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- Optimal P2Y12 Inhibitor After Myocardial Infarction: Can Angio-IMR Guide
Treatment Selection'-
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PubDate: 2025-07-01
- Finerenone in Heart Failure with Preserved or Mildly Reduced Ejection
Fraction: A Promising Therapeutic Advancement-
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PubDate: 2025-07-01
- Factor XIa Inhibitors Versus Direct Oral Anticoagulants for Atrial
Fibrillation: A Systematic Review and Meta-analysis of Randomized
Controlled Trials-
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Abstract: Introduction Direct oral anticoagulants (DOACs) are the standard treatment for reducing thromboembolic risk in patients with atrial fibrillation (AF); however, bleeding remains a major concern. Factor XIa inhibitors have emerged as a potential alternative, but evidence about their therapeutic potential remains unclear. We performed a systematic review and meta-analysis to evaluate the comparative efficacy and safety of Factor XIa inhibitors versus DOACs for AF. Methods PubMed, Embase, and Cochrane Library were systematically searched until February 15, 2025, to identify RCTs comparing Factor XIa inhibitors with DOACs in AF patients. Risk ratios (RR) with 95% confidence intervals (CI) were pooled using a random-effects model. Statistical analysis was performed in RevMan 5.4 with p-value
PubDate: 2025-06-25
- Correction to: Non-Invasive Local Acoustic Therapy Ameliorates Diabetic
Heart Fibrosis by Suppressing ACE-Mediated Oxidative Stress and
Inflammation in Cardiac Fibroblasts-
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PubDate: 2025-06-25
- Key Insights for DOAC Management in Complex Patients
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PubDate: 2025-06-21
- Molecular Interplay of Gene Network Dynamics, Epigenetic Regulation, and
Therapeutic Mapping in Cardiovascular Disease-
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Abstract: Purpose Cardiovascular diseases (CVDs) continue to be the leading cause of death globally, driven by a complex interplay of genetic, epigenetic, and environmental factors. Traditional risk factors alone fail to explain the individual variability in disease susceptibility and progression. Recent advances in genomics and epigenomics have revealed key molecular mechanisms that regulate cardiovascular function, highlighting the importance of gene network dynamics and epigenetic regulation. Methods This review systematically analyzes peer-reviewed literature from the past decade sourced from electronic databases including PubMed and Google Scholar. It compiles the multifaceted roles of DNA methylation, histone modifications, chromatin remodeling, and noncoding RNAs in regulating cardiovascular gene expression, cellular phenotypes, and disease pathogenesis. Results DNA methylation influences the transcriptional activity of gene expression associated with atherosclerosis, myocardial infarction, and hypertension, while histone modifications and ATP-dependent chromatin remodeling regulate cardiac hypertrophy, fibrosis, and regeneration. Noncoding RNAs further act as critical regulators of angiogenesis, inflammation, and myocardial remodeling. Therapeutically, these findings have facilitated the development of epigenetic drugs and gene-editing technologies targeting specific molecular pathways involved in CVD progression. Emerging technologies such as CRISPR/Cas9, RNA-based therapies, and small-molecule inhibitors of epigenetic enzymes hold potential for correct abnormal gene expression patterns. Moreover, integrative multi-omics and systems biology approaches are advancing personalized treatment strategies, improving the accuracy and effectiveness of cardiovascular interventions. Conclusion Collectively, unraveling the complex molecular interactions among gene networks, epigenetic alterations, and targeted therapeutic mapping aims to combat CVD with better precision and efficacy. Graphical Abstract
PubDate: 2025-06-20
- Clinical Implication of Quantitative Flow Ratio to Predict Clinical
Outcomes in De Novo Coronary Lesions After Drug-Coated Balloon Angioplasty
