The gut microbiome is known to modulate metabolic health, yet its role in coronary heart disease (CHD) and heart failure with preserved ejection fraction (HFpEF) remains unclear. In the present study, we profiled the gut microbiome of 234 participants using shotgun metagenomic sequencing across controls (n = 43), individuals with low-risk atherosclerosis (LRAS, n = 23), and patients with CHD + HFpEF (n = 168). Species richness was significantly increased in CHD + HFpEF, with no disruption in taxonomic evenness. LRAS did not diverge significantly in alpha metrics. In contrast, beta diversity analysis demonstrated significant divergence of both LRAS and CHD + HFpEF taxonomic structure from controls, with the greatest divergence in CHD + HFpEF, particularly in older patients. Notably, all differences were attenuated when comparing obese controls and disease groups. However, significant heterogeneity in multivariate dispersion was observed, and a contribution of differences in variation cannot be excluded. Further differential analysis, adjusting for age, BMI, sex, and glucose and lipid profiles, revealed significant associations between specific taxa and CHD + HFpEF, including depletion of the saccharolytic fermenter Bifidobacterium and enrichment of taxa linked to proteolytic or inflammatory metabolism (notably Prevotella and Bilophila), regardless of age and BMI. Subsequent analysis of inferred functional features indicated increased potential for L-citrulline, L-glutamate, L-lysine, and pyrimidine metabolism in CHD + HFpEF. Collectively, the present analysis suggests that CHD + HFpEF is associated with distinct compositional and functional shifts in the gut microbiome. Further longitudinal and interventional research is required to determine which of these microbial features contribute to disease progression and to better characterize underlying mechanisms.

Cardiovascular disease (CVD) is the primary cause of morbidity and mortality in individuals with rheumatoid arthritis (RA) and other rheumatic diseases (RDs), contributing to an approximate 50% increased cardiovascular risk relative to the general population. In addition to conventional cardiovascular risk factors, disease-specific processes such as chronic inflammation, endothelial dysfunction, and immunological dysregulation substantially accelerate atherosclerosis. This thorough analysis brings together the most recent information on how to measure cardiovascular risk, how to understand the underlying causes of RA and other rheumatic diseases, and how to treat them all together. In RA, long-term inflammation throughout the body causes atherosclerosis through several different mechanisms that are not related to common risk factors. To lower the risk of heart disease, rheumatologists, cardiologists, dietitians, physiotherapists, and immunologists must all work together. Evidence supports the targeting of disease activity, the management of conventional cardiovascular risk factors such as hypertension, dyslipidemia, diabetes, and the use of non-pharmacological therapies.

Atherosclerosis, a condition causing the narrowing of the arteries, is a major contributor to the development of cardiovascular diseases. This emphasizes the importance of examining the rheological behavior of blood flow through such arteries. The mathematical model serves as a framework to gain an understanding of the flow and thermal properties of blood. Thus, we employed a non-Newtonian Bingham-Papanastasiou model to explore the hemodynamics of blood through a catheterized stenotic artery, which is inclined with a progressively irregular stenosis geometry, incorporating the integrated influence of electroosmosis, thermal radiation, a magnetic field, and Joule heating, providing new insights into blood flow dynamics. The equations are solved numerically using an explicit finite difference method and visualized using MATLAB software by plotting velocity, wall shear stress, flow rate, resistance to flow, and temperature profiles. Results show that the axial velocity decreases by 36.66% with increasing catheter radius from 0.1 to 0.3, which can lead to insufficient blood supply. The axial velocity is seen to increase by 42.41% on increasing the electroosmotic parameter from 2 to 3.5, while the reduction in resistance reaches 30.85%. The streamline analysis reveals that increasing the Helmholtz-Smoluchowski velocity stabilizes the flow, while higher stenosis depth enhances the flow disturbance. The temperature is also seen to increase by 34.01% when Joule heating increases from 0 to 4. Thus, our study examines the blood flow behavior and its thermal properties providing useful insight into various medical applications.

Chest radiotherapy has improved cancer survival in various thoracic malignancies, including breast cancer, Hodgkin lymphoma, and lung cancer. However, inadvertent radiation exposure to the heart is associated with a broad spectrum of cardiovascular toxicities, collectively termed radiation-induced heart disease (RIHD). We aim to review the pathophysiology of RIHD and the current evidence for their incidence, risk factors, clinical management, and prevention strategies.

Atherosclerosis remains a major cause of cardiovascular morbidity and mortality. Growing evidence suggests that microbiota-host interactions contribute to atherosclerosis through systemic and local mechanisms. This review summarizes current evidence on gut microbiota, microbial metabolites, and plaque-associated microbial signals, and discusses their potential therapeutic implications. Gut dysbiosis may contribute to atherosclerosis through multiple metabolite-dependent, immune, vascular, and metabolic pathways. Recent multi-omics and experimental studies further indicate that microbiota influence vascular biology beyond compositional changes alone. In parallel, plaque-associated microbial signals, potentially originating from the oral cavity or gut, may contribute to local inflammation, oxidative stress, necrotic core expansion, and plaque vulnerability. We further discuss a putative gut-oral-intraplaque axis, a potential local microbial metabolite microenvironment within plaques, and possible cross-kingdom interactions between gut fungi and bacteria. Together, these findings support an integrated framework in which microbiota may shape atherosclerosis through interconnected systemic and local pathways, with potential implications for biomarker development and microbiota-targeted therapies.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD), the hepatic manifestation of cardiometabolic dysfunction, is closely linked to atherosclerosis, heart failure, and adverse cardiovascular outcomes. This review summarizes current evidence on the biological basis of the MASLD-heart axis, with particular emphasis on vascular injury and adverse cardiac remodeling. Methods: A narrative review of contemporary literature was conducted, including experimental studies, observational cohorts, meta-analyses, randomized clinical trials, and current guideline recommendations addressing the cardiohepatic axis. Results: The interaction between the liver and the heart involves interconnected mechanisms, including insulin resistance, lipotoxicity, oxidative stress, chronic inflammation, endothelial dysfunction, and neurohormonal activation. Experimental and translational evidence supports biologically plausible links between MASLD-related metabolic and inflammatory pathways and vascular or myocardial injury, while clinical studies consistently associate MASLD with arterial stiffness, microvascular dysfunction, atherosclerotic disease, adverse cardiac remodeling, heart failure, atrial fibrillation, and cardiovascular events. Several of these associations persist after adjustment for conventional cardiometabolic risk factors, although residual confounding and shared risk determinants limit causal inference. Non-invasive tools, including the Fibrosis-4 (FIB-4) score and transient elastography, may help identify patients at higher risk of advanced fibrosis and cardiometabolic complications. Lifestyle interventions remain the cornerstone of management, while glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, and fibroblast growth factor-21 analogs may provide combined hepatic and cardiovascular benefits. Conclusions: The cardiohepatic axis is an important component of cardiometabolic disease, linking hepatic dysfunction with vascular and myocardial injury through shared biological pathways. Incorporating hepatic assessment into cardiovascular risk evaluation may support earlier identification of high-risk patients.