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- Can We Leave No Metal Behind' DCB vs. DES in Large Coronary Arteries
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PubDate: 2024-08-23
- Effect of Preoperative Mitral Regurgitation on LVAD Outcomes in Patients
with Elevated Pulmonary Vascular Resistance-
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Abstract: Purpose In patients with end-stage heart failure who undergo left ventricular assist device (LVAD) implantation, higher pulmonary vascular resistance (PVR) is associated with higher right heart failure rates and ineligibility for heart transplant. Concomitant mitral regurgitation (MR) could potentially worsen pulmonary hemodynamics and lead to worse outcomes; however, its effects in this patient population have not been specifically examined. Methods Using an institutional database spanning November 2003 to August 2017, we retrospectively identified patients with elevated PVR who underwent LVAD implantation. Patients were stratified by concurrent MR: moderate/severe (PVR + MR) vs. mild/none (PVR − MR). Cumulative incidence functions and Fine-Gray competing risk regression were performed to assess the effect of MR on heart transplant rates and overall survival during index LVAD support. Results Of 644 LVAD recipients, 232 (171 HeartMate II, 59 HeartWare, 2 HeartMate III) had baseline PVR > 3 Woods units; of these, 124 (53%) were INTERMACS 1–2, and 133 (57%) had moderate/severe MR (≥ 3 +). Patients with PVR + MR had larger a baseline left ventricular end-diastolic diameter than patients with PVR − MR (87.9 ± 38.2 mm vs. 75.9 ± 38.0 mm; P = 0.02). Median clinical follow-up was 18.8 months (interquartile range: 4.7–36.4 months). Moderate/severe MR was associated with lower mortality rates during index LVAD support (adjusted hazard ratio 0.64, 95% CI 0.41–0.98; P = 0.045) and higher heart transplant rates (adjusted odds ratio 2.86, 95% CI 1.31–6.25; P = 0.009). No differences in stroke, gastrointestinal bleeding, or right heart failure rates were observed. Conclusions Among LVAD recipients with elevated preoperative PVR, those with moderate/severe MR had better overall survival and higher transplant rates than those with mild/no MR. These hypothesis-generating findings could be explained by incremental LVAD benefits resulting from reduction of MR and better LV unloading in a subset of patients with larger ventricles at baseline. In patients with preoperative elevated PVR, MR severity may be a prognostic sign that can inform patient selection for end-stage heart failure therapy. Graphical 
PubDate: 2024-08-20
- Flow Matters: Optimizing Invasive Coronary Physiology to Improve Long-Term
Outcomes-
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PubDate: 2024-08-17
- Efficacy and Safety of Non-Vitamin K Antagonist Oral Anticoagulants
Compared with Vitamin K Antagonists in Patients with Atrial Fibrillation
and Type 2 Valvular Heart Disease: A Systematic Review and Meta-Analysis-
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Abstract: Purpose This meta-analysis aimed to evaluate the efficacy and safety of non-vitamin K antagonist oral anticoagulants (NOACs) compared with vitamin K antagonists (VKAs) in patients with atrial fibrillation (AF) and type 2 valvular heart disease (VHD). Methods We searched the PubMed, LILACS, and MEDLINE databases to retrieve, randomized controlled trials (RCTs) comparing NOACs and VKAs in patients with AF and type 2 VHD, excluding mitral stenosis (moderate to severe, of rheumatic origin) or mechanical heart valves. The efficacy outcomes assessed were stroke and systemic embolism (SE), while safety outcomes included major bleeding and intracranial hemorrhage (ICH). Results Seven RCTs, including 16,070 patients with AF and type 2 VHD, were included. NOACs reduced the risk of stroke/SE (relative risk [RR], 0.75; 95% confidence interval [CI], 0.64–0.89; P = 0.0005), with no significant difference in major bleeding (RR, 0.88; 95% CI, 0.64–1.21; P = 0.43). The risk of ICH was reduced with NOACs (RR, 0.46; 95% CI, 0.27–0.77; P = 0.003). For patients with AF and bioprosthetic heart valve (five trials, 2805 patients), stroke/SE risks (RR, 0.65, 95% CI, 0.44–0.96) with NOACs were superior to VKAs. Major bleeding risks without ENVISAGE TAVI AF trial (RR, 0.53; 95% CI, 0.30–0.94; P = 0.03) with NOACs were superior to VKAs. The risks of ICH (RR, 0.61; 95% CI 0.34–1.09; P = 0.09) with NOACs were comparable to VKAs. Conclusions NOACs demonstrate efficacy and safety in patients with AF and type 2 VHD and reduce the risk of stroke/SE and ICH when compared with those with VKAs.