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Abstract: Purpose The association between the intra-procedure quantitative flow ratio (QFR) and clinical outcomes after drug-coated balloon (DCB) angioplasty has not been investigated. This study aimed to investigate the clinical predictive value of pre-DCB QFR, a functional assessment of lesion preparation, for clinical outcomes in de novo coronary lesions after DCB angioplasty. Methods This retrospective study included 170 consecutive patients undergoing DCB angioplasty for 177 de novo coronary lesions between January 2021 and December 2022. The QFR was computed at baseline, pre-DCB, and post-DCB. The primary endpoint was major adverse cardiac events (MACE), defined as a composite of all-cause death, cardiac death, target vessel myocardial infarction, and target lesion revascularization. Results During 2-year follow-up, 37 patients with 38 lesions have experienced MACE. The pre-DCB QFR, measured after pre-dilation, was significantly lower in the MACE group. Receiver operator characteristic curve analysis showed the optimal pre-DCB QFR cut-off value for predicting MACE was 0.925 (area under curve = 0.782, 95% confidence interval [CI] 0.702–0.861, sensitivity = 78.9%, specificity = 74.8%, p
PubDate: 2025-06-20
- Impact of Percutaneous Coronary Interventions on Coronary Microvascular
System: Coronary Stenting Versus Drug-Coated Balloon Angioplasty-
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PubDate: 2025-06-20
- Direct Oral Anticoagulants in Valvular Diseases and Prosthetic Valves: Why
Not'-
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Abstract: Valvular heart disease (VHD) and atrial fibrillation (AF) often coexist and lead to a prothrombotic state that necessitates the use of anticoagulants for the prevention of thromboembolic events. Direct oral anticoagulants (DOACs) are a significant advancement in anticoagulation therapy for patients with AF and VHD, leading to comparable efficacy and improved safety outcomes compared to vitamin K antagonists (VKAs). However, their role in patients with severe mitral stenosis, mechanical heart valves, and rheumatic heart disease remains limited due to the lack of robust data from clinical trials. As such warfarin continues to be the anticoagulant of choice for these populations. For patients with bioprosthetic valves or following transcatheter aortic valve implantation (TAVI), DOACs may be a viable alternative, but individualized risk assessment is crucial. The EHRA classification provides a practical framework for the management of patients with AF, but there are still challenges in its clinical application due to mixed valvular pathologies and patient-specific factors. Clinicians must carefully weigh the risk of thromboembolic and bleeding events, consider the patients’ preferences, and advise regular follow-up to optimize the treatment outcomes. Overall, while DOACs offer convenience and similar efficacy and safety compared to VKAs, VKAs remain the anticoagulant of choice for specific subgroups, underscoring the need for personalized approaches regarding anticoagulation therapy.
PubDate: 2025-06-20
- Pericardial Administration of Extracellular Vesicles Derived from Bone
Marrow Stem Cells Improved Doxorubicin-induced Heart Failure with Mid
Range Ejection Fraction (HFmrEF) in Rats-
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Abstract: Purpose This study investigates the therapeutic effects of extracellular vesicles (EVs) derived from bone marrow mesenchymal stem cells (BMSCs) on heart failure in rats through intrapericardial injection. Methods Initially, doxorubicin was used to induce apoptosis in H9C2 cells, and the protective effects of EVs on these cells were evaluated. EVs were injected into the pericardial cavity of rats with heart failure, followed by real-time in vivo imaging and immunofluorescence detection to confirm the implantation of EVs in the myocardium. Cardiac function was assessed via echocardiography after the pericardial injection. Immunohistochemical techniques were employed to measure the expression of BNP, IL-6, CD31, and VEGFA in rat heart tissue. Additionally, the collagen fiber content in the heart tissue was detected using Masson staining. Results The results showed that EVs derived from BMSCs at a concentration of 100 μg/ml most effectively promoted the proliferation of H9C2 cells and protected them from doxorubicin-induced damage. Compared to the heart failure group, EV treatment significantly increased LVEF, LVFS, and CO. Following intrapericardial injection of BMSCs, in vivo imaging revealed high-intensity fluorescence signals in the cardiac region, and immunofluorescence confirmed the implantation of EVs in the myocardium. Post-EV treatment, the expression levels of BNP and IL-6 and collagen content in myocardial tissue were significantly reduced, whereas the levels of CD31 and VEGFA were significantly increased. Conclusion EVs derived from BMSCs, when injected into the pericardial cavity, significantly improved cardiac function in heart failure rats through anti-inflammatory and pro-angiogenic mechanisms.
