Cardiovascular & hematological agents in medicinal chemistry最新文献

{"title":"Novel Pathway and Recent Advances for Targeting Sickle Cell Anemia through Novel Drug Delivery System.","authors":"Savita Chouhan, Ajazuddin, Parag Jain","doi":"10.2174/0118715257325911241113075950","DOIUrl":"https://doi.org/10.2174/0118715257325911241113075950","url":null,"abstract":"<p><p>Red blood cells with sickle cell anemia (SCA) have an irregular shape, and it is a genetic blood condition that can cause several problems and shorten life expectancy. Traditional treatments have focused on symptom management, but recent advancements in drug delivery systems offer promising pathways for targeted therapies. This abstract explores novel approaches to combat SCA through innovative drug delivery systems, gene therapy, and new pharmaceutical interventions. One novel pathway for targeting SCA involves utilizing advanced drug delivery systems to enhance the effectiveness of therapeutic agents. Nanotechnology-based delivery systems, such as nanoparticles and liposomes, offer precise drug targeting, controlled release, and improved bioavailability. These systems can encapsulate anti-sickling agents, like hydroxyurea, and enable their specific delivery to affected cells, reducing side effects and enhancing therapeutic outcomes. Additionally, therapy has become a ground-breaking method of treating SCA. CRISPR/Cas9 technology presents a groundbreaking opportunity to correct the genetic mutation responsible for sickle hemoglobin production. By precisely editing the HBB gene, which encodes the abnormal hemoglobin, researchers aim to restore normal hemoglobin expression, potentially offering a curative treatment for SCA. Furthermore, recent advancements in drug development have led to the discovery of promising candidates targeting specific pathways involved in SCA pathophysiology. Experimental drugs, such as voxelotor and crizanlizumab focus on modifying hemoglobin properties or inhibiting cell adhesion, respectively, thereby preventing sickle cell-related complications and reducing vaso-occlusive crisis frequency.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775463","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":"Anti-thrombotic Mechanisms of Echinochrome A on Arterial Thrombosis in Rats: In-Silico, In-Vitro and In-Vivo Studies.","authors":"Marina Lotfy Khalaf, Amel Mahmoud Soliman, Sohair Ramadan Fahmy, Ayman Saber Mohamed","doi":"10.2174/0118715257332064241104114546","DOIUrl":"https://doi.org/10.2174/0118715257332064241104114546","url":null,"abstract":"<p><strong>Background: </strong>Arterial thrombosis is one of the most significant healthcare concerns in the world. Echinochrome A (Ech-A) is a natural quinone pigment isolated from sea urchins. It has a variety of medicinal values associated with its antioxidant, anticancer, antiviral, anti-diabetic, and cardio-protective activities.</p><p><strong>Objective: </strong>The current study aims to investigate the effect and mechanism of Ech-A to inhibit thrombus formation induced by ferric chloride in rats.</p><p><strong>Methods: </strong>Twenty-four rats were assigned into four groups (n= 6); sham and thrombotic model groups were orally administered 2% DMSO, while the other groups were treated with two dosages of Ech-A (1 and 10 mg/kg, body weight). After seven days of administration, all groups were exposed to 50% ferric chloride for 10 min, except the sham group exposure to normal saline.</p><p><strong>Results: </strong>The molecular docking showed the free binding energies of Ech-A and vitamin K (Vit. K) with Vit. K epoxide reductase were -8.5 and -9.8 kcal/mol, which confirm the antithrombotic activity of Ech-A. The oral administration of Ech-A caused a significant increase in partial thromboplastin time, prothrombin time, clotting time, platelet count, fibrinogen levels, factor VIII, glutathione reduced, catalase, nitric oxide, and glutathione S-transferase. While white blood cells count, calcium level, and malondialdehyde concentration significantly decreased. The histological examination revealed a definite improvement in the carotid and cardiac tissues in the Ech-A groups.</p><p><strong>Conclusion: </strong>The study results showed that Ech-A prevented thrombosis by several mechanisms, including chelating calcium ions, increasing the NO concentration, suppressing oxidative stress, and antagonizing Vit. K.