascular death (adjusted [adj] odds ratio [OR] per 1 SD, 0.82; 95% CI, 0.68–0.98) that was primarily driven by 27% lower odds of sudden cardiac death (adj OR per 1 SD, 0.73; 95% CI, 0.55–0.97). Long‐chain ω3‐PUFA levels in the top quartile were associated with 51% lower odds of cardiovascular death (adj OR 0.49; 95% CI, 0.27–0.86) and 63% lower odds of sudden cardiac death (adj OR, 0.37; 95% CI, 0.16–0.56). An attenuated relationship was seen for α‐linolenic acid and subsequent odds of cardiovascular (adj OR, 0.92; 95% CI, 0.74–1.14) and sudden cardiac death (adj OR, 0.91; 95% CI, 0.67–1.25). No significant relationship was observed between any ω3‐PUFAs and the odds of cardiovascular death unrelated to sudden cardiac death, myocardial infarction, atrial fibrillation, or early post‐acute coronary syndrome ventricular tachycardia. Conclusions: In patients after non–ST‐segment–elevation‐acute coronary syndrome, plasma long‐chain ω3‐PUFAs are inversely associated with lower odds of sudden cardiac death, independent of traditional risk factors and lipids. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00099788.

Diabetic cardiomyopathy is a complex condition characterized by structural and functional changes in the heart, which are not explained by other known cardiovascular risk factors in patients with diabetes. Since Rubler first described this condition in 1972, there has been significant progress in understanding the multifactorial mechanisms that contribute to the development and progression of heart failure in diabetic patients. In this review, we provide a comprehensive discussion of the key mechanisms that underlie the development of diabetic cardiomyopathy, including chronic hyperglycemia, autonomic neuropathy, altered substrate utilization, and dysregulated insulin pathways. We also compare the distinct characteristics of heart failure in type 1 and type 2 diabetes and review the effects of antidiabetic medications on heart failure in diabetic patients with a particular emphasis on ongoing clinical trials.

Background: Recent randomized controlled trials did not show benefit of early/immediate coronary angiography (CAG) over a delayed/selective strategy in patients with out-of-hospital cardiac arrest (OHCA) and no ST-segment elevation. However, whether selected subgroups, specifically those with a high pretest probability of coronary artery disease may benefit from early CAG remains unclear. Methods: We included all randomized controlled trials that compared a strategy of early/immediate versus delayed/selective CAG in OHCA patients and no ST elevation and had a follow-up of at least 30 days. The primary outcome of interest was all-cause death. Odds ratios (OR) were calculated and pooled across trials. Interaction testing was used to assess for heterogeneity of treatment effects. Results: In total, 1512 patients (67 years, 26% female, 23% prior myocardial infarction) were included from 5 randomized controlled trials. Early/immediate versus delayed/selective CAG was not associated with a statistically significant difference in odds of death (OR 1.12, 95%-CI 0.91–1.38), with similar findings for the composite outcome of all-cause death or neurological deficit (OR 1.10, 95%-CI 0.89–1.36). There was no effect modification for death by age, presence of a shockable initial cardiac rhythm, history of coronary artery disease, presence of an ischemic event as the presumed cause of arrest, or time to return of spontaneous circulation (all P-interaction > 0.10). However, early/immediate CAG tended to be associated with higher odds of death in women (OR 1.52, 95%-CI 1.00–2.31, P = 0.050) than in men (OR 1.04, 95%-CI 0.82–1.33, P = 0.74; P-interaction 0.097). Conclusion: In OHCA patients without ST-segment elevation, a strategy of early/immediate versus delayed/selective CAG did not reduce all-cause mortality across major subgroups. However, women tended to have higher odds of death with early CAG. Graphical

Epstein–Barr virus (EBV) reactivation may be involved in long-COVID symptoms, but reactivation of other viruses as a factor has received less attention. Here we evaluated the reactivation of parvovirus-B19 and several members of the Herpesviridae family (DNA viruses) in patients with long-COVID syndrome. We hypothesized that monovalent COVID-19 vaccines inhibit viral interference between SARS-CoV-2 and several DNA viruses in patients with long-COVID syndrome, thereby reducing clinical symptoms. Clinical and laboratory data for 252 consecutive patients with PCR-verified past SARS-CoV-2 infection and long-COVID syndrome (155 vaccinated and 97 non-vaccinated) were recorded during April 2021–May 2022 (median 243 days post-COVID-19 infection). DNA virus–related IgG and IgM titers were compared between vaccinated and non-vaccinated long-COVID patients and with age- and sex-matched non-infected, unvaccinated (pan-negative for spike-antibody) controls. Vaccination with monovalent COVID-19 vaccines was associated with significantly less frequent fatigue and multiorgan symptoms (p < 0.001), significantly less cumulative DNA virus–related IgM positivity, significantly lower levels of plasma IgG subfractions 2 and 4, and significantly lower quantitative cytomegalovirus IgG and IgM and EBV IgM titers. These results indicate that anti-SARS-CoV-2 vaccination may interrupt viral cross-talk in patients with long-COVID syndrome (ClinicalTrials.gov Identifier: NCT05398952).