PubDate: 2024-08-17
- Exercise Enhances Anti-contractile Effects of PVAT Through Endogenous H2S
in High-Fat Diet–Induced Obesity Hypertension-
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Abstract: Purpose Hydrogen sulfide (H2S) secreted by perivascular adipose tissue (PVAT) is a critical vasodilator, which might be involved during the pathogenesis of hypertension. The present study aimed to investigate the exact role of H2S on the regulation of PVAT anti-contraction by long-term exercise in obesity hypertension. Methods After the establishment of obesity hypertension (24 weeks) through a high-fat diet, male Sprague–Dawley rats were randomly assigned to control group (HC), exercise group (HE), cystathionine γ-lyase (CSE) blocking group (HCB), and exercise combined with CSE blocking group (HEB). Exercise and CSE inhibitor regimens were performed throughout 13 weeks. Results After 13 weeks of intervention, blood pressure was significantly decreased by long-term exercise (HC vs. HE, P < 0.05) but not by exercise combined with the CSE inhibitor regimen. Meanwhile, the CSE inhibitor significantly blocked the production of H2S in PVAT even after exercise (HE vs. HEB, P < 0.05). Furthermore, long-term exercise altered the expressions of voltage-dependent K+ (Kv) channel subunits 7 (KCNQs), which were diminished by CSE inhibition in mesenteric arteries. As for vascular tension assessment, after incubation with or without KCNQ opener (retigabine), the anti-contractile effect of PVAT (with or without transferred bath solution of PVAT) was significantly enhanced by long-term exercise and eliminated by the CSE inhibitor regimen (P < 0.05); KCNQ inhibitor (XE991) blunted this effect except for HE. Conclusions These results collectively suggest that endogenous H2S is a strong regulator of the anti-contractile effect of PVAT in obesity hypertension by long-term exercise, and KCNQ in the resistance artery might be involved during this process but not the only target channel mediated by H2S.
PubDate: 2024-08-12
- How Much Is Enough'
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PubDate: 2024-08-08
- Levosimendan: A New Therapeutical Strategy in Patients with Renal
Insufficiency-
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Abstract: Abstract Levosimendan, a Ca2 + sensitizer with positive inotropic effects, is primarily employed for the short-term treatment of acute decompensated heart failure (ADHF). Levosimendan exerts renal function protection through various mechanisms, including anti-apoptosis, anti-inflammatory, and antioxidant effects in vivo. Additionally, levosimendan may have a protective effect on individuals with heart failure and renal insufficiency, as well as on renal function impairment after cardiac surgery. However, the application of levosimendan in patients with severe renal dysfunction remains controversial. This article delves into the use of levosimendan in severe renal insufficiency, explores its impact on renal function, and provides a comprehensive overview of its impact on renal function after cardiac surgery.
