Cardiovascular & hematological disorders drug targets最新文献

{"title":"Cost-effectiveness of Empagliflozin in Chronic Heart Failure: A Markov Model-based Analysis in Uzbekistan.","authors":"Nargiza Sultanbayeva, Shakhnoz Umarova, Shokhista Iskandarova, Guzal Mullabaeva, Shohista Mukhamedova","doi":"10.2174/011871529X495679261009064725","DOIUrl":"https://doi.org/10.2174/011871529X495679261009064725","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic Heart Failure (CHF) is a major public health challenge associated with high morbidity, mortality, and healthcare costs. Empagliflozin has demonstrated clinical benefits across the spectrum of heart failure; however, evidence on its economic value in low- and middle-income countries remains limited. To evaluate the cost-effectiveness of adding empagliflozin to standard therapy for patients with chronic heart failure from the perspective of the healthcare payer.</p><p><strong>Materials and methods: </strong>A cohort-based Markov model with a 3-month cycle length and a 20- year time horizon was developed to simulate disease progression in CHF. Health states included no complications, cardiovascular complications, renal complications, and death. Outcomes were measured in Life Years (LYs), Quality-Adjusted Life Years (QALYs), total costs, and Incremental Cost-Effectiveness Ratios (ICERs). Both deterministic and probabilistic sensitivity analyses were conducted.</p><p><strong>Results: </strong>Quality-adjusted life expectancy increased from 11.595 to 12.224 QALYs. Total discounted costs were 48,133,588 UZS for empagliflozin versus 43,261,361 UZS for standard therapy. The Incremental Cost-Effectiveness Ratio (ICER) was 7,738,951 UZS per QALY gained, which was substantially below the national willingness-to-pay threshold of 141.6 million UZS.</p><p><strong>Discussions: </strong>Since the ICER for empagliflozin compared with placebo is substantially lower than the calculated willingness-to-pay threshold, empagliflozin can be considered a costeffective treatment option.</p><p><strong>Conclusions: </strong>Adding empagliflozin to standard therapy for CHF is a cost-effective intervention in the Republic of Uzbekistan and provides meaningful clinical and economic benefits.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149221137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Gut Microbiome-derived Trimethylamine N-oxide and Short-chain Fatty Acids in Heart Failure Outcomes: A Narrative Review.","authors":"Sidhartha Gautam Senapati, Debabrata Mukherjee","doi":"10.2174/011871529X494489260914114458","DOIUrl":"https://doi.org/10.2174/011871529X494489260914114458","url":null,"abstract":"<p><strong>Introduction: </strong>HF continues to be a serious medical problem all over the world, resulting in significant morbidity and mortality despite advancements in therapeutic strategies. Current research indicates the involvement of the gut-heart axis in HF. Gut microbiome metabolites, including TMAO and SCFAs, affect heart structure, function, and outcomes.</p><p><strong>Methods: </strong>We conducted a review of experimental, observational, and clinical studies to evaluate alterations in gut microbiota and metabolome in patients with HF. The literature was analyzed to study mechanisms of observed alterations, clinical associations, their potential role as biomarkers, and therapeutic strategies associated with TMAO and SCFAs.</p><p><strong>Results: </strong>Higher TMAO levels generated by gut microbes from choline- and L-carnitinecontaining foods contributed to increased mortality, inflammation, and myocardial injury in HF. Conversely, SCFAs, such as acetate, propionate, and butyrate, produced during bacterial fermentation of dietary fibers promoted cardioprotection by maintaining gut integrity, enhancing immune and metabolic pathways, and promoting energy utilization in HF. In HF, the gut microbiome showed lower species diversity, reduced abundance of beneficial organisms responsible for SCFA production, and enrichment of microorganisms capable of producing TMAO. Diet played an essential role, with increased intake of dietary fiber leading to enhanced SCFAs levels and a high choline and fat content causing elevated TMAO levels.</p><p><strong>Discussion: </strong>Our analysis demonstrates that gut microbiome-derived metabolites exert both harmful and beneficial effects in HF. Gut-based dietary and microbiome modulation therapy might prove useful, although well-designed prospective clinical trials are needed to confirm its efficacy.</p><p><strong>Conclusion: </strong>Gut microbiome-derived metabolites, particularly TMAO and SCFAs, are promising mechanistic and prognostic markers in HF. However, routine clinical measurement and microbiome- targeted therapy require prospective validation, standardized assays, and interventional trials before implementation in HF care.