Cardiology最新文献

Introduction: The effectiveness and safety of oral anticoagulants (OACs) in patients with chronic kidney disease (CKD) and non-valvular atrial fibrillation (NVAF) in frail elderly patients have not been fully established. We aimed to evaluate the safety and effectiveness of OACs in frail elderly patients with atrial fibrillation (AF) and stage II-III CKD.

Methods: Frail elderly patients ≥65 years with AF and CKD who received OAC from January 2022 to June 2024 were retrospectively identified. Primary endpoints were composite of ischemic stroke and systemic embolism (IS/SE), and composite of intracranial hemorrhage (ICH) and/or gastrointestinal (GI) bleeding. Secondary endpoints included any bleeding.

Results: The study enrolled 365 patients, of whom 141 (38.6%) initiated warfarin therapy and 224 (61.3%) initiated DOACs. CHA2DS2-VASc score was nonsignificant (2.6 ± 1.01 vs. 2.8 ± 0.89, p value 0.054), for GFR ≥60 and GFR <60 mL/min/1.73 m2 patients, respectively. HAS-BLED score (1.9 ± 0.67 vs. 2.3 ± 0.70, p value 0.071) for GFR ≥60 and GFR <60 mL/min/1.73 m2 patients respectively. While the observed incidence of ICH/GI bleeding was numerically higher in patients with GFR <60 mL/min/1.73 m2, Cox proportional hazards regression did not demonstrate a statistically significant difference in hazard between the groups. The incidence of composite IS/SE was 8.5% in GFR ≥60 mL/min/1.73 m2 versus 8.7% in GFR <60 mL/min/1.73 m2 (HR 1.02, 95% CI: 0.60-1.74, p = 0.24). Composite ICH/GI bleeding occurred in 7.1% versus 9.3% (HR 2.15, 95% CI: 0.91-4.56, p = 0.41).

Conclusion: In this study comparing frail elderly patients with NVAF and CKD stage II versus stage III receiving OACs, we observed no significant difference in the risk of IS/SE or ICH/GI bleeding between groups. These findings suggest that within moderate CKD (eGFR 30-89 mL/min), renal function stage may not independently influence OAC-related outcomes when anticoagulation is well managed. Our results may not generalize to less frail populations or those with advanced CKD. Further prospective studies with larger sample size are needed to provide clearer guidance on the optimal use of OACs in this challenging clinical scenario.

Introduction: Myocardial infarction (MI) is one of the leading causes of death from cardiovascular diseases (CVDs). Despite various drugs and treatments, the outcomes have often been unsatisfactory. The purpose of this meta-analysis aimed to analyze the effects of polypill intervention on the incidence of MI and the related risk factors, blood pressure, and blood lipids.

Methods: We conducted a systematic search of appropriate randomized controlled trials (RCTs) in various databases, utilizing preset search terms. Then, we performed a meta-analysis of individual participant data, including studies that investigated the effectiveness of polypill (a fixed-dose combination drug) as compared to usual care in preventing MI. The primary outcomes are MI, CVD mortality, major adverse cardiovascular event (MACE), and all-cause mortality. Secondary outcomes include blood pressure levels (systolic blood pressure [SBP], diastolic blood pressure [DBP]), serum lipid levels (total cholesterol [TC], low-density lipoprotein cholesterol [LDL], and high-density lipoprotein cholesterol [HDL]).

Results: A total of 14 trials (N = 59,346) were included, with a mean age of 63.2 ± 10.0 years. The results showed that compared to the usual care group, polypill group was associated with a significant reduction of the incidence of MI (OR = 0.76; 95% CI: 0.59 to 0.99; p = 0.04) and MACE (OR = 0.79; 95% CI: 0.65 to 0.97; p = 0.03). The risk reduction for CVD mortality (OR = 0.85; 95% CI: 0.65 to 1.11; p = 0.20) and all-cause mortality (OR = 0.99; 95% CI: 0.95 to 1.03; p = 0.59) did not reach statistical significance contrast with the usual care group. Participants who were in polypill group was observed that the change of SBP level (SMD = -0.13; 95% CI: -0.25 to 0.00; p = 0.04), DBP level (SMD = -0.13; 95% CI: -0.19 to -0.06; p = 0.00), and LDL level (SMD = -0.21; 95% CI: -0.36 to -0.06; p = 0.01) reached statistical significance. However, the change of HDL level (SMD = -0.01; 95% CI: -0.06 to 0.04; p = 0.62) and TC level (SMD = -0.15; 95% CI: -0.32 to 0.01; p = 0.06) did not show remarkable difference.

Conclusion: These findings suggested that polypill not only is highly effective for preventing MI and reducing the incidence of MACE but also can lower blood pressure levels and blood lipid levels.

Introduction: Patent foramen ovale (PFO) is a prevalent congenital heart malformation closely linked with migraine. The effect of PFO size on migraine remains controversial.

Methods: This study analyzed migraine patients who underwent PFO closure at our institution from January 2020 through December 2022. Based on transthoracic echocardiography findings, the patients were classified into two groups through two distinct classification approaches: method A - permanent shunt (PS) group or non-PS group, and method B - large shunt under Valsalva maneuver (LSVM) group or small-to-moderate shunt under Valsalva maneuver (SMSVM) group. Migraine improvement and adverse events after PFO closure were recorded.