PubDate: 2024-08-07
- Iron Status Screening in Individuals with Heart Failure Before Initiating
Sodium-Glucose Cotransporter 2 Inhibitor Therapy: Is It Necessary'-
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PubDate: 2024-08-01
- Left Ventricular Thrombus After Myocardial Infarction: Opinions and
Equipoise-
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PubDate: 2024-08-01
- Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy
Target for Atherosclerosis-
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Abstract: Abstract Nowadays, as a type of orderly and active death determined by genes, programmed cell death (PCD), including apoptosis, pyroptosis, ferroptosis, and necroptosis, has attracted much attention owing to its participation in numerous chronic cardiovascular diseases, especially atherosclerosis (AS), a canonical chronic inflammatory disease featured by lipid metabolism disturbance. Abundant researches have reported that PCD under distinct internal conditions fulfills different roles of atherosclerotic pathological processes, including lipid core expansion, leukocyte adhesion, and infiltration. Noteworthy, emerging evidence recently has also suggested that oxidative stress (OS), an imbalance of antioxidants and oxygen free radicals, has the potential to mediate PCD occurrence via multiple ways, including oxidization and deubiquitination. Interestingly, more recently, several studies have proposed that the mediating mechanisms could effect on the atherosclerotic initiation and progression significantly from variable aspects, so it is of great clinical importance to clarify how OS-mediated PCD and AS interact. Herein, with the aim of summarizing potential and sufficient atherosclerotic therapy targets, we seek to provide extensive analysis of the specific regulatory mechanisms of PCD mediated by OS and their multifaceted effects on the entire pathological atherosclerotic progression.
PubDate: 2024-08-01
- Clinical Efficacy and Safety of Early Intravenous Administration of
Beta-Blockers in Patients Suffering from Acute ST-Segment Elevation
Myocardial Infarction Without Heart Failure Undergoing Primary
Percutaneous Coronary Intervention: A Study-Level Meta-Analysis of
Randomized Clinical Trials-
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Abstract: Background Several clinical studies have produced diverse results regarding the efficacy and safety of early intravenous beta-blockers in patients with acute ST-segment elevation myocardial infarction (STEMI). A study-level meta-analysis of randomized clinical trials (RCTs) comparing early intravenous beta-blockers versus placebo or routine care in STEMI patients undergoing primary percutaneous coronary intervention (PCI) was performed. Methods A database search was conducted using PubMed, EMBASE, the Cochrane Library, and Clinicaltrials.gov for randomized clinical trials (RCTs) that compared intravenous beta-blockers versus placebo or routine care in STEMI patients who underwent primary PCI. The efficacy outcomes were infarct size (IS, % of LV) and the myocardial salvage index (MSI) based on magnetic resonance imaging, electrocardiographic findings, heart rate, ST-segment reduction percent (STR%), and complete STR. Safety outcomes included arrhythmias in the first 24 h (ventricular tachycardia and fibrillation [VT/VF], atrial fibrillation [AF], bradycardia, and advanced atrioventricular [AV] block), cardiogenic shock and hypotension during hospitalization, left ventricular ejection fraction (LVEF), and major adverse cardiovascular events (cardiac death, stroke, reinfarction, and heart failure readmission) at follow-up. Results Seven RCTs with 1428 patients were included in this study, with 709 patients in the intravenous beta-blockers and 719 in the control group. Intravenous beta-blockers improved MSI compared to the control group (weighted mean difference [WMD] 8.46, 95% confidence interval [CI] 3.12–13.80, P = 0.002, I2 = 0%), but no differences were observed in IS (% of LV) between groups. Compared to the control group, the intravenous beta-blockers group had a lower risk of VT/VF (relative risk [RR] 0.65, 95% CI 0.45–0.94, P = 0.02, I2 = 35%) without an increase of AF, bradycardia, and AV-block and significantly decreased HR, hypotension. LVEF at 1 week ± 7 days (WMD 2.06, 95% CI 0.25–3.88, P = 0.03, I2 = 12%) and 6 months ± 7 days (WMD 3.24, 95% CI 1.54–4.95, P = 0.0002, I2 = 0%) was improved in the intravenous beta-blockers group compared to the control group. Subgroup analysis showed that intravenous beta-blockers before PCI decreased the risk of VT/VF and improved LVEF compared to the control group. Furthermore, sensitivity analysis showed that patients with a left anterior descending (LAD) artery lesion had a smaller IS (% of LV) in the intravenous beta-blockers group compared to the control group. Conclusion Intravenous beta-blockers improved the MSI, decreased the risk of VT/VF in the first 24 h, and were associated with increased LVEF at 1 week and 6 months following PCI. In particular, intravenous beta-blockers started before PCI is beneficial for patients with LAD lesions.