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SGLT-2 Inhibitors and GLP-1 Receptor Agonists in Managing Metabolic Syndrome Among Patients with Type 2 Diabetes Mellitus - A Narrative Review.","authors":"Hadeeqah Zayaan Riaz Ahamed, Sulthan Al Rashid, Rajkapoor Balasubramanian, Naina Mohamed Pakkir Maideen","doi":"10.2174/011871529X480529260812061106","DOIUrl":"https://doi.org/10.2174/011871529X480529260812061106","url":null,"abstract":"<p><strong>Introduction: </strong>Metabolic syndrome (MetS) is a cardiometabolic disorder defined by the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III). It is closely linked with type 2 diabetes mellitus (T2DM). The main features of this condition include central obesity, high triglyceride levels, low high-density lipoprotein cholesterol (HDL-C), high blood pressure, and impaired fasting glucose. The bidirectional relationship between MetS and T2DM significantly increases the risk of cardiovascular and metabolic diseases. This review examines the role of sodium-glucose co-transporter-2 (SGLT-2) inhibitors and glucagon-like peptide- 1 (GLP-1) receptor agonists in addressing the different issues associated with MetS. It also discusses their effect on blood sugar control and their benefits for heart and kidney health in people with T2DM.</p><p><strong>Methods: </strong>This study conducted a thorough review of clinical trials, meta-analyses, and guideline recommendations to gather evidence about how SGLT-2 inhibitors and GLP-1 receptor agonists work and their benefits in managing MetS in T2DM.</p><p><strong>Results: </strong>Both SGLT-2 inhibitors and GLP-1 receptor agonists have shown improvements in body weight, lipid levels, blood pressure control, and blood sugar management. Furthermore, there is strong evidence supporting their protective effects on heart and kidney health, underlining their importance as key treatments for high-risk patients with T2DM and MetS.</p><p><strong>Discussion: </strong>Several clinical studies have examined the role of SGLT-2 inhibitors and GLP-1 receptor agonists in addressing MetS, including central obesity, hypertriglyceridemia, low HDL levels, fasting hyperglycaemia, and hypertension.</p><p><strong>Conclusion: </strong>SGLT-2 inhibitors and GLP-1 receptor agonists form an effective strategy for managing MetS in the context of T2DM. Their broad effects on metabolism and well-known heart and kidney benefits make them vital parts of modern treatment for cardiometabolic conditions.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Silent Vascular Shift: Endothelial Dysfunction and Cardiovascular Risk in Menopausal Women.","authors":"Arti Saini, Inderjeet Verma, Ruby Bhatia","doi":"10.2174/011871529X448903260820091109","DOIUrl":"https://doi.org/10.2174/011871529X448903260820091109","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular disease (CVD) is the leading cause of death among women worldwide, with the risk significantly increasing after menopause. Hormonal changes during menopause influence the pathophysiology of endothelial dysfunction and atherosclerosis. Lowering levels of estrogen causes vascular hardening, decreased nitric oxide bioavailability, and a sharpened inflammatory response, which may contribute to increased cardiovascular risk during middle life in women. To review the role of endothelial health in cardiovascular risk among postmenopausal women, discuss the underlying mechanisms, and explore current management strategies aimed at reducing the incidence and impact of coronary artery disease.</p><p><strong>Methods: </strong>A comprehensive literature search via PubMed, Scopus, and Web of Science (2015-- 2025) via search strings (menopause OR perimenopause OR postmenopause) AND (endothelial dysfunction OR endothelial function OR nitric oxide OR vascular inflammation) AND (cardiovascular disease OR atherosclerosis OR cardiovascular risk) was conducted, with a focus on large epidemiological cohorts, randomized controlled trials, and mechanistic studies.</p><p><strong>Results: </strong>Postmenopausal women have a higher risk of developing CVD, and they have comparatively deteriorated endothelial dysfunction.</p><p><strong>Discussion: </strong>Compared with men, women experience unique changes in lipid profiles, metabolic syndrome, and fat distribution during and after menopause, which increase their cardiovascular risk. Traditional risk factors, such as hypertension, diabetes, smoking, physical inactivity, and obesity, also affect women differently. Hormonal changes during menopause further influence the pathophysiology of endothelial dysfunction and atherosclerosis. Lifestyle interventions, such as structured exercise, show promise for reducing risk, but evidence supporting the use of phytoestrogens and nutraceuticals is limited and heterogeneous.</p><p><strong>Conclusion: </strong>Menopause is a high-risk critical phase of increased cardiovascular risk through endothelial dysfunction. Multifaceted prevention measures, such as primary early intervention and individualized responses, are necessary to minimize long-term morbidity and mortality.