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142634552","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":"Cardio-metabolic Disorders Affected by Genetic Polymorphisms Related to Premature Menopause.","authors":"Mohammad Reza Mirinezhad, Hamideh Safarian Bana, Maliheh Aghsizadeh, Mohammad Amin Mohammadi, Hamideh Ghazizadeh, Ali Ebrahimi Dabagh, Sayyedeh Helya Mir Nourbakhsh, Hassan Kiani Shahvandi, Alireza Ghodsi, Mahdie Aghsizadeh, Faezeh Taghipour, Elahe Hasanzadeh, Nazanin Sheikh Andalibi, Hamed Khedmatgozar, Gordon A Ferns, Tayebeh Hamzehloei, Alireza Pasdar, Majid Ghayour-Mobarhan","doi":"10.2174/0118715257297949241023053739","DOIUrl":"10.2174/0118715257297949241023053739","url":null,"abstract":"<p><strong>Background: </strong>Premature menopause (PM) is defined as the end of ovulation before the age of 40 years, a condition commonly referred to as primary ovarian insufficiency. It has been shown there is an association between early menopause and a high risk of cardiovascular disease.</p><p><strong>Aim: </strong>This study aimed to evaluate the effect of genetic polymorphisms related to premature menopause on cardio-metabolic disorders Objective: We aimed to investigate the single nucleotide polymorphisms associated with PM and the risk of cardio-metabolic disorders in the MASHAD cohort study.</p><p><strong>Methods: </strong>In this cross-sectional study, a total of 117 women with PM were recruited and compared with 183 healthy women. All participants were assessed for anthropometric indices and genotyped for eight selected polymorphisms within seven different genes.</p><p><strong>Results: </strong>A significant difference was observed in physical activity level (PAL) between the groups. Individuals with rs4806660 CC genotype had a 3.63-fold increased risk of metabolic syndrome. Moreover, individuals with a TT genotype of the rs2303369 polymorphism had a 3.11-- fold increased risk of obesity.</p><p><strong>Conclusion: </strong>Our findings showed that genetic variations are risk factors related to cardio- metabolic disorders in women with premature menopause.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142592416","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":"Factor Xa Inhibitors and Low Molecular Weight Heparins in Perioperative Surgical Thromboprophylaxis: A Network Meta-Analysis.","authors":"Vijeta Bajpai, Tejas Patel, Priyanka Dwivedi, Ankita Kabi, Amrita Mishra, Ravi Shankar Sharma, Astha Gupta, Pradeepika Gangwar, Richa Agarwal, Surekha Kishore","doi":"10.2174/0118715257331706240919172310","DOIUrl":"https://doi.org/10.2174/0118715257331706240919172310","url":null,"abstract":"<p><strong>Background: </strong>venous thromboembolism (VTE) prophylaxis is crucial for reducing the risk of deep vein thrombosis (DVT) and pulmonary embolism (PE). This network metaanalysis was carried out to determine the most effective intervention among selective Xa inhibitors and low molecular weight heparins (LMWHs) for perioperative surgical thromboprophylaxis in major abdominal, pelvic, lumbar spine, and lower limb surgeries.</p><p><strong>Methods: </strong>A systematic literature search was conducted for randomized controlled trials (RCTs) comparing selective factor Xa inhibitors, LMWHs, and placebo as thromboprophylaxis agents in major abdominal, pelvic, lumbar spine, and lower limb surgeries. A Bayesian network metaanalysis was performed to compare all interventions for the risk of developing DVT, VTE, major VTE, total bleeding, and major bleeding. The surface under the cumulative ranking curves was used to rank all interventions.</p><p><strong>Results: </strong>Of 1788 retrieved references, 42 RCTs comparing 11 anticoagulants were included. As compared to enoxaparin, the risk of DVT was significantly reduced in patients treated with fondaparinux [RR: 0.53 (95% CrI: 0.31, 0.93)] and rivaroxaban [RR: 0.42 (95% CrI: 0.27, 0.64)]; VTE in patients treated with bemiparin [RR: 0.09 (95% CrI: 0, 0.7)], edoxaban [RR: 0.43 (95% CrI: 0.18, 0.96)], fondaparinux [RR: 0.55 (95% CrI: 0.34, 0.91)] and rivaroxaban [RR: 0.56 (95% CrI: 0.34, 0.85)]; major VTE in patients treated with rivaroxaban [RR: 0.26 (95% CrI: 0.11, 0.6)]. According to the surface under the cumulative ranking curves (SUCRA) value, fondaparinux and bemiparin increase the risk of serious bleeding more than other factor Xa inhibitors and LMWHs.</p><p><strong>Conclusion: </strong>Rivaroxaban, fondaparinux, edoxaban, and bemiparin are superior perioperative thromboprophylaxis agents than enoxaparin in major surgeries. Fondaparinux and bemiparin have shown the highest risk of major bleeding compared to other factor Xa inhibitors and LMWHs.