PubDate: 2024-08-01
- Acute Biomechanical Effects of Empagliflozin on Living Isolated Human
Heart Failure Myocardium-
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Abstract: Purpose Multiple randomized controlled trials have presented SGLT2 inhibitors (SGLT2i) as novel pharmacological therapy for patients with heart failure, resulting in reductions in hospitalization for heart failure and mortality. Given the absence of SGLT2 receptors in the heart, mechanisms of direct cardioprotective effects of SGLT2i are complex and remain to be investigated. In this study, we evaluated the direct biomechanical effects of SGLT2i empagliflozin on isolated myocardium from end-stage heart failure patients. Methods Ventricular tissue biopsies obtained from 7 patients undergoing heart transplantation or ventricular assist device implantation surgery were cut into 27 living myocardial slices (LMS) and mounted in custom-made cultivation chambers with mechanical preload and electrical stimulation, resulting in cardiac contractions. These 300 µm thick LMS were subjected to 10 µM empagliflozin and with continuous recording of biomechanical parameters. Results Empagliflozin did not affect the maximum contraction force of the slices, however, increased total contraction duration by 13% (p = 0.002) which was determined by prolonged time to peak and time to relaxation (p = 0.009 and p = 0.003, respectively). Conclusion The addition of empagliflozin to LMS from end-stage heart failure patients cultured in a biomimetic system improves contraction and relaxation kinetics by increasing total contraction duration without diminishing maximum force production. Therefore, we present convincing evidence that SGLT2i can directly act on the myocardium in absence of systemic influences from other organ systems.
PubDate: 2024-08-01
- Pharmacokinetic Interactions Between Abiraterone, Apalutamide,
Darolutamide or Enzalutamide and Antithrombotic Drugs: Prediction of
Clinical Events and Review of Pharmacological Information-
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Abstract: Purpose Abiraterone, apalutamide, darolutamide and enzalutamide are second-generation hormone therapies used for advanced prostate cancer; the majority of patients receiving these treatments are elderly, poly-medicated patients. Since their first market authorizations, their pharmacokinetic (PK) characteristics are increasingly well known. A potential risk of drug-drug interaction (DDI), especially with cardiovascular drugs, needs to be considered. In the case of antithrombotics, treatment imbalance can lead to severe consequences. Objectives To describe PK profiles of hormone therapies and antithrombotics and to predict DDIs and potentially related clinical events. Methods PK profiles (CYP450 and P-gp substrate, inducer or inhibitor) are described by cross-referencing data sources (summary of product characteristics, European public assessment reports, PubMed database, Micromedex®, etc.); a description of the potential interactions with anti-cancer drugs for each DDI and related clinical events is provided. We discuss management recommendations, including those set out in international guidelines. Results Antithrombotics are mainly metabolized by CYP 2C9, 2C19 or 3A4. For abiraterone (CYP 2C8, 2D6 inhibitor) and darolutamide (CYP 3A4 inducer), no interaction was identified with antithrombotics. For apalutamide (CYP 2C9, 2C19, 3A4 and P-gp inducer) and enzalutamide (CYP 2C9, 2C19, 3A4 inducer and P-gp inhibitor), several PK interactions were identified with antithrombotics, which could lead to various clinical events (haemorrhage or thromboembolism). Conclusion Numerous interactions are expected between enzalutamide or apalutamide and antithrombotics, for which management should be deployed on a case-by-case basis. PK and pharmaco-epidemiological studies could shed light on whether or not there are clinically significant events related to DDIs with antithrombotics.
