Cardiovascular diseases (CVDs) are a leading cause of global morbidity and mortality, significantly driven by chronic inflammation. Interleukin-6 (IL-6) and interleukin-1β (IL-1β) are critical inflammatory cytokines implicated in CVD progression. This systematic review evaluates the roles of IL-6 and IL-1β in CVDs by synthesizing data from relevant studies to understand their impact on cardiovascular outcomes and identify potential therapeutic interventions. A comprehensive literature search was conducted using PubMed and Embase, covering studies from January 2014 to December 2024. Inclusion criteria encompassed studies investigating IL-6 and/or IL-1β in CVDs, including human and relevant animal models, and reporting clinical outcomes, molecular mechanisms, or therapeutic interventions. Data extraction and quality assessment were performed independently by two reviewers. Our review included 12 studies focusing on the roles of IL-6 and IL-1β in various CVDs. Elevated IL-6 levels were significantly associated with peripheral artery disease, myocardial infarction, and heart failure, while IL-1β levels were linked to worse outcomes in coronary artery disease and heart failure. Meta-analyses indicated a significant association between higher IL-6 and IL-1β levels and increased risk of adverse cardiovascular events. These findings suggest that targeting IL-6 and IL-1β could offer promising therapeutic strategies for reducing inflammation and improving cardiovascular outcomes.

Short-chain fatty acids (SCFAs), produced through fermentation of dietary fibers by gut bacteria, play a central role in modulating cardiovascular function and heart failure (HF) development. The progression of HF is influenced by intestinal barrier dysfunction and microbial translocation, where SCFAs serve as key mediators in the gut–heart axis. This review examines the complex metabolic interactions between SCFAs and other gut microbiota metabolites in HF, including their relationships with trimethylamine N-oxide (TMAO), aromatic amino acids (AAAs), B vitamins, and bile acids (BAs). We analyze the associations between SCFA production and clinical parameters of HF, such as left ventricular ejection fraction (LVEF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and glomerular filtration rate (GFR). Gaining insights into metabolic networks offers new potential therapeutic targets and prognostic markers for managing heart failure, although their clinical significance needs further exploration.

Background: Apolipoprotein B (ApoB), a key component of atherogenic lipoproteins, has been increasingly implicated in cardiometabolic disorders beyond dyslipidemia. However, its role in glycemic dysregulation remains unclear. This study aimed to investigate the association between ApoB levels and glycemic parameters, including fasting glucose, insulin resistance, and glycated hemoglobin (HbA1c), in individuals without diagnosed diabetes. Methods: This study was conducted at the National Research Cardiac Surgery Center (Kazakhstan) over the period between 2023 and 2024 as a cross-sectional analysis. Adults aged ≥ 20 years without diagnosed diabetes and with complete data on their ApoB and glycemic markers were included. Associations between ApoB and fasting plasma glucose (FPG), HbA1c, and HOMA-IR were assessed using multivariable linear and logistic regression models adjusted for demographic, lifestyle, and metabolic covariates. Results: Higher ApoB levels were significantly associated with increased fasting glucose (β = 2.07 mg/dL per 1-SD increase in ApoB, p < 0.001), higher HbA1c (β = 0.06%, p < 0.001), and elevated HOMA-IR (β = 0.54, p < 0.001). Participants in the highest ApoB quartile had 53% higher odds of prediabetes (adjusted OR = 1.53; 95% CI: 1.22–1.91; p < 0.001) compared to the lowest quartile. These associations remained significant after adjusting for BMI, lipid levels, and other confounders. Conclusions: Elevated ApoB is independently associated with adverse glycemic profiles in nondiabetic individuals, suggesting its potential role in early glucose metabolism disturbances.

Myocardial injury following polytrauma is a significant yet often underdiagnosed condition that contributes to acute cardiac dysfunction and long-term cardiovascular complications. This review examines the role of systemic inflammation, oxidative stress, neuro-hormonal activation, and immune dysregulation in trauma-induced myocardial damage. Key immunological markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and adhesion molecules (ICAM-1, VCAM-1), are implicated in endothelial dysfunction, myocardial apoptosis, and ventricular remodeling. The interplay between these factors potentially exacerbates cardiac injury, increasing the risk of heart failure. Biomarker-guided approaches for early detection, combined with advanced imaging techniques such as speckle-tracking echocardiography and cardiac MRI, offer promising avenues for risk stratification and targeted interventions. Anti-inflammatory and oxidative stress-modulating therapies may mitigate myocardial damage and improve outcomes. This article highlights the clinical relevance of integrating immunological markers into diagnostic and therapeutic strategies to enhance the management of trauma-related cardiac dysfunction and reduce long-term morbidity.

Post-traumatic cardiac dysfunction is a clinically under-recognized complication of polytrauma, often occurring in the absence of overt structural injury. Traditional diagnostic tools frequently fail to detect early or subclinical myocardial impairment, underscoring the need for more sensitive assessment methods. This review explores the utility of global longitudinal strain (GLS), derived from speckle-tracking echocardiography (STE), as a sensitive biomarker for identifying and managing cardiac dysfunction following traumatic injury. It outlines the complex pathophysiology of trauma-induced myocardial impairment, including mechanical injury, systemic inflammation, oxidative stress, and neuro-hormonal activation. The limitations of conventional diagnostic approaches, such as electrocardiography, left ventricular ejection fraction (LVEF), and cardiac biomarkers, are critically assessed and contrasted with the enhanced diagnostic performance of GLS. GLS has demonstrated superior sensitivity in detecting subclinical myocardial dysfunction even when LVEF remains preserved and is associated with increased risk of long-term cardiovascular complications, including arrhythmias and heart failure. The manuscript highlights the clinical utility of GLS in early diagnosis, risk stratification, treatment monitoring, and long-term follow-up. Integration of GLS with inflammatory and oxidative biomarkers (e.g., IL-6, TNF-α, and MPO) and artificial intelligence-based diagnostic models offers potential for improved precision in trauma cardiology.

Background/Objectives: Cardiovascular diseases remain the leading cause of global mortality, with the gut microbiome emerging as a critical factor. This study aimed to characterize gut microbiome composition and metabolic pathways in individuals with low cardiovascular risk (LCR) compared to healthy controls to reveal insights into early disease shifts. Methods: We performed shotgun metagenomic sequencing on fecal samples from 25 LCR individuals and 25 matched healthy controls. Participants underwent a comprehensive cardiovascular evaluation. Taxonomic classification used MetaPhlAn 4, and functional profiling employed HUMAnN 3. Results: Despite similar alpha diversity, significant differences in bacterial community structure were observed between groups (PERMANOVA, p < 0.05). The LCR group showed enrichment of Faecalibacterium prausnitzii (p = 0.035), negatively correlating with atherogenic markers, including ApoB (r = −0.3, p = 0.025). Conversely, Fusicatenibacter saccharivorans positively correlated with ApoB (r = 0.4, p = 0.006). Metabolic pathway analysis revealed upregulation of nucleotide biosynthesis, glycolysis, and sugar degradation pathways in the LCR group, suggesting altered metabolic activity. Conclusions: We identified distinct gut microbiome signatures in LCR individuals that may represent early alterations associated with cardiovascular disease development. The opposing correlations between F. prausnitzii and F. saccharivorans with lipid parameters highlight their potential roles in cardiometabolic health. These findings suggest gut microbiome signatures may serve as indicators of early metabolic dysregulation preceding clinically significant cardiovascular disease.