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367866","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":"Iron Deficiency and its Relationship with Chronic Heart Failure- A Review.","authors":"Arshdeep Kaur, Ranjeet Kumar","doi":"10.2174/0118715257313681240913112017","DOIUrl":"https://doi.org/10.2174/0118715257313681240913112017","url":null,"abstract":"<p><p>Iron Deficiency (ID) is common in patients with cardiovascular disease. More than 64 million patients are suffering from chronic heart failure. The prevalence of iron deficiency increases with the severity of cardiac and renal dysfunction and is probably more common amongst women.</p><p><strong>Aim: </strong>This review article discusses multifactorial pathophysiology, the relationship between clinical characteristics, functional and absolute ID, and the advantages of medicinal intervention in chronic heart failure (CHF). It also covers how iron shortage affects other body parts.</p><p><strong>Approach: </strong>The most recent publications that included substantial scientific data on the connection between CHF and ID, with or without anaemia, were selected.</p><p><strong>Discussion: </strong>Complex physiopathological interactions, including higher hepcidin levels, systemic inflammation, and activation of the renin-angiotensin-aldosterone system, have been identified in these patients. These mechanisms exacerbate the outcomes for patients by amplifying the severity of anemia, chronic heart failure (CHF), and Chronic kidney disease (CKD). Research in this area has been limited and has shown inconsistent findings. Still, it has also examined evidence-based treatment approaches and diagnostic guidelines, especially in relation to iron supplements and erythropoietin-stimulating medications.</p><p><strong>Conclusion: </strong>Anemia is a frequent chronic heart failure consequence and a poor prognostic factor. We still don't completely understand the many complex causes of anemia. Iron deficiency screening is highly recommended for people with cardiac ailments because of its significance for their prognoses. Due to the paucity of research proving its effectiveness, the high incidence of unfavourable gastrointestinal side effects, and the prolonged length of time required for treatment to boost haemoglobin levels, an oral iron supplement is not advised for people with chronic heart failure. An insufficient amount of iron not only impacts the heart but also various other body components.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334357","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 Effect of CD31 on Coronary Collateral Development.","authors":"Huseyin Akcali, Mustafa Begenc Tascanov, Kenan Toprak, Halil Fedai, Asuman Bicer, İbrahim Halil Altiparmak, Zulkif Tanriverdi, Recep Demirbag, Ismail Koyuncu","doi":"10.2174/0118715257300068240819071920","DOIUrl":"https://doi.org/10.2174/0118715257300068240819071920","url":null,"abstract":"<p><strong>Background: </strong>Coronary collaterals are the feeding bridges between the main epicardial arteries, and research has shown that this collateral development plays a crucial role in myocardial performance, especially in patients with coronary artery disease. However, the evolution of these collaterals has not been fully explained.</p><p><strong>Objective: </strong>In this study, we aimed to reveal the effect of CD31 on coronary collateral development.</p><p><strong>Methods: </strong>As a result of coronary angiography performed in our clinic, 89 patients with coronary artery disease and 90 patients with normal coronary arteries were included in the study. Collateral development degrees were recorded from the angiographic images of the subjects. CD31 values were compared between the group with coronary artery disease and the control group. In addition, the coronary artery disease group was divided into subgroups according to the collateral development in terms of good collateral development and poor collateral development, and the factors that may affect the collateral development were tried to be determined.</p><p><strong>Results: </strong>CD31 levels were significantly higher in the group with coronary artery disease compared to the control group (p <0.001). In addition, CD31 levels in the subgroup with good collateral were significantly higher than in the group with weak collateral (p <0.001). In the correlation analysis, a significant positive correlation was found between serum CD31 level and SYNTAX score, age, glucose, and rentrop grade. Multivariate logistic regression analysis showed CD31 to be an independent predictor of good coronary collateral development.