Tyler Shugg, Tk Nguyen, Xuesi Hua, Blair Richards, James Rae, Robert Dess, Daniel Perry, Bradley Kay, Salim S Hayek, Monika Leja, Jasmine A Luzum
{"title":"Factors Associated With the Recovery of Left Ventricular Ejection Fraction in Patients With Anthracycline-Induced Left Ventricular Dysfunction.","authors":"Tyler Shugg, Tk Nguyen, Xuesi Hua, Blair Richards, James Rae, Robert Dess, Daniel Perry, Bradley Kay, Salim S Hayek, Monika Leja, Jasmine A Luzum","doi":"10.1177/10742484241304304","DOIUrl":"10.1177/10742484241304304","url":null,"abstract":"<p><strong>Background: </strong>Neurohormonal blocking drugs, like beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor blockers (ARBs), are recommended for treating anthracycline-induced left ventricular dysfunction (AILVD). However, there is limited evidence supporting their benefit. Therefore, this study evaluated associations of neurohormonal blockers and other clinical factors with recovery of left ventricular ejection fraction (LVEF) in patients with AILVD.</p><p><strong>Methods: </strong>This retrospective chart review assessed patients treated with at least one dose of anthracycline, then had ≥10% LVEF reduction or post-anthracycline LVEF value <50%, and then had a follow-up LVEF measurement ≥90 days later. The primary endpoint was LVEF recovery (highest follow-up LVEF-lowest LVEF post-anthracycline). Variables from univariable tests with <i>P</i> < .1 were incorporated in a multiple linear regression model for independent factors significantly associated with LVEF recovery (<i>P</i> < .05).</p><p><strong>Results: </strong>Out of 104 patients, 83% were female, 86% self-reported white race, 53% had breast cancer, median (IQR) age was 52 (22) years, and LVEF recovery was 14% (16%). The final multivariable model included 2 significant variables: beta-blocker dose after anthracycline exposure (every 25 mg increase in beta-blocker dose was associated with 5.0% increase in LVEF recovery; <i>P</i> = .0005) and the time between the start of the anthracycline and the lowest LVEF post-anthracycline (every 5-year increase in time was associated with 1.8% decrease in LVEF recovery; <i>P</i> = .0379).</p><p><strong>Conclusions: </strong>In patients with AILVD, a higher beta-blocker dose and earlier detection of LVEF reduction post-anthracycline were significantly and independently associated with improved LVEF recovery. These findings need to be validated in a larger, independent cohort.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484241304304"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11831319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Thanks to Reviewers.","authors":"","doi":"10.1177/10742484251315246","DOIUrl":"https://doi.org/10.1177/10742484251315246","url":null,"abstract":"","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251315246"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sarah K Gharib, Abid M Sadiq, Faryal M Raza, Sophia S Muhali, Annette A Marandu, Norman J Kyala, Eliasa K Ndale, Venance P Maro, William P Howlett, Elifuraha W Mkwizu, Nyasatu G Chamba, Furaha S Lyamuya, Elichilia R Shao, Kajiru G Kilonzo
{"title":"Vitamin K Antagonist Use and Level of Anticoagulation Control Among Patients at a Tertiary Hospital in Northern Tanzania.","authors":"Sarah K Gharib, Abid M Sadiq, Faryal M Raza, Sophia S Muhali, Annette A Marandu, Norman J Kyala, Eliasa K Ndale, Venance P Maro, William P Howlett, Elifuraha W Mkwizu, Nyasatu G Chamba, Furaha S Lyamuya, Elichilia R Shao, Kajiru G Kilonzo","doi":"10.1177/10742484251315104","DOIUrl":"10.1177/10742484251315104","url":null,"abstract":"<p><strong>Background: </strong>Vitamin K antagonists (VKA) continue to be the principal anticoagulants for both the treatment and prevention of venous thromboembolism. The use of VKA often requires regular monitoring to avoid over-anticoagulation and prevent thromboembolic complications. The aim was to determine the indication for VKA use and factors associated with suboptimal anticoagulation control among patients in northern Tanzania.