PubDate: 2024-08-01
- Levosimendan Reverses Cardiac Malfunction and Cardiomyocyte Ferroptosis
During Heart Failure with Preserved Ejection Fraction via Connexin 43
Signaling Activation-
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Abstract: Purpose In recent decades, the occurrence of heart failure with preserved ejection fraction (HFpEF) has outweighed that of heart failure with reduced ejection fraction by degrees, but few drugs have been demonstrated to improve long-term clinical outcomes in patients with HFpEF. Levosimendan, a calcium-sensitizing cardiotonic agent, improves decompensated heart failure clinically. However, the anti-HFpEF activities of levosimendan and underlying molecular mechanisms are unclear. Methods In this study, a double-hit HFpEF C57BL/6N mouse model was established, and levosimendan (3 mg/kg/week) was administered to HFpEF mice aged 13 to 17 weeks. Different biological experimental techniques were used to verify the protective effects of levosimendan against HFpEF. Results After four weeks of drug treatment, left ventricular diastolic dysfunction, cardiac hypertrophy, pulmonary congestion, and exercise exhaustion were significantly alleviated. Junction proteins in the endothelial barrier and between cardiomyocytes were also improved by levosimendan. Among the gap junction channel proteins, connexin 43, which was especially highly expressed in cardiomyocytes, mediated mitochondrial protection. Furthermore, levosimendan reversed mitochondrial malfunction in HFpEF mice, as evidenced by increased mitofilin and decreased ROS, superoxide anion, NOX4, and cytochrome C levels. Interestingly, after levosimendan administration, myocardial tissue from HFpEF mice showed restricted ferroptosis, indicated by an increased GSH/GSSG ratio; upregulated GPX4, xCT, and FSP-1 expression; and reduced intracellular ferrous ion, MDA, and 4-HNE levels. Conclusion Regular long-term levosimendan administration can benefit cardiac function in a mouse model of HFpEF with metabolic syndromes (namely, obesity and hypertension) by activating connexin 43-mediated mitochondrial protection and sequential ferroptosis inhibition in cardiomyocytes.
PubDate: 2024-08-01
- Impact of Heart Failure History at Baseline on Cardiovascular Effects of
GLP-1 Receptor Agonists in Type 2 Diabetes: a Meta-analysis-
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Abstract: Purpose Effects of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in type-2 diabetes mellitus (T2DM) with or without prior heart failure (HF) have been inconsistent across cardiovascular outcome trials. This study aimed to investigate the impact of HF history at baseline on cardiovascular effects of GLP-1 RAs in T2DM. Methods PubMed, Embase, Web of Science, and clinical trial registries were searched for randomized controlled trials (RCTs) or post hoc analyses (≥ 24 weeks) reporting HF hospitalizations and/or cardiovascular death (HHF/CVD), major adverse cardiovascular events (MACE) comprising of cardiovascular death, myocardial infarction, and stroke in adults with T2DM with or without HF history (PROSPERO:CRD42022367633). Hazard ratios (HRs) in GLP-1RAs versus placebo arms were pooled together using the generic inverse variance method in fixed-effects model. Subgroup analysis was performed. Results We identified 5 eligible studies, pooling data retrieved from six RCTs and 48,489 individuals with T2DM. On pooled analysis, GLP1RA treatment versus placebo significantly reduced risk of HHF/CVD in only T2DM without HF history (HR = 0.84; 95%CI, 0.77–0.91; I2 = 14%; p < 0.001), but not in those with HF history (HR = 0.96; 95%CI, 0.85–1.08; I2 = 14%; p = 0.4) (p-interaction < 0.1). GLP-1RAs reduced incident HHF in T2DM with or without HF history (HR = 0.89; 95%CI, 0.80–0.98; I2 = 41%; p < 0.05) (p-interaction = 0.28). Sensitivity analysis excluding REWIND trial accentuated the impact of baseline HF history on both HHF/CVD and HHF (p-interaction < 0.05). Benefits on MACE with GLP-1RAs were consistently seen in T2DM regardless of HF history (p-interaction = 0.8). Conclusion GLP-1RAs consistently prevented HF hospitalizations and MACE in T2DM regardless of baseline HF history, whereas significant attenuation of benefits on composite HHF/CV death were observed in those with HF history.