</p><p><strong>Conclusion: </strong>CD31, a marker of angiogenesis, may be involved in coronary collateral development.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142115916","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":"WITHDRAWN: Pyridazine Derivatives: Molecular Docking ADMET Prediction and Synthesis for Antihypertensive Activity","authors":"Gagandeep Kaur, Ankur Thakur, Lovish Sharma, Nidhi Rani","doi":"10.2174/0118715257316272240807075752","DOIUrl":"10.2174/0118715257316272240807075752","url":null,"abstract":"<p><p>The article has been withdrawn at the request of the authors of the journal Cardiovascular & Hematological Agents in Medicinal Chemistry.</p><p><p>Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.</p><p><p>The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php</p><p><strong>Bentham science disclaimer: </strong>It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142006103","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":"Mavacamten: A Review of a Novel Therapeutic Approach for Hypertrophic Cardiomyopathy.","authors":"Ayesha Abdul Qadir Memon, Areeba Shamim, Sanoober Mirza, Muhammad Osama, Iyad Naeem Muhammad, Calvin R Wei","doi":"10.2174/0118715257283752240325082733","DOIUrl":"https://doi.org/10.2174/0118715257283752240325082733","url":null,"abstract":"Hypertrophic Cardiomyopathy (HCM) is a heart disease that can cause left ventricular hypertrophy, arrhythmias, heart failure, and sudden cardiac death. Currently, pharmacological treatment is limited and ineffective. Mavacamten (CamzyosTM) is a cardiac myosin inhibitor developed as a therapeutic option to reduce myocardial contractility and restoration of myocardial function. The Food and Drug Administration (FDA) approved the use of Mavacamten in 2022 for HCM symptoms. Clinical studies have proven that Mavacamten can reduce Left Ventricular Outflow Tract (LVOT) involvement, cardiac hypercontraction, and hypertrophy. This review provides an overview of HCM, its pathophysiology, current treatments, synthesis of Mavacamten, and the clinical trials of Mavacamten.","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":"8 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140739047","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":"Redox-signalling and Redox Biomarkers in Cardiovascular Health and Disease.","authors":"Yasmin Sultana, Damanpreet Kaur Lang, Thomson Santosh Alex, Rakhi Khabiya, Akanksha Dwivedi, Saikat Sen, Raja Chakraborty","doi":"10.2174/0118715257282030240130095754","DOIUrl":"https://doi.org/10.2174/0118715257282030240130095754","url":null,"abstract":"<p><p>Overproduction of reactive nitrogen and oxygen species (RNS and ROS) has been linked to the pathogenesis of diabetes, hypertension, hyperlipidemia, stroke, angina, and other cardiovascular diseases. These species are produced in part by the mitochondrial respiratory chain, NADPH oxidase, and xanthine oxidase. RNS and ROS both contribute to oxidative stress, which is necessary for the development of cardiovascular disorders. In addition to ROS species like hydroxyl ion, hydrogen peroxide, and superoxide anion, RNS species like nitric oxide, peroxynitrous acid, peroxynitrite, and nitrogen dioxide radicals have also been linked to a number of cardiovascular conditions. They promote endothelial dysfunction, vascular inflammation, lipid peroxidation, and oxidative damage, all of which contribute to the development of cardiovascular pathologies. It's crucial to understand the mechanisms that result in the production of RNS and ROS in order to identify potential therapeutic targets. Redox biomarkers serve as indicators of oxidative stress, making them crucial tools for diagnosing and predicting cardiovascular states. The advancements in proteomics, metabolomics, genomics, and transcriptomics have made the identification and detection of these small molecules possible. The following redox biomarkers are notable examples: 3-nitrotyrosine, 4-hydroxy-2-nonenal, 8- iso-prostaglandin F2, 8-hydroxy-2-deoxyguanosine, malondialdehyde, Diacron reactive oxygen metabolites, total thiol, and specific microRNAs (e.g. miRNA199, miRNA21, miRNA1254, miRNA1306-5p, miRNA26b-5p, and miRNA660-5p) are examples. Although redox biomarkers have great potential, their clinical applicability faces challenges. Redox biomarkers frequently have a short half-life and exist in small quantities in the blood, making them challenging to identify and measure. The interpretation of biomarker data may also be influenced by confounding factors and