PubDate: 2025-06-11
- Anticoagulation Therapy in VTE: Is a Lower Dose the Safer Choice'
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PubDate: 2025-06-10
- Effects of Angiotensin-Converting Enzyme Inhibitors/Angiotensin II
Receptor Blockers on Prognosis in Acute Coronary Syndrome Patients with
Preserved Ejection Fraction Undergoing Regular Dialysis-
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Abstract: Purpose The utilization of angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) following myocardial infarction (MI) is substantiated by evidence derived from trials conducted during the thrombolysis era. However, limited evidence suggests that ACEI/ARB confer benefits to patients with preserved left ventricular ejection fraction (LVEF). Notably, these studies typically exclude patients undergoing regular dialysis. In this study, we examined the association between the use of ACEI/ARB and the 5-year outcomes in patients with acute coronary syndrome (ACS) who are on regular dialysis and possess preserved left ventricular function. Methods This multicenter retrospective study enrolled a total of 1249 dialysis patients diagnosed with coronary heart disease (CAD). A total of 603 patients meeting the inclusion and exclusion criteria were analyzed. Results The mean age of the cohort was 61.7 years, with 70.6% being male; 313 (51.9%) patients were treated with ACEI/ARB. Over a 5-year follow-up period, the use of ACEI/ARB had no benefit on the composite outcome of major adverse cardiovascular events (MACE) (31.3% vs. 29.0%, p = 0.988). However, ACEI/ARBs reduced mortality across all causes (24.9% vs. 33.1%, p = 0.012) and cardiovascular deaths (14.7% vs. 21.4%, p = 0.015). Furthermore, ACEI/ARB demonstrated a more pronounced cardiovascular mortality benefit in patients with poorer left ventricular function (LVEF 50–60%). Conclusion In dialysis patients with ACS and preserved left ventricular function, ACEI/ARB reduces all-cause and cardiovascular mortality. Additionally, a more pronounced survival benefit is observed in patients with impaired LVEF (50–60%). However, no benefit was found regarding MACE.
PubDate: 2025-06-10
- Thrombocytopenia and Antiphospholipid Syndrome
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PubDate: 2025-06-06
- Macrophage CBX4 Potentiates Atherosclerosis by its SUMO E3 Ligase Activity
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Abstract: Atherosclerosis (AS) is the leading cause of cardiovascular disease and mortality worldwide. Despite extensive research, there remains an urgent need for novel therapeutic strategies. By integrating genomic da...
PubDate: 2025-06-06
- Coronary Artery Bypass Grafting With or Without Concomitant Surgical
Ventricular Reconstruction in Ischemic Cardiomyopathy Patients-
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Abstract: The present study aims to compare the long-term outcomes of surgical ventricular reconstruction (SVR) combined with coronary artery bypass grafting (CABG) versus CABG alone in patients with ischemic cardiomyop...
