Progress in cardiovascular diseases最新文献

Objective: To evaluate the independent and joint associations of social determinants of health (SDOH) and healthy lifestyle factors with life expectancy among adults with cardiovascular-kidney-metabolic (CKM) syndrome.

Research design and methods: We analyzed two prospective population-based cohorts: the UK Biobank (2006-2010) and the US National Health and Nutrition Examination Survey (NHANES, 1999-2018). Adults with CKM at baseline and complete data on SDOH and lifestyle indicators were included. Cox proportional hazards models were used to estimate mortality risk by CKM stage, SDOH, and lifestyle adherence. Life expectancy at age 50 was calculated using life table methods, stratified by CKM stage and levels of SDOH and lifestyle.

Results: A total of 213,738 UK Biobank participants (6.69 % deaths) and 10,345 NHANES participants (9.48 % deaths) were included. Advanced CKM stages were associated with significantly higher mortality risk and shorter life expectancy in both cohorts. Individuals with higher SDOH weighted scores or lower healthy lifestyle scores had elevated mortality risks. The joint effects of poor CKM status, adverse SDOH, and unhealthy lifestyle were additive. In NHANES, life expectancy at age 50 ranged from 33.9 years (CKM stage 0 with healthy lifestyle) to 13.2 years (CKM stage 4 with unhealthy lifestyle). In the UK Biobank, the corresponding figures were 34.2 and 21.7 years.

Conclusions: In two large cohorts, poorer CKM health, greater social disadvantage, and unhealthy lifestyles were each independently and jointly associated with lower life expectancy. These findings support the need for integrated strategies targeting both social and behavioral factors to improve outcomes in CKM populations.

The implantable cardioverter-defibrillator (ICD) is a cornerstone therapy for the prevention of sudden cardiac death (SCD). However, with the global population aging, the application of ICD therapy to elderly patients presents a significant clinical and ethical challenge. The main clinical trials that established the efficacy of ICDs largely excluded or underrepresented individuals over the age of 75, as well as those with significant frailty and comorbidities. We critically examine the evidence for primary and secondary prevention, highlighting the concept of competing risks of non-arrhythmic death, which attenuates the potential benefit of ICDs with advancing age. The risk-benefit ratio is further complicated by a heightened risk of procedural and long-term complications, including device-related infections and pocket integrity issues such as skin erosion. The decision to perform a generator replacement at the time of battery depletion is a crucial opportunity for a new goals-of-care discussion rather than a routine procedure, as evidence shows high mortality rates and a low likelihood of appropriate therapy post-exchange in the very elderly. Finally, we address the management of the ICD at the end of life, summarizing the ethical and legal consensus supporting device deactivation as a critical component of palliative care to prevent suffering from futile shocks. This review calls for a paradigm shift away from criteria based solely on left ventricular ejection fraction and chronological age towards a holistic, individualized approach integrating comprehensive geriatric assessment, comorbidity burden, and structured shared decision-making.

Background: Visceral adipose tissue (VAT) is a metabolically active fat depot strongly associated with cardiometabolic diseases. Current cardiovascular risk models, including the PREVENT equation, do not incorporate direct measures of visceral fat. This study evaluates whether MRI-derived VAT enhances the discrimination and calibration of the PREVENT model for atherosclerotic cardiovascular disease (ASCVD), heart failure (HF), and total cardiovascular disease (CVD) in a large, population-based cohort.

Methods: We included 38,373 UK Biobank participants who underwent abdominal MRI and had no known CVD at baseline. VAT volume was quantified using standardized MRI protocols. We assessed whether adding VAT to the PREVENT model improved model performance for incident ASCVD, HF, and total CVD, using C-statistics and net reclassification improvement (NRI).

Results: The mean age was 54.86 years (SD 7.49), and 52 % of participants were female. The median VAT volume was 3.58 L (IQR:2.14-5.33). Using the overall median VAT value as the threshold, higher visceral adiposity (>3.58 L) was associated with significantly increased risk of ASCVD (HR: 1.32, 95 % CI: 1.15-1.51), heart failure (HR: 1.55, 95 % CI: 1.27-1.89), and total CVD (HR: 1.38, 95 % CI: 1.23-1.55) adjusting for age and sex. Adding VAT to the PREVENT model did not significantly improve discrimination for ASCVD (C-statistic 0.731 vs. 0.729, p = 0.85), nor for HF or total CVD. However, VAT significantly improved reclassification: NRI for ASCVD was 0.37 (95 % CI: 0.30-0.33), for HF was 0.48 (95 % CI: 0.35-0.61), and for total CVD was 0.37 (95 % CI: 0.28-0.46). The association between VAT and all outcomes remained robust after adjustment for age and sex.

