Abstract: Clopidogrel, as an antiplatelet drug, is important for the treatment of the secondary prevention of ischemic stroke according to the latest guidelines on ischemic stroke management. However, some patients still fail to achieve a drug response and experience ischemic events despite taking clopidogrel because of differences in the production of active metabolites attributable to specific factors. Although platelet function testing plays a crucial role in evaluating the efficacy of antiplatelet drugs, research on their application remains relatively limited in the ischemic stroke population; thus, it is necessary to clarify their role in guiding individualized treatment for patients with ischemic stroke. In this review, we synthesize the current state of research on clopidogrel resistance (CR) in patients with ischemic stroke, covering key aspects such as the pharmacological mechanisms and metabolism of clopidogrel, the risk factors associated with CR, and the clinical application of platelet function testing in ischemic stroke. Our study aims to explore the prevalence and predictors of CR among patients with ischemic stroke, identify its potential impact on recurrent ischemic stroke, and thereby offer insights for the development of personalized and precision treatment strategies for clopidogrel treatment in these patients.
Chronic alcohol consumption causes serious damage to the liver and cardiovascular system and leads to neoplastic lesions in various organs such as the esophagus, liver, and breast. In our study, we evaluated the protective effects of standard and high doses of dapagliflozin against alcohol-related cardiac damage by utilizing its anti-inflammatory, anti-fibrotic, and anti-cardiac remodeling effects with biochemical and pathological parameters. Twenty male and twenty female Sprague-Dawley rats were used in the experiments. The animals were randomly divided into 5 groups, with 4 males and 4 females in each group. The experimental groups (ALCOHOL, ALCOHOL+DAP, and ALCOHOL+hDAP groups) were given 20% ethyl alcohol intraperitoneally (i.p.) once daily for 28 days. Dapagliflozin (DAP, ALCOHOL+DAP, and ALCOHOL+hDAP groups) and saline solution (CONT and ALCOHOL groups) were administered orally via gavage (o.g.). In the hearts of animals exposed to alcohol, cardiomyocyte hypertrophy, irregular myofiber arrangement, widespread or focal infiltration of inflammatory cells such as neutrophils and lymphocytes, and marked cytoplasmic vacuolization were observed. Treatment with high-dose dapagliflozin alleviated these structural changes. Alcohol caused significant proximal tubular damage. High-dose dapagliflozin resulted in a greater reduction in alcohol-induced renal damage. Although standard dose dapagliflozin improved alcohol-induced impaired Caspas-3, Cytokeratin 18-M30, Cytokeratin 18-M65, TAS, TOS, OSI, MDA, IL-1β, TNF-α, HsCRP, Endothelin-1, IMA, total thiol, native thiol, and disulfide levels, high dose dapagliflozin provided significant improvements (p<0.001). This study suggests that high-dose dapagliflozin (3 mg/kg) may have the potential to regulate mitochondrial function and thiol/disulfide balance in alcohol-related heart damage by inhibiting fibrosis, hypertrophy, apoptosis, inflammation, and oxidative stress through various mechanisms.
In dialysis-dependent end-stage renal disease patients (ESRD), statin use remains an evidence-use dilemma: randomized controlled trials (RCTs) suggested limited benefit from statin initiation, whereas observational cohort studies reported lower mortality and cardiovascular events. This discordance creates uncertainty in prescribing, resource allocation, guideline interpretation, and shared decision-making. This analysis assessed whether this apparent conflict reflects true inconsistency, risk of bias, indirectness, or limitations in translating evidence into recommendations. Using narrative synthesis, GRADE-informed appraisal, and evidence-to-decision principles, an evidence-based, patient-centered approach is proposed based on the current available evidence.
Left ventricular thrombus (LVT) is a serious complication of anterior ST-elevation myocardial infarction (STEMI). Despite guideline endorsement of prophylactic anticoagulation in selected high-risk patients, the supporting evidence remains of low certainty. Aim of our systematic review and meta-analysis is to evaluate the efficacy and safety of triple antithrombotic treatment (TAT) versus dual antiplatelet treatment (DAPT) alone for LVT prevention in patients with anterior STEMI treated with primary percutaneous coronary intervention (pPCI). Three electronic databases (EMBASE, MEDLINE, Cochrane Library) were systematically searched from inception to February 2026, following PRISMA 2020 guidelines. Eligible studies enrolled adult patients with anterior STEMI revascularised by pPCI, compared prophylactic TAT with DAPT alone, and reported LVT outcomes. Data were pooled as risk ratios (RR) with 95% confidence intervals (CI) using random-effects models. The primary outcome was LVT formation; secondary outcomes were major bleeding and systemic embolism. Six studies including 2,021 patients were analyzed. Pooled analysis demonstrated no statistically significant reduction in LVT formation with TAT (RR 0.54, 95% CI 0.21-1.40; p=0.21; I2=61%), whereas major bleeding risk was significantly increased (RR 2.69, 95% CI 1.40-5.19; p=0.003; I2=14%). A non-significant trend toward reduced systemic embolism was observed (RR 0.44, 95% CI 0.18-1.07; p=0.07; I2=0%). The addition of prophylactic anticoagulation to DAPT in patients with anterior STEMI treated with pPCI does not show a statistically significant reduction in LVT formation while significantly increasing major bleeding risk. These findings do not support routine prophylactic TAT in unselected patients with anterior STEMI.