</p><p><strong>Methods: </strong>This was a retrospective cohort study that examined the anticoagulation data of patients on long-term VKA from 1<sup>st</sup> January 2020 to 31<sup>st</sup> December 2022. Eligible participants were those on VKAs for at least 7 days and with at least 3 international normalized ratio (INR) results. The level of anticoagulation control was determined through the calculation of the time-in-therapeutic range (TiTR) using the Rosendaal and the percent of INR in therapeutic range methods.</p><p><strong>Results: </strong>TiTR was found to be 17% using the direct method and 16% using the Rosendaal formula. 102 tests out of 365 were within the target range (28%). Absence of health insurance (aRR: 1.24, 95% CI: 1.06-1.44, <i>P</i> = .007), alcohol consumption (aRR: 1.37, 95% CI: 1.15-1.62, <i>P</i> < .001), and prolonged intervals between tests of 14 to 28 days (aRR: 1.34, 95% CI: 1.05-1.74, <i>P</i> = .018) showed association with INR being out of range.</p><p><strong>Conclusion: </strong>Patients who achieved target therapeutic anticoagulation control were less than the acceptable 65%. Anticoagulation outcomes were better in patients with frequent INR monitoring and those with health insurance. Alcohol consumption carries a high risk of poor anticoagulation control. Further studies are needed to enforce better INR control.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251315104"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Steven Hopkins, Faiz Baqai, Saivaroon Gajagowni, Gavin Hickey
{"title":"Direct Cardiac Mechanisms of the Sodium Glucose Co-Transporter 2 Inhibitor Class.","authors":"Steven Hopkins, Faiz Baqai, Saivaroon Gajagowni, Gavin Hickey","doi":"10.1177/10742484251323428","DOIUrl":"https://doi.org/10.1177/10742484251323428","url":null,"abstract":"<p><p>BackgroundSodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated significant cardiovascular benefits in clinical trial. While their role in reducing heart failure hospitalizations and cardiovascular mortality is well established, the precise mechanisms underlying their direct cardiac effects remain unclear. This literature review aims to synthesize current knowledge on the molecular and physiological pathways by which SGLT2 inhibitors may exert effects on cardiac tissue, independent of glycemic control.MethodsA comprehensive review of peer-reviewed articles, randomized controlled trials, meta-analyses, and mechanistic studies published in PubMed and related databases was conducted. The search focused on studies examining the direct impact of SGLT2 inhibitors on cardiac function, remodeling, metabolism, and intracellular signaling pathways. Only studies evaluating the cardiac effects separate from their glucose-lowering action were included in the analysis.ResultsThis review identified several key mechanisms by which SGLT2 inhibitors may benefit the heart directly, including reductions in oxidative stress, inflammation, and myocardial fibrosis. Emerging evidence suggests that these drugs modulate key pathways such as sodium-hydrogen exchange (NHE) inhibition, improvement of mitochondrial function, and promotion of ketone body utilization in cardiomyocytes.ConclusionsSGLT2 inhibitors appear to confer direct cardioprotective effects. These include anti-inflammatory, anti-fibrotic, and energy efficiency improvements in the myocardium. The findings highlight new potential therapeutic mechanisms and provide a foundation for further research into the non-diabetic use of SGLT2 inhibitors in heart failure and other cardiac conditions. Understanding these direct effects could lead to optimized treatment strategies for patients with and without diabetes.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251323428"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shanshan Geng, Zhongbao Ruan, Lianghong Ying, Zhou Liu
