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- 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
- The Application of Machine Learning in Warfarin Dose Precision for
Diabetic Patients Treated with Statins: A Comparative Study-
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Abstract: Purpose To evaluate the impact of statin therapy on warfarin dose requirements in diabetic patients and to assess the performance of various machine learning algorithms in predicting optimal warfarin dosing. Methods The datasets available for total participants of 628 (216 diabetics and 412 non-diabetic patients) were analyzed. We categorized the patients according to height, weight, gender, race, and age, plasma international normalized ratio (INR) on reported therapeutic dose of warfarin, target INR, warfarin dose, statin therapy, and indications for warfarin. Various models were tested on data of patients from the International Warfarin Pharmacogenetics Consortium (IWPC). Data preprocessing involves structuring and handling missing values. Six predictive models, including least absolute shrinkage and selection operator (LASSO), k-nearest neighbors (KNN), support vector regression (SVR), linear regression (LR), decision tree, and random forest (RF), were employed in predicting optimal warfarin dosage. The best dose for each patient will be predicted using one of the six regression models. Results This comparative study showed that the mean (and the standard deviation) of warfarin dose for diabetic and non-diabetic patients were 38.73 (15.37) and 34.50 (18.27) mg per week, respectively. Furthermore, the impact of various statin they use is considered and patient undergoing atorvastatin and rosuvastatin therapy against the necessity of high dose warfarin if the diabetic patients use lovastatin and fluvastatin. Conclusion Diabetic patients under statin therapy, considering the specific statin used, require different warfarin dose. Through the application of advanced machine learning, models as dosing predictors may attenuate the adverse effects of warfarin.
PubDate: 2025-05-31
- Amiodarone for the Management of Acute Atrial Arrhythmias After Lung
Transplant-
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Abstract: Purpose Dosing, safety, and outcomes of amiodarone in acute post-operative atrial arrhythmias (POAAs) after lung transplantation are not well understood. Current literature suggests amiodarone may increase mortality in lung transplant recipients (LTRs). This study described outcomes associated with amiodarone use in POAAs after lung transplantation. Methods This single-center, retrospective cohort study analyzed LTRs who received amiodarone after developing a POAA within 30 days of transplant surgery and prior to hospital discharge from their index transplant admission. Primary safety outcomes included mortality and the incidence of adverse drug reactions (ADRs). Secondary efficacy outcomes included time to normal sinus rhythm (NSR) attainment, intensive care unit (ICU) and hospital length of stay, and atrial arrhythmia (AA) recurrence. Results A total of 131 LTRs who developed an acute POAA received amiodarone. The 1-year mortality did not differ between this cohort and our overall lung transplant population, and ADR incidence was similar to that observed in non-LTRs. The median time to NSR attainment was 28 h after amiodarone initiation; ICU and hospital lengths of stay were 4.5 and 18.5 days, respectively; and AA recurrence occurred in 32.8% of patients. Conclusion The findings of this study suggest that amiodarone use may be safe in LTRs with acute atrial arrhythmias, and may also effectively terminate acute POAAs in this population.
PubDate: 2025-05-30
- Revealing the Process of Vein Graft Failure: A Panoramic Review from
Etiology Analysis to Mechanism Explanation and Treatment Strategy-
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Abstract: Although coronary artery bypass grafting remains the primary surgical intervention for coronary heart disease, the occurrence of postoperative vascular stenosis is a limiting factor that negatively impacts the long-term efficacy of the procedure and increases the risk of associated postoperative and cardiovascular complications. Therefore, it is imperative to establish a more complete understanding of the physiological and pathological changes and risk factors related to vein graft stenosis, including the underlying mechanisms, to improve preventive measures and treatment strategies for the management of saphenous vein graft failure. The aim of this comprehensive review was to summarize the known etiological mechanisms that drive vein graft failure development and progression and to explore strategies for its prevention and management, including surgical techniques, pharmacological interventions, gene therapy, and other treatment modalities that may improve clinical outcomes, such as those that target specific signaling pathways. Table 1 lists the abbreviations used in this article.
