The pathophysiology of ST-elevated myocardial infarction (STEMI) extends beyond coronary artery occlusion to include microvascular and endothelial dysfunction, both of which critically influence outcomes. Endocan, a soluble dermatan sulfate proteoglycan secreted by endothelial cells, has emerged as a novel biomarker of endothelial activation and dysfunction. Recent studies suggest that elevated endocan levels may carry prognostic significance in patients with STEMI, particularly those undergoing percutaneous coronary intervention (PCI). A comprehensive search of PubMed, Cochrane Library, and Google Scholar was conducted to identify studies evaluating endocan as a prognostic biomarker in STEMI. Review articles, case reports, case series, and experimental studies were excluded. Seven clinical studies, comprising sample sizes ranging from 80 to 320 patients, met the inclusion criteria. Across these studies, endocan levels were analyzed in relation to established prognostic markers and clinical outcomes. Key findings demonstrated that higher endocan levels correlated with stress hyperglycemia (r = 0.21, p < 0.05), higher SYNTAX scores, and worse in-hospital outcomes. A cutoff value of 1.7 ng/mL predicted STEMI with 76.1% sensitivity and 73.6% specificity. Elevated endocan levels also showed positive correlations with the TIMI risk score, major adverse cardiovascular events (MACE), and were identified as independent predictors of incomplete ST-segment resolution (STR) (p = 0.044) and no-reflow phenomenon (NRP) (p < 0.001, OR = 2.39, 95% CI = 1.37–4.15). Collectively, the evidence indicates that endocan is strongly associated with endothelial dysfunction, MACE, NRP post-PCI, and impaired reperfusion. Moreover, traditional prognostic indices such as TIMI and SYNTAX scores appear to correlate with circulating endocan levels. However, variability in reported cutoff values across studies highlights the need for larger, multicenter trials with standardized endpoints to establish endocan’s diagnostic and prognostic utility in STEMI.

Introduction/Objective: The Gut Microbiome (GM) plays a critical role in cholesterol metabolism through the production of metabolites such as trimethylamine N-oxide and shortchain fatty acids, contributing to inflammation, endothelial dysfunction, and host gene regulation. This study aims to taxonomically characterize gut microbial profiles, evaluate their association with coronary artery disease, and explore the potential therapeutic implications of microbiome- mediated cardiometabolic pathways. Methods: We pooled data from six Mendelian Randomization studies that utilized the MiBio- Gen consortium and CAD, and cardiovascular risk GWAS data from CARDIoGRAMplusC4D, FinnGen, and UK Biobank databases. Within the phylum Firmicutes, inverse variance weighted analysis was used to estimate the association between: (1) protective effects of Clostridiales vadinBB60 group, Genus Butyricicoccus, Genus Ruminococcus UCG010, Coprococcus 1, Intestinibacter, Ruminiclostridium 6, Anaerotruncus, and Family Acidaminococcaceae; and (2) causative effects of Clostridium innocuum group, Genus Turicibacter, Eisenbergiella, Holdemanella, Eubacterium, Coprostanoligenes group, Ruminococcaceae UCG005, and Genus Catenibacterium on CAD. Results: Higher levels of phylum Firmicutes exhibit a statistically significant protective effect on CAD (OR: 0.880, 95% CI: 0.853–0.907), with low heterogeneity (I² = 20%, P = 0.857). Conversely, an increased abundance of Firmicutes also correlates with a higher risk of CAD (OR: 1.10, 95% CI: 1.06–1.14), showing low heterogeneity (I² = 20%, P = 0.90). Leave-one-out sensitivity analyses confirmed the robustness of these results. Discussion: The findings highlight a significant relationship between gut microbiome dysbiosis and adverse cardiometabolic outcomes, potentially mediated through inflammatory pathways, metabolic signaling, and microbial metabolite production. These results support the growing role of microbiome-targeted interventions as emerging strategies for cardiometabolic risk modification. Conclusion: Firmicutes exhibit both protective and causative effects on CAD. These findings highlight the complexity of the gut microbiome’s role in cardiovascular diseases. Further detailed research on the mechanisms by which specific bacteria at the lower taxonomic levels exert this effect is imperative to understand this complex relationship and its clinical implications.

Inflammation and malnutrition are important contributors to adverse outcomes in heart failure (HF). The neutrophil percentage-to-albumin ratio (NPAR), derived from routinely available laboratory parameters, integrates inflammatory burden and nutritional status and may provide prognostic value. We conducted a systematic review in accordance with the PRISMA 2020 guidelines to evaluate the association between baseline or admission NPAR and all-cause mortality in adults with HF. Two independent reviewers performed study selection and data extraction, and methodological quality was assessed using the Newcastle–Ottawa Scale. Because of heterogeneity in study populations, NPAR cutoff values, and outcome definitions, meta-analysis was not performed and findings were synthesized narratively. Five observational cohort studies comprising more than 4900 patients were included. Across all studies, elevated NPAR was consistently associated with increased short-term (30–90 days) and long-term (1–5 years) all-cause mortality in diverse HF populations, with reported hazard ratios ranging from 1.52 to 2.18. Several studies also demonstrated superior prognostic performance of NPAR compared with neutrophil percentage or serum albumin alone. However, reported NPAR cutoff values varied and remain unstandardized. Elevated NPAR is consistently associated with increased all-cause mortality in patients with HF and may serve as a simple, cost-effective tool for clinical risk stratification. Prospective studies are needed to establish standardized thresholds and validate its prognostic utility across HF phenotypes and clinical settings.

Cannabis use and low socioeconomic status are recognized as distinct risk factors for cardiovascular pathologies. This retrospective cross-sectional study aims to investigate the association between income status and cardiovascular disease risk among young hospitalized adults with recreational cannabis use or cannabis use disorder (CUD). We analyzed young adult hospitalizations (18-44 years) with known CUD from the 2020 National Inpatient Sample. Propensity score-matched analysis (1:1) was used to compare comorbidities and major adverse cardiac and cerebrovascular events (MACCE) between the high-income quartile (HIQ) and low-income quartile (LIQ) within the CUD cohort. Out of the young adult admissions, a total of 286,855 individuals were identified as recreational cannabis users. After propensity matching, we divided the CUD cohort into 63,355 patients with HIQ (41.1% female) and LIQ (41.4% female). While both cohorts exhibited comparable ages and racial distribution (> 65% white), the individuals from the LIQ cohort were predominantly from the South (45.7% vs. 27.9%), visiting rural hospitals (13.9% vs. 1.3%), with Medicaid (56.3% vs. 41.1%) as the predominant payer. Additionally, the LIQ cohort had a higher prevalence of drug abuse (65.5% vs. 58.4%), tobacco use (24.9% vs. 22.6%), HTN (17% vs. 14.7%), chronic pulmonary disease (13.2% vs. 12.7%), DM (8% vs. 6.6%), and obesity (10.9% vs. 10.0%). Additionally, in-hospital outcomes like MACCE (2% vs. 0.8%) and acute ischemic stroke (AIS) (0.5% vs. 0.3%) were higher in the LIQ cohort (Graphical Abstract). After adjusting for confounding factors, the risk of AIS in the HIQ cohort was 37% lower than in the LIQ cohort (OR: 0.63 [95% CI: 0.42-0.96]). All p values < 0.05. Higher prevalence of CVD risk factors in the LIQ-CUD group and lower odds of AIS-related admissions in the HIQ-CUD group warrant targeted interventions and policy measures to understand and address the behavioral risk of cannabis use by economic status and disparities in MACCE.