Type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are closely linked chronic disorders and leading causes of morbidity and mortality worldwide. Increasing evidence identifies the gut microbiota (GM), including its microbial genes and metabolites, as potential modifiers of these processes. This narrative review summarizes mechanistic, translational, and clinical evidence linking GM dysbiosis with T2D and atherosclerosis and evaluates microbiota-directed therapeutic strategies. Converging mechanistic, translational, and clinical evidence supports GM dysbiosis as a plausible shared contributor to T2D and atherosclerosis through interconnected pathways involving impaired intestinal barrier integrity and metabolic endotoxemia, TLR4/NF-κB- and inflammasome-mediated inflammation, and microbial metabolites, including short-chain fatty acids (SCFAs), bile acids (BAs), trimethylamine N-oxide (TMAO), phenylacetylglutamine (PAGln), and tryptophan-derived indoles. These pathways can influence glucose and lipid metabolism, insulin signaling, immune activation, endothelial function, and vascular inflammation, providing a biological framework linking dysglycemia with increased cardiovascular risk and supporting the GM as a potential therapeutic target. However, the field remains limited by predominantly observational and confounded human data, incomplete causal evidence, and heterogeneous responses to microbiota-directed interventions. Dietary modification, prebiotics, probiotics, synbiotics, next-generation probiotics and postbiotics, fecal microbiota transplantation, and microbiota-modulating antidiabetic therapies have shown signals of benefit on metabolic or vascular surrogate endpoints, but evidence for durable clinical benefit remains limited and inconsistent across strains, populations, and study designs. Future progress in GM manipulation to improve cardiometabolic outcomes will require function-focused, causally grounded research and adequately powered, outcome-driven clinical trials incorporating GM-guided patient stratification. Until such evidence is available, the GM should be viewed as a biologically compelling and promising, but not yet clinically actionable, link between metabolic and atherosclerotic disease.
Physical performance and frailty have emerged as potential markers of physiological reserve and cardiovascular vulnerability after acute myocardial infarction (AMI). This review examines the prognostic significance of gait speed, lower-extremity physical performance, frailty, and sarcopenia after AMI and acute coronary syndrome (ACS) and discusses their underlying pathophysiological mechanisms and clinical implications. Slow gait speed, impaired Short Physical Performance Battery (SPPB) scores, and frailty are associated with mortality, rehospitalization, heart failure, and adverse cardiovascular events after AMI or ACS. Gait speed and SPPB may provide incremental prognostic information beyond conventional cardiovascular risk assessment and established risk scores. These associations may reflect an interconnected cardiac–vascular–muscle axis involving reduced cardiac reserve, vascular dysfunction, impaired skeletal muscle perfusion, sarcopenia, and physical deconditioning. Importantly, emerging evidence suggests that targeted cardiac rehabilitation may improve gait speed, muscle strength, and overall physical performance in vulnerable patients. Physical performance represents a clinically relevant and potentially modifiable dimension of post-AMI cardiovascular vulnerability. Incorporating gait speed, SPPB, and frailty assessment into conventional risk stratification may improve patient phenotyping and identify individuals requiring more intensive rehabilitation and follow-up. Further prospective studies are needed to standardize assessment strategies and determine whether improving physical performance translates into better cardiovascular outcomes.
Blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C) are leading cardiovascular disease (CVD) risk factors yet remain suboptimally controlled. Digital health technologies may help bridge the gap between guideline recommendations and improved cardiovascular (CV) outcomes. We review digital health interventions for hypertension and dyslipidemia management. Mobile health (mHealth) interventions, including Corrie, LINKED-BP, Hello Heart, and Mass General Brigham platforms, demonstrate meaningful improvements in BP and LDL-C, particularly when paired with clinical support. In contrast, low-intensity text messaging alone produces modest or inconsistent benefits. Electronic Health Record (EHR)-based alerts can support therapy intensification but require thoughtful integration and clinician co-design. Artificial Intelligence (AI) may identify nonadherence and automate prescription refills, although further study is needed. Equitable implementation among high-risk and underserved populations remains essential. Digital health can promote treatment adherence, patient activation, earlier intervention, and access to care, with potential to improve CVD prevention at scale.
This review examines whether worsening air quality, as represented by the Air Quality Index (AQI), and its constituent pollutant exposures, is associated with atherosclerotic cardiovascular disease (ASCVD) risk in South Asia. South Asian populations have a genetic predisposition to cardiovascular disease and several modifiable risk factors; however, research examining the interaction between air quality and these factors remains understudied. Large population-based health studies consistently demonstrate a positive correlation between elevated levels of air pollutants, including PM₂.₅, PM₁₀, NO₂, CO, O₃, and NO, and ASCVD risk. Poor air quality may compound traditional ASCVD risk factors. Policy and pollution-reduction efforts may help, but evidence for South Asia-specific interventions remains limited. This review synthesizes evidence from population studies to establish air quality as a potentially modifiable risk factor for cardiovascular disease and stresses the need for improved surveillance and targeted risk-mitigation strategies to address the ASCVD burden in South Asia.
Statin intolerance remains a significant barrier to achieving lipid goals and reducing atherosclerotic cardiovascular disease (ASCVD) risk. Bempedoic acid (BA), an oral ATP-citrate lyase inhibitor activated predominantly in the liver, offers a non-statin lipid-lowering option with a low propensity for muscle-related adverse effects. This review seeks to discuss BA use in real-world practice. This review summarizes BA pharmacology, cardiovascular outcomes, safety, combination strategies, and real-world implementation in individuals who are either statin intolerant or unwilling to take statins. The CLEAR clinical trial series established BA's lipid-lowering effect and safety profile, culminating in CLEAR Outcomes, which further demonstrated fewer major adverse cardiovascular events among patients with established ASCVD or at high cardiovascular risk. Although these findings are compelling, they are limited to this population, and the impact in low- to borderline-risk populations remains unclear. In practice, clinicians should assess the potential contribution of the nocebo effect, distinguish partial versus complete statin intolerance, preserve any tolerated statin exposure, define the residual lipid-lowering gap, and align treatment intensity with cardiovascular risk and patient preferences. BA may then be considered within a guideline-directed framework that accounts for treatment access, tolerability, and shared decision-making. Combination therapy with BA and ezetimibe represents a practical oral option, whereas PCSK9-targeted therapy may be preferred when the gap to lipid goals is sufficiently large or the patient is at high ASCVD risk. Clinicians should also provide risk-based counseling and monitoring for potential adverse effects, including hyperuricemia, gout, and tendon injury. Overall, BA represents a valuable addition to the lipid-lowering armamentarium.
