Reviews in cardiovascular medicine最新文献

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), originally developed for glycemic control in type 2 diabetes, have emerged as transformative agents with broad therapeutic applications across multiple organ systems. This review explores the expanding role of GLP-1 RAs in managing cardiometabolic diseases, including obesity, heart failure (particularly with preserved ejection fraction), chronic kidney disease (CKD), and metabolic dysfunction-associated steatotic liver disease (MASLD). Robust clinical trial data support the efficacy of GLP-1 RAs in promoting weight loss, improving cardiovascular outcomes, and preserving renal function, with additional trials underway to further strengthen and expand the evidence base. Despite the growing utility of GLP-1 RAs, challenges related to cost, access, adherence, and implementation persist, particularly for indications beyond diabetes. However, innovations such as oral formulations and combination therapies may help improve accessibility and sustained use. As clinical guidelines evolve, targeted integration of GLP-1 RAs into care models may transform the prevention and treatment landscape for complex, chronic diseases.

Background: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have been shown to reduce major adverse cardiovascular events (MACEs) in patients with type 2 diabetes mellitus (T2DM) and high cardiovascular risk. However, the efficacy of GLP-1 RAs on the outcomes of MACEs across different racial and sex groups among patients with and without T2DM remains underexplored. Thus, this study aimed to evaluate the association between GLP-1 RAs and MACEs in patients with and without T2DM based on race and sex.

Methods: We conducted a systematic literature search on the PubMed and Scopus databases, as well as ClinicalTrials.gov, for relevant randomized controlled trials (RCTs) from inception to July 5, 2025. Trials were eligible for inclusion if the included adults (≥18 years) had been randomized to a GLP-1 RA versus placebo group, and MACEs were reported as an outcome. Trials combining GLP-1 RAs with other investigational glucose-lowering agents were excluded. Risk ratios (RRs) and 95% confidence intervals (CIs) were pooled using a random-effect model, and a p-value of <0.05 was considered statistically significant.

Results: Nine RCTs involving 81,266 patients were included in the analysis. The mean age of patients was 65 years. Compared with the placebo, GLP-1 RAs significantly reduced the risk of MACEs in males (RR, 0.82; 95% CI: 0.77-0.86; p < 0.001) and females (RR, 0.81; 95% CI: 0.75-0.88; p < 0.001). Meanwhile, across racial groups, GLP-1 RAs significantly reduced the risk of MACEs in Caucasian patients (RR, 0.87; 95% CI: 0.79-0.96; p < 0.001) compared with placebo. However, no significant difference was observed for the risk of MACEs in Black patients (RR, 1.05; 95% CI: 0.72-1.53; p = 0.80) when comparing GLP-1 RAs with placebo.

Conclusion: This meta-analysis demonstrates that GLP-1 RAs significantly reduce the risk of MACEs in both males and females, as well as across various racial groups in patients with or without T2DM. However, the lack of significant benefit in Black patients suggests potential racial disparities in the enrollment and efficacy of GLP-1 RAs for cardiovascular outcomes.

Atherosclerosis, a lipid-driven chronic inflammatory disease, is the primary pathological basis of cardiovascular diseases, characterized by endothelial injury, lipid deposition, immune cell infiltration, and chronic inflammation. The NOD-like Receptor Pyrin Domain-Containing 3 (NLRP3) inflammasome has emerged as a crucial mediator of inflammation in atherosclerosis, with caspase recruitment domain family member 8 (CARD8) acting as a key regulatory component. Indeed, CARD8, a member of the caspase recruitment domain family, regulates immune responses by modulating inflammasome activity, particularly NLRP3. Recent studies suggest that CARD8 influences various aspects of atherosclerotic development, including lipid accumulation, oxidative stress, vascular inflammation, smooth muscle cell proliferation, and plaque instability. Thus, this review summarizes the latest findings on the role of CARD8 in the pathogenesis of atherosclerosis, with a focus on the regulatory effects of this component on immune cells and inflammatory pathways. We also discuss the potential of targeting CARD8 as a therapeutic strategy for atherosclerosis, exploring the current preclinical and clinical evidence.