PubDate: 2024-08-01
- Comparison of His–Purkinje Conduction System Pacing with
Atrial–Ventricular Node Ablation and Pharmacotherapy in HFpEF Patients
with Recurrent Persistent Atrial Fibrillation (HPP-AF study)-
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Abstract: Background There is currently no particularly effective strategy for patients with persistent atrial fibrillation accompanying heart failure with preserved ejection fraction (HFpEF), especially with recurrent atrial fibrillation after ablation. In this study, we will evaluate a new treatment strategy for patients with persistent atrial fibrillation who had at least two attempts (≧2 times) of radio-frequency catheter ablation but experienced recurrence, and physiologic conduction was reconstructed after atrioventricular node ablation or drug therapy, to control the patient's ventricular rate to maintain a regular heart rhythm, which is called His–Purkinje conduction system pacing (HPCSP) with atrioventricular node ablation. Methods and results This investigator-initiated, multicenter prospective randomized controlled trial aimed to recruit 296 randomized HFpEF patients with recurrent atrial fibrillation. All the enrolled patients were randomly assigned to the pacing group or the drug treatment group. The primary endpoint is differences in cardiovascular events and clinical composite endpoints (all-cause mortality) between patients in the HPCSP and drug-treated groups. Secondary endpoints included heart failure hospitalization, exercise capacity assessed by cardiopulmonary exercise tests, quality of life, echocardiogram parameters, 6-minute walk distance, NT-ProBNP, daily patient activity levels, and heart failure management report recorded by the CIED. It is planned to compete recruitment by the end of 2023 and report in 2025. Conclusions The study aims to determine whether His–Purkinje conduction system pacing with atrioventricular node ablation can better improve patients' symptoms and quality of life, postpone the progression of heart failure, and reduce the rate of rehospitalization and mortality of patients with heart failure. Clinical trial registration number: ChiCTR1900027723, URL:http://www.chictr.org.cn/edit.aspx'pid=46128&htm=4
PubDate: 2024-08-01
- A Comprehensive Review of the Pleiotropic Effects of Ticagrelor
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Abstract: Aims This review summarizes the findings of preclinical studies evaluating the pleiotropic effects of ticagrelor. These include attenuation of ischemia–reperfusion injury (IRI), inflammation, adverse cardiac remodeling, and atherosclerosis. In doing so, it aims to provide novel insights into ticagrelor’s mechanisms and benefits over other P2Y12 inhibitors. It also generates viable hypotheses for the results of seminal clinical trials assessing ticagrelor use in acute and chronic coronary syndromes. Methods and Results A comprehensive review of the preclinical literature demonstrates that ticagrelor protects against IRI in the setting of both an acute myocardial infarction (MI), and when MI occurs while on chronic treatment. Maintenance therapy with ticagrelor also likely mitigates adverse inflammation, cardiac remodeling, and atherosclerosis, while improving stem cell recruitment. These effects are probably mediated by ticagrelor’s ability to increase local interstitial adenosine levels which activate downstream cardio-protective molecules. Attenuation and augmentation of these pleiotropic effects by high-dose aspirin and caffeine, and statins respectively may help explain variable outcomes in PLATO and subsequent randomized controlled trials (RCTs). Conclusion Most RCTs and meta-analyses have not evaluated the pleiotropic effects of ticagrelor. We need further studies comparing cardiovascular outcomes in patients treated with ticagrelor versus other P2Y12 inhibitors that are mindful of the unique pleiotropic advantages afforded by ticagrelor, as well as possible interactions with other therapies (e.g., aspirin, statins, caffeine).