Results: A total of 201 migraine patients were included in this study, 110 (54.7%) had PS and 118 (58.7%) had LSVM. The PS and LSVM groups experienced less migraine burden (57.1 ± 64.5 vs. 88.5 ± 96.5 h, p = 0.035; 59.7 ± 67.3 vs. 88.9 ± 96.6 h, p = 0.039). The LSVM group had shorter headache episode durations (11.0 ± 8.2 vs. 14.4 ± 12.3 years, p = 0.045). The PS and LSVM groups showed less absolute reduction in migraine burden (33.8 ± 55.2 vs. 71.2 ± 84.9 h, p = 0.032; 33.9 ± 50.5 vs. 76.3 ± 92.8 h, p = 0.008). The LSVM group had a lower rate of alleviation (79.7% vs. 95.2%, p = 0.018). Medium-to-large residual shunt (MLRS) and SMSVM were independent predictors of migraine improvement, and a history of cryptogenic stroke (CS) was a predictor of migraine termination.

Conclusion: SMSVM PFO in migraine patients has significant clinical implications and positive intervention outcomes. Both SMSVM and MLRS are associated with migraine relief, and a history of CS is a predictor of migraine termination.

Introduction: Fasting plasma glucose (FPG) fluctuations are increasingly recognized as potential prognostic markers in cardiovascular diseases. However, the association between changes in FPG before and after heart failure (HF) diagnosis and long-term mortality remains unclear. This study aimed to evaluate the impact of FPG changes surrounding HF diagnosis on all-cause mortality to inform individualized HF management strategies.

Methods: This prospective cohort study was conducted using data from the Kailuan study. A total of 3,533 patients newly diagnosed with HF were included after excluding individuals with a history of HF, malignancies, or missing FPG data. FPG levels measured before and after HF diagnosis were used to classify participants into five groups: significant decrease (Q1), mild decrease (Q2), stable (Q3), mild increase (Q4), and significant increase (Q5). The primary outcome was all-cause mortality, with follow-up through December 31, 2021. Survival outcomes were evaluated using Kaplan-Meier curves and multivariate Cox regression models.

Results: During a mean follow-up of 5.63 ± 3.80 years, 1,446 all-cause deaths were recorded. Kaplan-Meier analysis demonstrated a significantly higher mortality risk associated with greater changes in FPG levels (log-rank p < 0.0001). In multivariable Cox models, both the Q1 (significant decrease) and Q5 (significant increase) groups exhibited elevated mortality risks compared to the Q3 (stable) group, with adjusted hazard ratios of 1.37 (95% CI: 1.12-1.67) and 1.35 (95% CI: 1.12-1.62), respectively.

Conclusion: Significant changes in FPG before and after HF diagnosis are independently associated with increased all-cause mortality. These findings highlight the importance of maintaining glycemic stability and support the need for personalized glucose management strategies in patients with HF.

Introduction: The progression of heart failure (HF) has been independently linked to both tissue inhibitor of metalloproteinase-4 (TIMP4) and the equilibrium between regulatory T (Treg) as well as T helper 17 (Th17) cells. Despite these associations, the interplay between TIMP4 and the Th17/Treg ratio remains poorly understood. Our research sought to elucidate the impact of TIMP4 on HF pathogenesis, with a particular emphasis on its influence on Th17 and Treg lymphocyte populations.

Methods: Bioinformatics analysis of the GSE196656 dataset was conducted. An isoprenaline-induced Sprague-Dawley rat model of HF was used, with rats divided into groups: HF alone, HF with TIMP4 overexpression, and HF with TIMP4 knockdown. HF in primary myocardial cell cultures was induced using Angiotensin II, and extracellular vesicles were collected from the culture medium. ELISA, Western blot, TUNEL staining, qRT-PCR, and RNA extraction analyzed the impact of TIMP4 on HF. Additionally, purified naïve CD4+ T cells from rats were used in vitro to investigate TIMP4's influence on Th17 and Treg cell differentiation.

Results: Analysis of the GSE196656 dataset revealed significant upregulation of TIMP4 in HF. Myocardial exosomal TIMP4 was significantly elevated in the HF model. In the experimental rat model, TIMP4 overexpression significantly reduced plasma levels of biomarkers related to heart injury as well as inflammation, enhanced indicators of heart function and suppressed cell death in the heart muscle. Furthermore, TIMP4 overexpression decreased IL-17 levels and the Th17 cell proportion while promoting Treg cell differentiation and increasing IL-10 levels. In vitro studies demonstrated that TIMP4 effectively inhibits the differentiation of Th17 cells and promotes the growth of Treg cells. These effects were observed to vary depending on the dosage.

Conclusion: TIMP4 overexpression exerts a protective effect in HF by inhibiting myocardial injury, inflammation, and apoptosis, and by regulating immune cell balance. These findings imply that targeting TIMP4 could potentially serve as a therapeutic strategy for HF, as it has the ability to regulate immune responses and minimize damage to the myocardium.