Background: Coronary artery calcium (CAC) reflects the overall atherosclerotic burden. The CAC density is inversely associated with plaque vulnerability. Intravascular ultrasound (IVUS)-defined attenuated plaques represent unstable lesions, which are linked to adverse clinical outcomes. Meanwhile, the determination as to whether coronary computed tomography angiography (CCTA)-derived CAC metrics can serve as noninvasive markers of attenuated plaques remains uncertain.

Methods: This retrospective study included coronary artery disease (CAD) patients who underwent both CCTA and IVUS between January 2023 and December 2024 at our medical center. CCTA was used to quantify plaque volume, density, and composition (lipid, fiber, and calcium), while IVUS was employed to characterize the plaques as attenuated and non-attenuated.

Results: Among 94 patients with 150 coronary plaques, calcium volume showed a very strong correlation with total plaque volume (r _s = 0.953, p < 0.0001). Meanwhile, attenuated plaques exhibited significantly lower calcium density (321.00 vs. 499.00 Hounsfield units (HU); p = 0.0004), calcium volume (55.20 vs. 168.10 mm³; p = 0.003), and calcium percentage (33.30% vs. 55.40%; p = 0.015) compared with the non-attenuated plaques. Multivariate logistic regression analysis identified lower CAC density as the only independent predictor of IVUS-confirmed attenuated plaques (odds ratio = 0.994, 95% confidence interval (CI): 0.990-0.997; p = 0.0002). The area under the receiver operating characteristic (AUROC) curve for CAC density in diagnosing attenuated plaques was 0.735 (95% CI: 0.603-0.868; p = 0.0004). At a cutoff of 461.50 HU, the sensitivity and specificity were 81.8% and 66.1%, respectively.

Conclusion: CCTA-derived CAC volume reflects the atherosclerosis (AS) burden, while lower CAC density independently predicts IVUS-confirmed attenuated plaques. A higher CAC density was associated with plaque stability, suggesting that the CCTA-derived CAC density may serve as a noninvasive marker of plaque stability, aiding in the assessment of plaque vulnerability and risk stratification.

Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors, a novel class of oral antihyperglycemic medications prescribed for type 2 diabetes mellitus, play a beneficial role in slowing the progression of heart failure. However, debate persists regarding the potential link of these inhibitors to acute kidney injury (AKI) in specific clinical conditions.

Methods: This study was a retrospective analysis of consecutive patients receiving off-pump coronary artery bypass grafting (OPCABG) at our institution between January 2018 and July 2023. A group of patients who had been administered SGLT2 inhibitors was systematically compared with non-users in a 1:3 ratio using propensity score matching. The principal endpoint was postoperative AKI after OPCABG. In addition, we performed a comprehensive meta-analysis of the associations between SGLT2 inhibitor therapy and AKI risk. The analytical approach combined institutional data with aggregated findings from existing literature.

Results: The analysis encompassed 403 patients who administered SGLT2 inhibitors and 1209 non-users. AKI developed in 54 cases (13.4%) post-OPCABG among individuals who received SGLT2 inhibitors, compared to 373 cases (30.9%) in the control cohort. Statistical analysis demonstrated significantly reduced AKI prevalence in the SGLT2 inhibitor cohort compared to non-users (p < 0.001). The meta-analysis results confirmed a protective association between SGLT2 inhibitor therapy and AKI risk reduction (odds ratio (OR) = 0.525, 95% confidence interval (CI) 0.437-0.631; p < 0.001).

Conclusion: In this study, SGLT2 inhibitor administration was associated with a decreased incidence of postoperative AKI in OPCABG patients.

Clinical trial registration: NCT05888168, https://clinicaltrials.gov/study/NCT05888168?cond=NCT05888168&rank=1.