PubDate: 2025-06-05
- Can Inclisiran Emerge in the Crowded Lipid-Lowering Therapy Landscape'
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PubDate: 2025-06-04
- Sotagliflozin: Two Birds with One Stone'
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Abstract: Purpose Sodium-glucose cotransporter 2 inhibitors (SGLT2i), initially developed as antidiabetic agents, have become a cornerstone in the treatment of heart failure (HF) due to their well-established cardio-renal benefits. Clinical trials with SGLT2i have shown a reduction in major adverse cardiovascular events (MACE) across a broad range of patients with no effect on atherothrombotic cardiovascular events such as myocardial infarction (MI) or stroke. On the other hand, sotagliflozin, the first of a new class of dual SLGT1-2 inhibitor (SGLT1-2i), reduces MACE, with independent reductions in MI and stroke, an effect not seen with SGLT2 inhibition alone. Method A comprehensive literature review was conducted using PubMed and Scopus, focusing on publications from the last 5 years. Articles were selected based on relevance, methodological rigor, and citation impact. Results SGLT1 and SGLT2 work complimentarily in urinary glucose reabsorption, while SGlT1 also regulates dietary glucose in the intestine. However, its function in other organs remains undefined. SGLT1 is overexpressed in the failing heart and has been associated with increased oxidative stress, cardiomyocyte hypertrophy, and fibrosis. Additionally, SGLT1 also plays an important role in platelet activation and thrombus formation. Experimental studies suggest that sotagliflozin, by inhibiting SGLT1, reverses the metabolic derangements associated with SGLT1 overexpression. Conclusion These observations suggest that dual SGLT1-2 inhibition may offer additional benefits over single SGLT2-i. Further comparative and mechanistic studies are required to understand and differentiate the clinical impact of SGLT2i vs. SGLT1-2i, particularly in non-diabetic HF patients.
PubDate: 2025-06-04
- Vagus Nerve Stimulation by Focused Ultrasound Attenuates Acute Myocardial
Ischemia/Reperfusion Injury Predominantly Through Cholinergic
Anti-inflammatory Pathway-
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Abstract: Purpose This study investigates the cardioprotective effects of focused ultrasound stimulation (FUS) as a novel, noninvasive intervention for mitigating acute myocardial ischemia/reperfusion (I/R) injury. Methods In rat I/R models (30-min left anterior descending coronary artery (LAD) occlusion followed by 2-/24-h reperfusion), FUS was applied to the right cervical vagus nerve during early reperfusion (10–60 min post-reperfusion). The effects of FUS were assessed by analyzing inflammatory markers, arrhythmia incidence, pathological changes, echocardiographic parameters, pro-/anti-oxidative biomarkers, myocardial fibrosis, and infarct size. To elucidate the underlying mechanism, vagotomy and atropine administration were performed. Results FUS significantly reduced heart rate and inflammation in the 2-h reperfusion model. Compared to the I/R group, the I/R + FUS group exhibited markedly decreased premature ventricular contractions (221.00 ± 166.93 vs 83.11 ± 34.08, p < 0.05), ventricular tachycardia and ventricular fibrillation (16.67 ± 10.68 vs. 3.67 ± 3.24, p < 0.01), and arrhythmia scores during reperfusion (2.44 ± 1.13 vs. 0.67 ± 0.50, p < 0.01). In the 24-h reperfusion model, FUS significantly reduced myocardial fibrosis and infarct size (infarct size/area at risk 49.60 ± 9.17% vs. 20.73 ± 4.91%, p < 0.001) and preserved left ventricular ejection fraction (35.68 ± 9.95% vs 56.73 ± 2.64%, p < 0.001). The protective effects of FUS were abolished by vagotomy or atropine, suggesting the cholinergic anti-inflammatory pathway as a potential mechanism. Conclusion Targeted FUS neuromodulation exerts acute and sustained cardioprotection against I/R injury primarily through cholinergic anti-inflammatory mechanisms, offering a safer and more accessible alternative to traditional treatments.
PubDate: 2025-06-02
- Risk of Contrast Induced Nephropathy for Patients on an SGLT2 Inhibitor
Undergoing Percutaneous Intervention-
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PubDate: 2025-05-31
- Macrophage Migration Inhibitory Factor: the Next Adjunct to Reperfusion
Therapy in Acute Myocardial Infarction'-
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PubDate: 2025-05-31
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