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Venous Congestion in Metabolic Heart Disease: Potential Indirect Role of Dual Incretin Agonists.","authors":"Sidhartha Gautam Senapati","doi":"10.2174/011871529X502187260803101832","DOIUrl":"https://doi.org/10.2174/011871529X502187260803101832","url":null,"abstract":"<p><strong>Introduction: </strong>Venous congestion is responsible for symptoms, organ dysfunction, and negative outcomes in heart failure. In obesity-related Heart Failure (HF) with preserved ejection fraction (HFpEF), metabolic dysfunction, inflammation, endothelial damage, and sodium retention might exacerbate venous congestion.</p><p><strong>Method: </strong>This structured narrative review provides an overview of the association between metabolic dysfunction, venous congestion, and incretin-based treatment in heart failure. Relevant literature was reviewed with special focus on original clinical trials, mechanism-of-action studies, and studies with venous congestion-related endpoints or surrogates.</p><p><strong>Results: </strong>Beneficial effects of GLP-1 receptor agonists and dual GIP/GLP-1 receptor agonists in obesity-related HFpEF patients have been shown in weight loss, symptom improvement, improvement in exercise tolerance, and reduced cardiovascular and heart failure outcomes. Nevertheless, there is still no evidence showing the direct effect of these agents in reducing venous pressure, preload, and systemic venous congestion.</p><p><strong>Discussion: </strong>The current available literature can explain the indirect mechanism by which weight loss, hypotensive action, improved insulin resistance, reduction of ectopic fat, and antiinflammatory properties improve the cardiometabolic physiology of HFpEF patients.</p><p><strong>Conclusion: </strong>Although the use of dual incretin agonists represents a novel therapeutic approach for obesity-related HFpEF, the ability of these drugs to decongest the venous system directly is not yet proven. Further studies are required to evaluate venous congestion endpoints such as right-sided filling pressures, venous Doppler indices, natriuretic peptides, need for diuretics, and VExUS score.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating AI in Cardiovascular Systems: Innovations in Diagnosis, Risk Prediction, and Management.","authors":"Srushti Bhupesh Patil, Yash Pramod Patil, Kunal Sharad Patil, Nagaraju Bandaru, Makarand Suresh Gambhire","doi":"10.2174/011871529X414660251209135356","DOIUrl":"https://doi.org/10.2174/011871529X414660251209135356","url":null,"abstract":"<p><p>Worldwide, cardiovascular diseases remain the leading contributors to illness and death, which hinders rapid diagnosis and efficient treatment. Recent developments in artificial intelligence (AI) have transformed cardiovascular medicine by enabling the integration and analysis of large and complex data sets from portable sensors, electronic health records, and medical images. AI algorithms, such as machine learning and deep learning models, excel in detecting detailed patterns and forecasting disease progression, improving risk assessment and diagnostic accuracy. These technologies enable the early diagnosis of disorders such as heart failure, arrhythmias, and coronary artery disease, resulting in more personalized treatment approaches and better patient outcomes. Automated image processing reduces human error and simplifies procedures, while continuous cardiac function can be monitored remotely. As AI systems advance further, they have the potential to revolutionize clinical decision-making by providing real-time information and predictive analyses that anticipate adverse cardiac events. Despite ongoing challenges with data quality, model transparency, and ethical considerations, the use of AI in cardiovascular care is expected to optimize resource allocation, reduce healthcare costs, and ultimately improve survival rates. Adopting this cutting-edge technology represents a crucial step toward a more precise, proactive, and patient-centered strategy with significant potential.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148610832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage Polarization and Endothelial Dysfunction in Response to Cigarette Smoke and Ketone Body Administration.","authors":"Meity Ardiana, Inna Maya Sufiyah, Fita Triastuti, Alivia Retra Kusumowardani","doi":"10.2174/011871529X437571251214200529","DOIUrl":"https://doi.org/10.2174/011871529X437571251214200529","url":null,"abstract":"<p><strong>Introduction: </strong>Cigarette smoking promotes endothelial dysfunction through inflammation and macrophage polarization toward a pro-inflammatory M1 phenotype. Ketone bodies have been reported to have vascular benefits and may represent a therapeutic approach by modulating macrophage responses. This study investigated the impact of cigarette smoke on macrophage polarization and whether ketone body administration could alter these effects in an animal model.