Background: Metabolic dysfunction significantly influences cardiovascular outcomes following ST-elevation myocardial infarction (STEMI). The triglyceride-glucose (TyG) index and triglyceride-glucose-body mass index (TyG-BMI) serve as surrogate markers of insulin resistance, whereas B-type natriuretic peptide (BNP) levels reflect cardiac dysfunction. However, the combined prognostic value of these biomarkers for predicting major adverse cardiovascular events (MACEs) in patients with STEMI remains underexplored.

Methods: We conducted a retrospective cohort study of 1177 consecutive patients with STEMI who underwent percutaneous coronary intervention between August 2018 and December 2023. Patients were stratified into four groups based on the TyG index (cutoff: 7.2), TyG-BMI (cutoff: 186), and BNP level (cutoff: 300 pg/mL). The primary endpoint was MACEs, defined as a composite of all-cause mortality, nonfatal myocardial infarction, ischemia-driven repeat revascularization, heart failure hospitalization, and cerebrovascular events. Cox proportional hazards models with progressive adjustment were employed to assess independent and combined prognostic significance.

Results: A total of 483 patients (41.0%) experienced MACEs during a median follow-up of 461 days (interquartile range (IQR): 79-672). Patients with both an elevated TyG index (≥7.2) and a high BNP concentration (≥300 pg/mL) demonstrated the highest cardiovascular risk profile and a more than twofold increased MACE risk (hazard ratio (HR) 2.18, 95% confidence interval (CI): 1.57-3.03; p < 0.001) compared with the reference group (those with a low TyG index and low BNP concentration). Similarly, patients with elevated TyG-BMIs (≥186) and BNP levels had an 81% increased risk (HR 1.81, 95% CI: 1.30-2.51; p < 0.001). Meanwhile, the combined TyG index + BNP model demonstrated superior predictive accuracy (area under the curve (AUC): 0.67) compared with the individual biomarkers and the established Global Registry of Acute Coronary Events (GRACE) score (AUC: 0.58). Subgroup analyses revealed particularly pronounced associations in older patients, females, and those with hypertension.

Conclusions: The combination of the TyG index or TyG-BMI with BNP provides enhanced prognostic stratification for predicting MACEs in STEMI patients, offering superior discriminatory capacity compared with that of individual biomarkers. This integrated approach may facilitate personalized risk assessment and guide therapeutic decision-making in clinical practice.

Transcatheter aortic valve implantation (TAVI) has evolved from an experimental, last-resort procedure in 2002 to a first-line therapy for aortic stenosis; moreover, the 2025 ESC/EACTS (European Society of Cardiology/European Association for Cardiothoracic Surgeons) guidelines marked a paradigm shift beyond traditional risk stratification toward earlier intervention and broader patient selection. Current evidence demonstrates the non-inferiority or superiority of TAVI to surgical aortic valve replacement across all risk categories, with the guidelines now recommending TAVI for patients aged ≥70 years and formally endorsing early intervention in asymptomatic severe stenosis when procedural risk is low. Meanwhile, critical challenges persist despite large-scale systematic reviews demonstrating significant mortality reduction following TAVI, including paravalvular leak rates of 10-25% compared to near-zero rates with surgery, and subclinical leaflet thrombosis affecting up to 30% of patients with unclear optimal management strategies. Moreover, the expansion toward younger populations exposes critical knowledge gaps, including unknown long-term durability beyond 10 years, structural valve degeneration rates of 4.8-13.3% at 5-7 years, and complex reintervention scenarios with reported mortality rates of 17.1% for surgical TAVI explantation. Thus, this review synthesizes contemporary evidence within the framework of the 2025 guidelines while examining unique aspects, including the pathophysiology of subclinical leaflet thrombosis, polymeric heart valve technologies as next-generation solutions, and the critical durability questions that will determine the role of TAVI in younger patients. Next-generation polymeric valves utilizing materials such as polyhedral oligomeric silsesquioxanes-polycarbonate urethane (POSS-PCU), poly(styrene-b-isobutylene-b-styrene) (SIBS), and siloxane polyurethane-urea have shown promising preclinical results in terms of enhanced durability and reduced thrombogenicity, although comprehensive clinical validation remains necessary. As TAVI practice evolves under new guideline recommendations emphasizing early intervention and simplified antithrombotic management, this thorough analysis can provide essential context for understanding both current capabilities and future directions in transcatheter valve therapy.

