Progress in cardiovascular diseases最新文献

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.

Background: Cardiomyopathies encompass a heterogeneous group of myocardial diseases with variable clinical manifestations and prognoses. Despite their complexity and association with high-risk outcomes, malpractice claims related to cardiomyopathies have not been well-characterized.

Objective: To characterize medicolegal claims associated with non-ischemic cardiomyopathies in the United States and identify common clinical and systemic contributors to liability.

Methods: A retrospective review of U.S. malpractice and negligence claims from inception to 2025 was conducted using Westlaw, vLex, and a sports cardiology litigation database. Included cases involved a diagnosis or clinical suspicion of cardiomyopathy directly linked to a legal claim. Case frequency, location, demographics, allegations, defendant profiles, and outcomes/awards were identified for all eligible cases.

Results: Of 421 cases reviewed, 63 (15 %) met inclusion criteria, spanning 1990-2025 with 1.8 cases/year. Hypertrophic (38 %) and dilated (31 %) cardiomyopathies were the most frequently litigated subtypes. Sudden cardiac arrest/death occurred in 79 % of cases. Leading allegations were failure to diagnose cardiomyopathy (37 %), inappropriate treatment (27 %) and communication failures (19 %). Non-cardiology providers, particularly primary care, were the most frequently named defendants (83 %), while cardiologists were implicated in 29 % of cases. Incarcerated individuals accounted for 16 % of cases. Most outcomes favored defendants (54 %), while 13 % resulted in plaintiff-favorable verdicts or settlements, with awards ranging from $100,000-$21,568,710 ($200,999 - $28,039,323 adjusted for inflation).

Conclusion: While rare, malpractice claims related to cardiomyopathies are often associated with preventable failures in diagnosis, treatment and communication. These findings underscore the need for improved provider education, standardized diagnostic pathways, and clinical decision support tools to mitigate liability and enhance patient safety.

Ischemic stroke is a significant global health challenge, accounting for approximately 66 % of all strokes worldwide. Recent data indicates that stroke was the third leading cause of death (10.7 % of all deaths), following ischemic heart disease and COVID-19. In 2021, nearly 94 million people were living with the consequences of a stroke, and about 12 million new cases were reported. Major risk factors for stroke include high systolic blood pressure, exposure to ambient particulate matter, smoking, and elevated levels of low-density lipoprotein cholesterol (LDL-C), with LDL-C contributing to nearly one-third of all ischemic strokes. In primary prevention, many at-risk individuals have undiagnosed or poorly managed lipid disorders, including elevated lipoprotein(a). The challenge persists in secondary prevention, where up to 40 % of individuals at risk of recurrent ischemic stroke experience a recurrence within five years. A key reason for this is the inadequate diagnosis and management of lipid disorders, underscoring the necessity for early and intensive (upfront) combination lipid-lowering therapy (LLT) to meet treatment goals promptly after an event. Unfortunately, data indicates that up to 40 % of post-stroke patients receive no LLT, and many more receive inadequate treatment. Additionally, existing guidelines for LLT in both primary and secondary stroke prevention are often inconsistent and outdated. Similarly, the understanding of the effects of LDL-C and LLT on the risks of haemorrhagic stroke and dementia remains limited, emphasizing the need for clear and practical guidance. Thus, within this Consensus Paper we aimed to provide consistent, easy-to-follow, and practical guidance on lipid targets, along with clear pathways for effectively treating patients with lipid disorders who are at risk for stroke and those who have experienced one. This approach is intended to help reduce the risk of recurrent ischemic strokes and their associated complications.