{"title":"Knockdown of AMFR Alleviates Atrial Fibrosis in Atrial Fibrillation by Stabilizing SOD1 Protein Expression.","authors":"Shanshan Geng, Zhongbao Ruan, Lianghong Ying, Zhou Liu","doi":"10.1177/10742484251356140","DOIUrl":"https://doi.org/10.1177/10742484251356140","url":null,"abstract":"<p><p>PurposeDemonstration of the role of autocrine motility factor receptor (AMFR) in atrial fibrillation (AF) mice.MethodsThe AF model was established by administering Ang II to mice and transfected with AMFR knockdown or AMFR overexpression plasmids by tail vein injection of the AAV vector. Atrial fibrosis was examined by Masson staining. The mRNA expression of inflammatory factors TNF-α, IL-1β, and IL-6 in atrial tissue was detected by PCR. Reactive oxygen species (ROS) production in atrial tissue was examined by dihydroethidium staining. Apoptotic cells of atrial tissue were examined by TUNEL staining. The expression levels of fibrosis-related genes (COL1A1 and α-SMA), apoptosis-related genes (cleaved-caspase3 and cleaved-PARP), and SOD1 were detected by western blot. The ubiquitination level of superoxide dismutase 1 (SOD1) was detected by ubiquitination assay.ResultsAng II resulted in increased AMFR expression in mouse atrial tissue, and knockdown of AMFR inhibited atrial fibrosis, inflammatory factors, and ROS production, as well as apoptosis in mice. In addition, the knockdown of AMFR inhibited the ubiquitination level of SOD1 and increased the protein expression level of SOD1, whereas overexpression of AMFR exerted the opposite effect and aggravated Ang II-induced AF.ConclusionKnockdown of AMFR promotes SOD1 expression by inhibiting SOD1 ubiquitination levels and attenuates atrial fibrosis in AF mice by regulating SOD1.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251356140"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ivana Kraljević, Mirsala Solak, Ante Mandić, Katarina Mlekuš Kozamernik, Maja Raičević, Anida Divanović Slato, Zlata Kovačević, Emir Muzurović
{"title":"Hypopituitarism and Cardiovascular Risk.","authors":"Ivana Kraljević, Mirsala Solak, Ante Mandić, Katarina Mlekuš Kozamernik, Maja Raičević, Anida Divanović Slato, Zlata Kovačević, Emir Muzurović","doi":"10.1177/10742484251332398","DOIUrl":"https://doi.org/10.1177/10742484251332398","url":null,"abstract":"<p><p>Hypopituitarism, resulting from a partial or complete deficiency of anterior or posterior pituitary hormones, is associated with increased cardiovascular (CV) morbidity and mortality. This heterogeneous endocrinological disorder may arise from various etiologies, including genetic mutations, pituitary tumors, traumatic brain injury, and autoimmune diseases. Hypopituitarism often results in multiple endocrine deficits that contribute to metabolic dysregulation characterized by insulin resistance, dyslipidemia, and increased visceral adiposity, all known risk factors for CV disease (CVD). Additionally, the presence of chronic inflammation and endothelial dysfunction further increases the risk of CVD in these patients. While standard hormone replacement therapy (HRT) is crucial for restoring hormonal balance, it can sometimes have adverse metabolic effects that can exacerbate atherosclerosis and CVD. Emerging evidence suggests that optimizing HRT regimens and addressing specific hormone deficiencies, such as growth hormone and cortisol, may reduce these risks and improve CV outcomes. This review comprehensively analyzes the etiology, pathophysiological mechanisms underlying CV risk in anterior pituitary dysfunction, and treatment strategies to mitigate CV morbidity and mortality in patients with hypopituitarism.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251332398"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mehmet Melek, Hasan Ari, Alper Karakuş, Selma Ari, Ahmet Tütüncü, Tahsin Bozat