PubDate: 2025-05-29
- Drug-coated Balloons for De Novo Lesions in Large Coronary Arteries–Are
They Ready for Prime Time'-
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PubDate: 2025-05-22
- Midkine Promote Atherosclerosis by Regulating the Expression of
ATP-Binding Cassette Transporter A1 via Activator Protein-1-
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Abstract: Purpose Midkine (MK) has been shown to facilitate atherosclerotic plaque formation by downregulating the expression of ATP-binding cassette transporter A1 (ABCA1). However, the mechanism by which MK regulates ABCA1 to promote atherosclerosis remains incompletely understood. In this study, we sought to investigate the molecular mechanism by which MK’s regulation of ABCA1 influences the pathogenesis of atherosclerosis. Methods Male apoE-/- mice were subjected to a high-fat diet to establish an atherosclerosis model. The model mice received intraperitoneal injections of MK and activator protein-1 (AP-l) inhibitor SR11302. The ATP-binding cassette transporter A1 (ABCA1) and AP1 expression were detected using immunohistochemistry (IHC), quantitative polymerase chain reaction (qPCR), and western blotting (WB). RAW264.7 macrophages were incubated with oxidized low-density lipoprotein (ox-LDL) to generate foam cells. These foam cells were treated with MK, SR11302, JNK inhibitor SP600125, and PI3K inhibitor wortmannin. The expression of ABCA1, AP-1, JNK, and PI3K were detected using qPCR and WB. The cholesterol efflux and lipid accumulation of cells were analyzed using scintillation counting and oil red O staining, respectively. Results MK-treated mice exhibited an accelerated development of atherosclerotic lesion (30% in the MK group vs. 20% in the control group), along with hepatic steatosis and lipid disorder. The expression of c-fos and AP-1 were up-regulated by MK in macrophages. Compared with the MK-treated group, inhibition of AP-1 using SR11302 or transfection with c-fos siRNA markedly enhanced the cholesterol efflux (12.73% in the MK + SR11302 group vs. 9.98% in the MK group, 12.73% in the MK + si-c-fos group vs. 10.02 % in the MK group), reduced lipid accumulation, and increased the protein levels of ABCA1 in macrophages. Compared to the MK-treated group, mice treated with both MK and SR11302 showed downregulated ABCA1 expression in aortic sinus lesions, a larger lesion area (22.59% vs. 18.54%), and significantly elevated levels of plasma total cholesterol (TC), low-density lipoprotein (LDL), and triglycerides (TG). These results suggest that MK-induced pharmacological inhibition of AP-1 augmented ABCA1 expression in plaques, ameliorated lipid disorders, and abrogated atherosclerosis progression in apoE-/- mice. In addition, in vitro experiments revealed that the MK-induced up-regulation of c-fos expression was effectively suppressed by inhibitors of JNK and PI3K. Conclusions Our findings unveil a novel mechanistic pathway in atherosclerosis, whereby MK promotes the development of atherosclerosis by up-regulating AP-1 in macrophages via the PI3K/AKT/JNK signaling cascade. Graphical Abstract
PubDate: 2025-05-22
- Effects of SGLT2 Inhibitor in Patients with Diabetes with Newly Diagnosed
Acute Myocardial Infarction: A Multicenter Prospective Cohort Study-
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Abstract: Purpose The purpose of the current study is to evaluate the role of sodium-glucose co-transporter 2 inhibitors (SGLT2i) in the treatment of patients with diabetes with newly diagnosed acute myocardial infarction (AMI). Methods This multicenter, prospective, cohort study included 1161 patients with diabetes with newly diagnosed AMI. The primary endpoint events included rehospitalization for heart failure (HF) and major adverse cardiovascular events (MACEs). The secondary endpoint events were recurrent MI and cardiac death. Results Patients were categorized into the SGLT2i group and the non-SGLT2i group. During a median follow-up of 1.8 (1.5–2.3) years, the risk of hospitalization for HF (HR 0.58; 95% CI 0.36–0.94; P = 0.026) and MACEs (HR 0.59; 95% CI 0.40–0.86; P = 0.006) were lower in the SGLT2i group, with a similar trend observed for cardiac death (HR 0.51; 95% CI 0.27–0.99; P = 0.046). SGLT2i appears to be a better choice for all such patients. However, our research further found the above trends were observed mainly in the LVEF
PubDate: 2025-05-22
- Early in-hospital use of SGLT2i in heart failure patients with ischemic
etiology-