Background: Recent advancements have introduced novel cardiac myosin inhibitors (CMIs) that have demonstrated significant efficacy in treating hypertrophic cardiomyopathy (HCM). This meta-analysis aimed to clarify the current understanding of the impact of CMIs on echocardiographic cardiac structure and function in patients with HCM.

Methods: A comprehensive search of the PubMed, Cochrane Library, and Embase databases was conducted from inception until September 14, 2025. The studies reporting the impact of CMIs on echocardiographic cardiac structure and function in HCM patients were included.

Results: Ultimately, this meta-analysis included 10 studies: five randomized controlled trials (RCTs), three echocardiographic sub-studies derived from RCTs, and two long-term cohort studies. A total of 938 patients were enrolled in these studies. This meta-analysis revealed that CMIs significantly reduce interventricular septum thickness (mean difference (MD): -1.77, 95% confidence interval (CI): -3.30 to -0.23; p = 0.0240). CMIs were also shown to significantly reduce left ventricular mass index (MD: -18.15, 95% CI: -32.65 to -3.65; p = 0.0141). Moreover, the pooled results demonstrated that administering CMIs can significantly reduce left ventricular ejection fraction (MD: -3.22, 95% CI: -5.60 to -0.85; p = 0.0078). CMIs also significantly improved echocardiographic parameters of left ventricular diastolic function, such as the left atrial volume index (MD: -5.75, 95% CI: -7.87 to -3.64; p < 0.0001) and septal E/e' ratio (MD: -3.80, 95% CI: -4.74 to -2.87; p < 0.0001). However, the results did not reveal an association between CMIs and the risk of atrial arrhythmias (risk ratio (RR): 0.98, 95% CI: 0.33 to 2.94; p = 0.9689).

Conclusions: CMIs have shown great efficacy in improving left ventricular structure and diastolic function in HCM patients. Additionally, CMIs can reduce left ventricular ejection fraction. However, the impact of CMIs on the risk of atrial arrhythmias remains unclear.

The prospero registration: CRD420251243904, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251243904.

Background: Rheumatic heart disease (RHD) is a global autoimmune disease that contributes significantly to cardiovascular mortality. However, a comprehensive investigation into age-specific mortality patterns across diverse regions remains limited. To address this issue, this study aimed to investigate alterations in RHD mortality and disease burden measured by disability-adjusted life years (DALY), and modifiable risk factors across 204 countries and regions during the preceding three decades. Additionally, this study endeavored to forecast the trends for RHD in the coming decade and to explore the associations with the age, period, and birth cohort by analyzing data from the Global Burden of Disease (GBD) 2019.

Methods: We present up-to-date mortality and DALY data for RHD sourced from the GBD 2019 data. We employed the age-period-cohort (APC) model to assess local and net drift, as well as the influences of age, period, and birth cohort. Additionally, we examine modifiable risk factors and provide projections for RHD mortality trends in the coming decade.

Results: Age-standardized mortality rates for RHD exhibited a net drift ranging from -5.59 (95% confidence interval (CI): -5.84 to -5.34) in high-middle sociodemographic index (SDI) regions, to -2.34 (95% CI: -2.42 to -2.25) in low SDI regions. Comparable trends were observed with DALY. High systolic blood pressure was the major metabolic risk factor in both 1990 and 2019. Projections indicate a global reduction in RHD mortality rates over the coming decade. Nevertheless, individuals in low-SDI regions are projected to bear a substantial mortality burden in both 2019 and 2029, accentuating a widening sex disparity.

Conclusions: In summary, this study found that age, period, and birth cohort effects for RHD were positive globally, except for low SDI regions. The widening health disparities between regions indicate an imminent threat of significant disease burden. Thus, this study underscores the imperative requirement for targeted interventions, enhanced healthcare accessibility, and sex-sensitive strategies to alleviate the burden of death and disability associated with RHD, particularly in low SDI regions.