</p><p><strong>Methods: </strong>A randomized post-test-only control group design was conducted in 20 male Wistar rats assigned to four groups: control, smoke-exposed without intervention, and smoke-exposed treated with ketone bodies at low (1.5 g/kg/day) or high (6 g/kg/day) doses. Wistar rats were exposed to cigarette smoke (40 cigarettes/day) for 4 weeks, followed by ketone body administration. Macrophage polarization was assessed by calculating the M1/M2 ratio.</p><p><strong>Results: </strong>Cigarette smoke exposure increased M1 macrophage expression and produced an M1- dominant phenotype compared with controls (K⁷ 14.11 ± 10.15 vs. K- 7.00 ± 9.93, p = 0.109). Ketone body administration showed a trend toward reduced M1 and M2 macrophage counts and lowered the M1/M2 ratio, with the lowest ratio observed at the highest ketone dose (K⁷ 6.96 ± 8.55 vs P2 2.88 ± 2.86, p = 0.348).</p><p><strong>Discussion: </strong>Cigarette smoke promoted M1-dominant polarization, supporting its proinflammatory role in endothelial dysfunction. Ketone body administration could shift the balance toward a more anti-inflammatory profile, with higher doses favoring M2 activity.</p><p><strong>Conclusion: </strong>These findings provide initial evidence that ketone bodies may affect macrophage polarization under cigarette smoke exposure, supporting their potential as modulators of vascular inflammation.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148610871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanotechnology - Driven Innovations in Anticoagulant Delivery and Antidote Development for Hemostasis Regulation.","authors":"Jitendra Maity, Sushil Kumar Singh, Sovan Lal Pal, Amlan Bishal","doi":"10.2174/011871529X423173251208100541","DOIUrl":"https://doi.org/10.2174/011871529X423173251208100541","url":null,"abstract":"<p><strong>Introduction: </strong>Hemostasis is a complex physiological mechanism that maintains normal blood flow and prevents excessive bleeding after vascular injury. Anticoagulant drugs are widely used to prevent systemic embolism, stroke, and recurrent venous thromboembolism (VTE). Conventional therapies such as heparins and vitamin K antagonists (VKAs) face challenges including parenteral administration, toxicity, and poor patient compliance, leading to an increased need for innovative delivery systems and reversal strategies.</p><p><strong>Methods: </strong>This review synthesises current evidence on nanotechnology-driven drug delivery systems (DDS) and antidote development for anticoagulants, drawing from recent preclinical and clinical studies. The focus is on liposomes, ethosomes, cubosomes, hydrogels, solid lipid nanoparticles (SLnPs), self-nanoemulsifying drug delivery systems (SNEDDS), and emerging antidotes such as idarucizumab, andexanet alfa, and ciraparantag.</p><p><strong>Results: </strong>Nanocarrier systems enhance anticoagulant therapy by improving solubility, stability, targeted delivery, and sustained release. Oral DDS approaches, including solid dispersions, fastdissolving platforms, and SNEDDS, show potential to replace invasive parenteral regimens. Antidote development has advanced rapidly, with idarucizumab approved for dabigatran reversal, andexanet alfa for factor Xa inhibitors, and ciraparantag demonstrating broad-spectrum activity in development.</p><p><strong>Discussion: </strong>Nanotechnology-based DDS address long-standing limitations of conventional anticoagulants, improving patient compliance and therapeutic safety. However, cost, immunogenicity, clearance pathways, and regulatory challenges remain barriers to widespread adoption. Antidotes, while effective, raise concerns about accessibility and affordability in low-resource settings.</p><p><strong>Conclusion: </strong>This review highlights the novelty of integrating nanotechnology-based delivery systems with targeted antidote strategies. Such convergence offers a patient-centred, safer, and more effective framework for anticoagulant therapy, while underscoring the need for future research in clinical translation, cost-effectiveness, and long-term safety.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148610876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Marine Products as Therapeutics for Atherosclerosis Through Modulation of Gut-heart Axis.","authors":"Fatima Khan, Kalyani Barve","doi":"10.2174/011871529X473049260710110225","DOIUrl":"https://doi.org/10.2174/011871529X473049260710110225","url":null,"abstract":"<p><strong>Introduction: </strong>A bidirectional relationship between cardiovascular health and gut microbiota, established by the gut-heart axis, is a major contributor to the development or prevention of atherosclerosis. Chronic immune-inflammatory and fibro-proliferative atherosclerosis remains a significant global cause of morbidity and death. Bile acids, Short-Chain Fatty Acids (SCFAs), and trimethylamine-N-oxide (TMAO) are examples of gut-derived metabolites that majorly impact inflammation, endothelial dysfunction, and plaque formation.