the complex interplay of various oxidative stress pathways. Therefore, in-depth validation studies and the development of sensitive and precise detection methods are needed to address these problems. In the search for redox biomarkers, cutting-edge techniques like mass spectrometry, immunoassays, and molecular diagnostics are applied. New platforms and technologies have made it possible to accurately detect and monitor redox biomarkers, which facilitates their use in clinical settings. Our expanding knowledge of RNS and ROS involvement in cardiovascular disorders has made it possible to develop redox biomarkers as diagnostic and prognostic tools. Overcoming the challenges associated with their utility and utilizing advanced detection techniques, which will improve their clinical applicability, will ultimately benefit the management and treatment of cardiovascular conditions.</p>","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140320123","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":"A Three-year Retrospective Study Looking at Preventing Hospital Acquired Thrombosis.","authors":"Vipin Kammath, Anuj Gupta, Alexander Bald, Gavin Hope, Nisheeth Kansal, Ahmad Al Samaraee, Vish Bhattacharya","doi":"10.2174/0118715257269027231228114930","DOIUrl":"10.2174/0118715257269027231228114930","url":null,"abstract":"<p><strong>Background: </strong>Hospital-acquired venous thromboembolism (HA-VTE) is defined as cases of venous thromboembolism (VTE) that occur in a hospital and within ninety days of a hospital admission. Deep vein thromboses (DVTs) most commonly occur within the deep veins of the pelvis and legs. If the thrombus dislodges and travels to the lungs, it can result in a pulmonary embolus (PE). VTE is associated with significant morbidity and mortality, accounting for almost 10% of all hospital deaths. If risk factors are correctly identified and VTE prophylaxis is prescribed, VTE can be a preventable condition. In 2010, NHS England launched The National Venous Thromboembolism Prevention Programme. This included NICE guidance, and a VTE risk assessment tool, which must be completed for at least 95% of patients on admission. The National Thrombosis Survey, published by Thrombosis UK, studied how this program was implemented locally, and audited HA-VTE prevention strategies nationally.</p><p><strong>Objectives: </strong>Using the Thrombosis Survey and NICE guidance as an aide, this study collects data about hospital-acquired DVT (HA-DVT) at the Queen Elizabeth Hospital in Gateshead (QEH) and aims to: 1. Identify cases of HA-DVT and understand the clinical circumstances surrounding these cases 2. Assess the quality of VTE preventative measures at QEH 3. Outline potential improvement in reducing the incidence of HA-VTE at this hospital Methods: This retrospective cohort study used electronic records to identify all cases of DVT between April 2019 and April 2022 at QEH. Cases of HA-DVT were defined as: a positive ultrasound doppler report and either the case occurring in the 90 days following an inpatient stay, or beyond two days into an admission. For these cases of HA-DVT, we recorded the: reason for admission; admitting specialty; presence of an underlying active cancer and deaths occurring within 90 days of diagnosis. We assessed the quality of VTE preventative measures, by recording the: completion of VTE risk assessments; prescription of weight-adjusted pharmacological VTE prophylaxis and provision of VTE prophylaxis on discharge. For HA-DVT cases occurring within 90 days of an inpatient stay, the preventative measures were assessed on the original admission. Electronic records were used to record the completion rate of the National VTE risk assessment tool for all inpatients during this time frame.</p><p><strong>Results: </strong>The VTE risk assessment tool was completed for 98.5% of all admissions. One hundred and thirty-five cases of HA-DVT were identified between April 2019 and April 2022. Sixteen patients with HA-DVT did not have VTE prophylaxis prescribed on admission. Eleven of these patients had a clearly documented reason why anticoagulation was avoided. In HA-DVT cases where pharmacological VTE prophylaxis was prescribed, 23% were prescribed an inappropriate dose for their weight. If anticoagulation was required on discharge, this was p","PeriodicalId":93924,"journal":{"name":"Cardiovascular & hematological agents in medicinal chemistry","volume":" ","pages":"212-222"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139577135","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}