{"title":"Impact of Intravenous Nitrate Treatment on Antiplatelet Effects of Clopidogrel in Acute Coronary Syndrome Patients: A Pilot Study.","authors":"Mehmet Melek, Hasan Ari, Alper Karakuş, Selma Ari, Ahmet Tütüncü, Tahsin Bozat","doi":"10.1177/10742484251357147","DOIUrl":"10.1177/10742484251357147","url":null,"abstract":"<p><p>BackgroundClopidogrel is a pro-drug that requires metabolic activation by hepatic cytochrome P450 (CYP) enzymes in two steps. Previous studies have shown that the administration of continuous nitrate significantly affects the activity of hepatic CYP. In this pilot study, we assess the impact of intravenous nitrate treatment on the antiplatelet effects of clopidogrel in patients with non-ST-elevation myocardial infarction (NSTEMI).MethodWe included 20 NSTEMI patients: 15 in the nitrate group and five in the control group. All patients received a 300 mg acetylsalicylic acid and a 600 mg clopidogrel loading dose. The nitrate group was administered an intravenous glyceryl trinitrate infusion at 10 µg/min for 48 h. After the drugs were initiated, blood samples were collected from patients at intervals of 30th minutes, 60th minutes, 120th minutes, fourth hour, sixth hour, and 48th hour to assess platelet function. The antiplatelet effect of clopidogrel was evaluated using the platelet reactivity unit (PRU) from the Verify-Now P2Y12 assay.ResultThe PRU values at baseline and the 30th, 60th, 120th minutes, and 48th hour were similar between the two groups (<i>P</i> > .05). However, PRU values at the fourth and sixth hours were significantly higher in the nitrate group than in the control group (274.1 ± 53.9 vs 162.4 ± 39.9; <i>P</i> = .002 and 272.0 ± 67.0 vs 185.6 ± 18.1; <i>P</i> = .03, respectively).ConclusionIntravenous nitrate therapy in patients with NSTEMI delayed the onset of the antiplatelet effect of orally loaded clopidogrel by at least 4 h. This point should be kept in mind in patients using clopidogrel and nitrate therapy together. (NCT06878638).</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251357147"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rafał Dąbrowski, Agnieszka Segiet-Święcicka, Stefan Sawicki, Ilona Kowalik, Krzysztof Jaworski, Michał Farkowski, Agata Kubaszek-Kornatowska, Piotr Michałek, Mirosław Dłużniewski, Hanna Szwed, Tomasz Hryniewiecki, Jarosław Karwowski
{"title":"Clinical Efficacy of Canrenone in Restoring Sinus Rhythm in Patients With Atrial Fibrillation-A Pilot, Randomized, Double-Blind Study.","authors":"Rafał Dąbrowski, Agnieszka Segiet-Święcicka, Stefan Sawicki, Ilona Kowalik, Krzysztof Jaworski, Michał Farkowski, Agata Kubaszek-Kornatowska, Piotr Michałek, Mirosław Dłużniewski, Hanna Szwed, Tomasz Hryniewiecki, Jarosław Karwowski","doi":"10.1177/10742484251356361","DOIUrl":"10.1177/10742484251356361","url":null,"abstract":"<p><p>Background and aimsRenin-angiotensin-aldosterone system (RAAS) inhibition is an upstream therapy for managing atrial fibrillation (AF). Of all RAAS-inhibiting agents, only canrenone in the form of potassium canrenoate, a specific inhibitor of mineralocorticoid receptors, is administered intravenously. We evaluated the clinical efficacy of intravenous potassium canrenoate in restoring sinus rhythm in patients with paroxysmal AF episodes.MethodsThis double-center, randomized, double-blind study comprised 52 patients with AF (lasting <48 h) in stable cardiopulmonary conditions who were eligible for cardioversion. The patients were randomly assigned to receive a slow intravenous bolus of 10 ml either as a placebo (0.9% saline) or canrenone (200 mg). The primary endpoint was the return of sinus rhythm within 2 h after drug administration.ResultsOf 52 patients, 27 (51.9%) and 25 (48.1%) were treated with placebo and canrenone, respectively. The median patient age was 68 years, and 27 patients (51.9%) were men. Sinus rhythm restoration during the follow-up period occurred in 3 (11.5%) and 4 (16.0%) patients in the placebo and canrenone arms (<i>P</i> = .477), respectively. Adverse events were observed in 2 (7.4%) and 0 (0.0%) patients in the placebo and canrenone arms, respectively (<i>P</i> = .170).ConclusionsIntravenous canrenone is not effective in the sinus rhythm restoration among the patients with paroxysmal AF.ClinicalTrials.gov. NCT03536806.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251356361"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dalyia Abu-Ghazaleh, David A Taylor, Louise Roberts, Indu Singh, Vinicius Cruzat, Roselyn B Rose'Meyer