</p><p><strong>Methods: </strong>Data were collected using keywords like 'marine', 'atherosclerosis', 'gut dysbiosis', 'short-chain fatty acids', and 'gut-heart axis' from databases such as PubMed, ScienceDirect, and Scopus. Relevant studies were analysed to evaluate mechanisms linking gut dysbiosis, metabolite modulation, and prevention of atherosclerosis.</p><p><strong>Results: </strong>Marine-derived bioactive compounds include peptides, carotenoids (Fucoxanthin), polysaccharides (Fucoidan, Alginate), and sterols (Fucosterol), which have anti-inflammatory, lipidlowering, and microbiome-balancing properties, making them promising therapeutic options. These bioactive compounds prevent the progression of atherosclerosis by lowering TMAO levels, increasing SCFA synthesis, improving lipid metabolism, and regulating genes associated with cholesterol metabolism.</p><p><strong>Discussion: </strong>The gut-heart axis is a critical contributor to the development and progression of atherosclerosis. Marine natural products have therapeutic potential in the management of atherosclerosis since they act as modulators of gut microbiota and cardiovascular health.</p><p><strong>Conclusion: </strong>Marine-derived natural products offer a novel therapeutic strategy for prevention and management of atherosclerosis by targeting the gut-heart axis.</p>","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety and Efficacy of Ticagrelor with Aspirin DAPT vs. Aspirin Alone in Patients Undergoing CABG Following ACS: A Systematic Review and Meta-Analysis.","authors":"Kunal Mahajan, Deep Dutta, A B M Kamrul-Hasan, Nitin Mahajan, Jaibharat Sharma, Surender Himral, Shekhar Vohra, Akshyaya Pradhan","doi":"10.2174/011871529X488257260710041631","DOIUrl":"https://doi.org/10.2174/011871529X488257260710041631","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;It remains uncertain whether Dual Antiplatelet Therapy (DAPT) or aspirin alone is better for patients following Coronary Artery Bypass Grafting (CABG) post-Acute Coronary Syndrome (ACS). Currently available Systematic Reviews and Meta-Analyses (SRMA) are limited to the analysis of different combinations of DAPT across various clinical conditions of cardiovascular disease and are not restricted to CABG post-ACS. This SRMA aimed to evaluate the safety and efficacy of Ticagrelor with Aspirin (TA) versus aspirin alone in patients who underwent CABG following ACS.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Electronic databases were searched for studies involving patients who underwent CABG after ACS and received TA in the intervention arm versus aspirin in the control arm. The primary outcomes were death and major bleeding. The secondary outcomes were Composite Cardiovascular Outcomes (CCO), Myocardial Infarction (MI), stroke, saphenous vein graft patency, revascularization, and side effects.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Data from five studies (4 RCTs and one cohort study; 9,659 patients) were analysed. The risk of death [OR 1.18 (95% CI 0.60-2.28); P =0.63; I²=46%] and major bleeding [OR 1.65 (95% CI 0.95-2.86); P =0.07; I²=44%] was numerically higher with TA than with aspirin alone, although these differences were not statistically significant. Composite cardiovascular outcomes [OR 0.96 (95% CI 0.74-1.24); P=0.74; I²=0%], myocardial infarction [OR 0.99 (95% CI 0.67- 1.46); P =0.94; I²=0%], stroke [OR 0.60 (95% CI 0.33-1.08); P =0.09; I²=0%], saphenous vein graft patency [OR 1.75 (95% CI 0.93-3.27); P =0.08; I²=75%], and revascularisation [OR 1.21 (95% CI 0.46-3.15); P =0.70; I²=49%] were similar between the two groups.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;These findings suggest that the theoretical advantage of intensified platelet inhibition with ticagrelor-based DAPT does not translate into improved clinical outcomes in patients undergoing CABG after ACS. The pathophysiology of graft failure, which is often driven by technical factors and progressive atherosclerosis rather than platelet-mediated thrombosis alone, may partly explain the absence of additional benefit from potent dual antiplatelet therapy. At the same time, the observed numerical increase in bleeding events highlights the potential trade-off associated with more aggressive platelet inhibition in the postoperative setting.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;In patients undergoing CABG following ACS, ticagrelor-aspirin DAPT does not confer significant improvement in ischemic outcomes compared with aspirin monotherapy and may increase bleeding risk. Aspirin alone appears to provide comparable protection, supporting its continued role as the cornerstone of antiplatelet therapy after surgical revascularization. Nevertheless, antiplatelet therapy after CABG should be individualised according to each patient's ischaemic/thrombotic and bleeding risk rather than applied ","PeriodicalId":93925,"journal":{"name":"Cardiovascular & hematological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148521387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}