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Abstract: Purpose SGLT2i role in the treatment of heart failure (HF) regardless of clinical presentation and left ventricular ejection fraction (LVEF) has been widely proven and real-world data regarding patients with HF and ischemic heart disease (IHD) and, in particular with recent acute coronary syndrome (ACS) and de novo HF, are lacking. We aim to evaluate the occurrence of the composite of cardiovascular death (CV)/ HF hospitalization (HFH), all-cause death, CV death and HFH at 6 months follow up, in patients with HF due to IHD as well as in recent ACS who introduced SGLT2i during the index hospitalization. Methods The present is an observational, prospective, single center study, enrolling patients with a diagnosis of HF due to IHD as primary etiology. According to SGLT2i introduction timing, two groups were created: pre-discharge (G1) or post-discharge (G2) introduction. A sub-analysis in patients admitted due to ACS has been performed. Results A total of 222 consecutive patients have been enrolled from April 2022 to April 2024 and were followed-up for a period of 6 months. At multivariate Cox regression analysis, statistically significant differences have been observed between the two groups in terms of the composite CV death/HFH (HR = 0.24; 95%CI [0.101–0.564]; p = 0.001), all-cause death (HR = 0.27; 95% CI [0.100–0.725]; p = 0.009), CV death (HR = 0.32; 95%CI [0.101–0.999] p = 0.045) and HFH (HR = 0.31; 95%CI [0.098–0.963]; p = 0.043). Patients with ACS treated with SGLT2i before discharge showed a reduced rate of CV death/HFH (log-rank p = 0.008), CV death (log-rank p = 0.015) and all-cause death (log-rank p = 0.005) compared to patients who were not treated with SGLT2i before discharge. In this subpopulation, no differences have been observed in terms of HFH (log-rank p = 0.155). Significant differences in term of CV death/HFH (log-rank p = 0.039) have been observed in de novo HF patients, but not in terms of the other study endpoints. Conclusions The early in-hospital introduction of SGLT2i reduced the occurrence of the composite CV death/HFH, all-cause death, CV death and HFH in patients with ischemic cardiomyopathy. In the subgroup analysis of patients admitted due to ACS, the introduction of SGLT2i during the index hospitalization resulted in a significant reduction of the composite CV death/HFH, CV death and all-cause death, but not in HFH. The same therapeutic strategy resulted in reduced rate of CV death/HFH in the de novo HF subpopulation.
PubDate: 2025-05-15
- Dissociation Between Mortality/Kidney Benefits and Neutral MACE Outcomes
with ARNi in Heart Failure and Post-dialysis AKD Recovery-
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PubDate: 2025-05-13
- The FUNCTION Study: A Randomized Controlled Trial on the Efficacy of
Sacubitril/Valsartan on the Success Rate of Catheter Ablation for
Nonparoxysmal Atrial Fibrillation-
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Abstract: Purpose The efficacy of radiofrequency catheter ablation (RFCA) alone for nonparoxysmal atrial fibrillation (NPAF) is unsatisfactory. This study investigated the effect of sacubitril/valsartan, a type of angiotensin receptor neprilysin inhibitor (ARNI), on NPAF patients with hypertension who underwent RFCA and analysed the possible influencing factors. Methods In this prospective, randomized clinical trial, 240 NPAF patients were randomly divided into a control group (n = 121) and an ARNI group (n = 119). The primary outcome was freedom from atrial fibrillation (AF) and atrial tachycardia/atrial flutter (AT/AFL) for ≥ 30 s without antiarrhythmic medications at 15 months after the 3-month blanking period. The secondary outcomes included recurrence types, blood pressure, echocardiographic parameters and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Results At 15 months, a higher maintenance rate of sinus rhythm was achieved in the ARNI group compared to the control group (79.8% vs. 69.4%, hazard ratio [HR] 0.59; 95% confidence interval [CI] 0.36–0.98; P = 0.04). Moreover, a smaller left atrial diameter (adjusted mean difference −1.9 mm [95% CI −3.2 to −0.5], P = 0.02) and lower NT-proBNP level (adjusted median difference −34 pg/ml [95% CI −62 to −6], P = 0.03) were observed in the ARNI group than in the control group at 15 months. Among the patients who recurred, a lower incidence of AF (50.0% vs. 62.2%, P = 0.01) was found in the ARNI group, but presented a significantly higher incidence of AT/AFL. In the subgroup analysis, compared with those in the control group, more patients in the ARNI group achieved success in patients with EF
PubDate: 2025-05-07
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