PubDate: 2024-08-01
- The Influence of the FFAR4 Agonist TUG-891 on Liver Steatosis in
ApoE-Knockout Mice-
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Abstract: Background Nonalcoholic fatty liver disease (NAFLD) constitutes an independent risk factor for the development of coronary heart disease. Low-grade inflammation has been shown to play an important role in the development of atherosclerosis and NAFLD. Free fatty acid receptor 4 (FFAR4/GPR120), which is involved in damping inflammatory reactions, may represent a promising target for the treatment of inflammatory diseases. Our objective was to evaluate the effect of TUG-891, the synthetic agonist of FFAR4/GPR120, on fatty liver in vivo. Methods The effect of TUG-891 on fatty liver was investigated in apoE−/− mice fed a high-fat diet (HFD), using microscopic, biochemical, molecular, and proteomic methods. Results Treatment with TUG-891 inhibited the progression of liver steatosis in apoE−/− mice, as evidenced by histological analysis, and reduced the accumulation of TG in the liver. This action was associated with a decrease in plasma AST levels. TUG-891 decreased the expression of liver genes and proteins involved in de novo lipogenesis (Srebp-1c, Fasn and Scd1) and decreased the expression of genes related to oxidation and uptake (Acox1, Ehhadh, Cd36, Fabp1). Furthermore, TUG-891 modified the levels of selected factors related to glucose metabolism (decreased Glut2, Pdk4 and Pklr, and increased G6pdx). Conclusion Pharmacological stimulation of FFAR4 may represent a promising lead in the search for drugs that inhibit NAFLD. Graphical abstract 
PubDate: 2024-08-01
- Antiplatelet Agents and Oral Anticoagulant Use in Patients with Atrial
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Abstract: Introduction People with atrial fibrillation (AF) frequently have competing mechanisms for ischaemic stroke, including extracranial carotid atherosclerosis. The objective of this study was to determine associations between use of oral anticoagulants (OACs) plus antiplatelet agents (APA) after ischaemic stroke and outcomes for patients with AF and carotid artery disease. Patients and Methods A retrospective cohort study was conducted. Participants receiving OACs with or without APA were propensity score–matched for age, sex, ethnicity, co-morbidities and presence of cardiac and vascular implants and grafts. Outcomes were 1-year mortality, recurrent stroke and major bleeding. Results Of 5708 patients, 24.1% (n=1628) received non-vitamin K antagonist OACs (NOACs) with no APA, 26.0% (n=1401) received NOACs plus APA, 20.7% (n=1243) received warfarin without APA and 29.2% (n=1436) received warfarin plus APA. There was no significant difference in risk of recurrent stroke between the groups. Compared to receiving NOACs without APA, receiving warfarin plus APA was associated with a higher risk of mortality (hazard ratio (HR) 1.51 (95% confidence interval (CI) 1.20, 1.89)) and major bleeding (HR 1.66 (95% CI 1.40, 1.96)). Receiving NOACs plus APA was also associated with a higher risk of major bleeding compared to NOACs without APA (HR 1.27 (95% CI 1.07, 1.51), respectively). Conclusions The results suggest for patients with AF and carotid artery disease after ischaemic stroke, receiving NOACs without APA is associated with a lower risk of major bleeding with no negative impact on recurrent stroke or mortality. Evidence from randomised trials is needed to confirm this finding.
PubDate: 2024-08-01
- Acute Hemodynamic Effects of Empagliflozin: Are They Relevant to the
Clinical Practice'-
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PubDate: 2024-06-18
DOI: 10.1007/s10557-024-07598-6
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