Conclusions: MRI-derived visceral adiposity is associated with increased risk of ASCVD, HF, and total CVD. While VAT did not improve overall discrimination of the PREVENT model, it significantly enhanced reclassification, particularly for HF risk. This suggests that VAT may improve individualized cardiovascular risk stratification and inform targeted preventive strategies.

Background: Transcatheter aortic valve replacement (TAVR) is increasingly utilized for severe aortic stenosis (AS), yet optimal risk stratification remains challenging, particularly in patients with preserved ejection fraction (EF). Diastolic dysfunction (DD) has been reported in up to 54.4 % of TAVR patients (predominantly grade 1) and severe (grade 3) DD in ∼13.4 % in prior cohorts and predicts poor outcomes. N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), a marker of ventricular stress, shows promise in enhancing risk assessment. This study evaluates NT-pro-BNP's utility in detecting DD and predicting outcomes in severe AS patients with preserved EF undergoing TAVR.

Methods: This retrospective study included 1594 patients with severe AS (aortic valve area < 1 cm²) and EF ≥50 % undergoing TAVR at Cleveland Clinic (2016-2020). Of these, 784 had complete echocardiographic DD data. Pre- and post-TAVR NT-pro-BNP levels, clinical, and echocardiographic parameters were analyzed. DD was classified using Mitral valve (MV) E/e', tricuspid regurgitation (TR) velocity, and left atrial volume index (LAVi). The Youden Index determined the optimal NT-pro-BNP cut-off, with outcomes assessed via Kaplan-Meier and Cox regression analyses.

Results: NT-pro-BNP correlated with DD severity, with a cut-off of 802 pg/ml (sensitivity 62.3 %, specificity 54.1 %) identified. Higher NT-pro-BNP tertiles were linked to worse baseline characteristics (e.g., NYHA III/IV 65.7 %-82.5 %, p = 0.02) and echocardiographic DD markers (e.g., LAVi 37.61-50.14 ml/m², p < 0.001). Post-TAVR, NT-pro-BNP >802 pg/ml predicted increased mortality, heart failure hospitalizations, and prolonged length of stay (p < 0.001), with Cox regression confirming NT-pro-BNP as an independent predictor (OR 1.645, 95 % CI: 1.244-2.174).

Conclusion: NT-proBNP should be considered a complementary biomarker of DD and predicts adverse outcomes in severe AS patients with preserved EF undergoing TAVR, supporting its integration into pre-procedural risk stratification to optimize management.

Mast cells have emerged as pivotal regulators of cardiovascular physiology and pathology, influencing key processes including fibrosis, angiogenesis, tissue regeneration, and atherosclerosis. This review synthesizes findings from 110 studies to delineate the multifaceted roles of mast cells across these domains. Historically associated with allergic responses, growing evidence now underscores their substantial contribution to the progression of cardiovascular diseases. In fibrotic remodeling, mast cells facilitate extracellular matrix deposition and fibroblast activation through the release of pro-fibrotic mediators such as tryptase and chymase. In the context of angiogenesis, mast cells enhance endothelial proliferation and vascular permeability, predominantly through VEGF-driven signaling pathways. Although the role of mast cells in cardiac regeneration remains underexplored, current evidence suggests a context-dependent function in modulating stem cell dynamics and inflammatory microenvironments. Additionally, mast cells can participate in the pathogenesis of atherosclerosis by promoting lipid accumulation, vascular inflammation, and plaque destabilization. Collectively, these findings highlight mast cells as integral components of cardiovascular disease mechanisms. Therapeutic targeting of mast cell-derived mediators and signaling pathways, through stabilizers, enzyme inhibitors, or selective modulators, represents an avenue worthy of investigation for clinical intervention. Future studies should refine these strategies, aiming to mitigate mast cell-driven pathogenesis while preserving their physiological roles in tissue homeostasis and immune defense.