{"title":"The Pathophysiology of Vasovagal Syncope and New Approaches to its Pharmacological Treatment.","authors":"Dalyia Abu-Ghazaleh, David A Taylor, Louise Roberts, Indu Singh, Vinicius Cruzat, Roselyn B Rose'Meyer","doi":"10.1177/10742484251351140","DOIUrl":"10.1177/10742484251351140","url":null,"abstract":"<p><p>Syncope refers to the transient loss of consciousness and the most common type of syncope is vasovagal syncope (VVS), usually occurring when a person is in an upright position, and/or after exposure to intense stress. The sequelae of VVS is caused by an increase in sympathetic tone and heart rate combined with an underfilled left ventricular chamber that leads to stimulation of cardiac afferent C fibers ultimately leading to bradycardia and vasodilation causing a reduction in venous return, cerebral hypoperfusion and VVS. Several treatment options have been tested including physical counter-pressure measures, electrical pacing, cardioneuroblation. Pharmacological interventions and clinical trials for VVS are summarized in this review; however, there is still limited evidence of their efficacy for reducing episodes of VVS. This review will examine studies using animal models of the vasovagal reflex arc to investigate the physiological mechanisms and neurotransmitters associated with VVS, the tilt-table test that induces VVS in patients and the potential sources of cardiac and platelet mediators that can activate cardiac afferent C fibers. This study will also consider how the previously investigated pharmacotherapies provide insight into the multiple mechanisms involved in VVS and propose new targets for the pharmacological treatment of VVS.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251351140"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Concomitant Therapy of Direct Oral Anticoagulants with Amiodarone in Atrial Fibrillation: A Meta-analysis.","authors":"Kazuhiko Kido, Mikiko Shimizu, Tsuyoshi Shiga, Masayuki Hashiguchi","doi":"10.1177/10742484251351148","DOIUrl":"10.1177/10742484251351148","url":null,"abstract":"<p><p>BackgroundThe concomitant therapy of amiodarone with direct oral anticoagulants (DOACs) significantly increases the concentrations of DOACs and may increase the bleeding risks. Multiple real-world studies compared the concomitant therapy of amiodarone and DOACs versus the DOAC alone, but their main findings were contradictory.MethodsA meta-analysis compared the concomitant therapy of amiodarone and DOACs versus DOACs monotherapy. Database searches through May 1, 2025, were performed. The primary outcome was major bleeding. The secondary outcomes included stroke or systemic embolism, any bleeding, all-cause mortality, gastrointestinal bleeding, and intracranial bleeding.ResultsThis meta-analysis included a total of nine studies. There were no significant differences in major bleeding between the concomitant therapy of amiodarone and DOAC and DOAC monotherapy groups (OR 1.12; 95% CI 0.98, 1.27; <i>P</i> = .09; <i>I</i><sup>2</sup> = 64%). No significant differences in any bleeding (OR 1.18; 95% CI 0.88, 1.57; <i>P</i> = .27; <i>I</i><sup>2</sup> = 77%), gastrointestinal bleeding (OR 0.97; 95% CI 0.84, 1.11; <i>P</i> = .65; <i>I</i><sup>2</sup> = 56%), and intracranial bleeding (OR 1.14; 95% CI 1.00, 1.30; <i>P</i> = .05; <i>I</i><sup>2</sup> = 32%) were also found between the two groups. No significant differences in stroke or systemic embolism were found between the two groups (OR 0.86; 95% CI 0.74, 1.00; <i>P</i> = .05; <i>I</i><sup>2</sup> = 34%).Conclusion and RelevanceThe concomitant therapy of amiodarone and DOACs did not significantly increase the bleeding risks or decrease the risk of stroke or systemic embolism compared to the DOAC monotherapy. The drug-drug interactions between amiodarone and DOACs may not be clinically significant.</p>","PeriodicalId":15281,"journal":{"name":"Journal of Cardiovascular Pharmacology and Therapeutics","volume":"30 ","pages":"10742484251351148"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}