Mineralocorticoid receptor activation contributes to cardiovascular and kidney injury through inflammation, fibrosis, oxidative stress, endothelial dysfunction, and adverse tissue remodeling. Eplerenone, a selective steroidal mineralocorticoid receptor antagonist developed to minimize the endocrine adverse effects associated with spironolactone, has demonstrated substantial clinical benefits in patients with post-myocardial infarction left ventricular dysfunction and heart failure with reduced ejection fraction, where its role is well established. This review examines the evolving evidence supporting eplerenone across cardiovascular and renal diseases, including hypertension, left ventricular hypertrophy, albuminuria, and broader cardiorenal risk reduction. Although accumulating data suggest potential benefits in these settings, the strength of evidence varies considerably across indications. Spironolactone remains the mineralocorticoid receptor antagonist with the strongest evidence for resistant hypertension, whereas finerenone has generated the most robust dedicated kidney outcomes data in patients with diabetic chronic kidney disease. We conclude that eplerenone should be viewed neither as simply an alternative for spironolactone intolerance nor as a universal substitute for newer mineralocorticoid receptor antagonists. Rather, it remains an evidence-based, well-tolerated therapy with a firmly established role in post-myocardial infarction left ventricular dysfunction and heart failure with reduced ejection fraction, together with a potentially valuable role in selected hypertensive and cardiorenal populations where selective mineralocorticoid receptor blockade and long-term tolerability are important clinical considerations.
Pericarditis is the most common cardiac manifestation of systemic lupus erythematosus (SLE), yet optimal management remains poorly defined. Glucocorticoids are frequently used but are associated with toxicity and increased recurrence risk. Interleukin-1 (IL-1) inhibition has demonstrated efficacy in recurrent pericarditis, though data in SLE-associated pericarditis is limited. In order to evaluate the clinical impact of IL-1 blockade on the treatment of SLE-associated recurrent pericarditis, we performed a retrospective case series of six patients with SLE-associated recurrent pericarditis treated with the IL-1 inhibitor rilonacept at a tertiary care cardio-rheumatology center. Clinical response, inflammatory markers, imaging findings, and use of concomitant therapies were assessed before and after IL-1 inhibition. Following initiation of rilonacept, all six patients achieved clinical improvement: three (50%) attained complete symptom resolution and three (50%) demonstrated partial symptomatic improvement. C-reactive protein normalized in all four patients with elevated baseline levels. Any post-treatment imaging, available in five of six patients (83.3%), demonstrated objective reduction in pericardial inflammation or effusion in all five. Use of concomitant therapies decreased substantially. IL-1 blockade with rilonacept was associated with clinical and imaging improvement and substantially reduced reliance on glucocorticoids and other anti-inflammatory agents in SLE-associated recurrent pericarditis. These findings support IL-1 inhibition as a targeted, steroid-sparing strategy in refractory disease and further prospective investigation.
Empagliflozin (EMPA), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, demonstrates cardioprotective effects in heart failure, and recent trials suggest benefits in acute myocardial infarction (MI). However, the mechanisms underlying its efficacy, particularly its impact on the post-MI inflammatory response, are not fully elucidated. This study aimed to investigate whether EMPA modulates post-MI inflammation and to uncover the underlying molecular pathways. C57BL/6J mice undergoing MI were randomized to receive EMPA or saline for 7 days. EMPA treatment significantly improved survival, reduced fibrosis, and enhanced cardiac function. EMPA attenuated the systemic inflammatory response at day 1 post-MI, as evidenced by lower serum levels of IL-1β, IL-6, and CXCL-1. In the infarcted myocardium at day 1 post-MI, EMPA suppressed infiltration of neutrophils and pro-inflammatory macrophages while increasing anti-inflammatory macrophages. Mechanistically, EMPA upregulated the ketone body metabolic enzyme β-hydroxybutyrate dehydrogenase 1 (BDH1), increasing cardiac β-hydroxybutyrate (β-HB) levels, and subsequently inhibited NF-κB p65 phosphorylation. In immortalized bone marrow-derived macrophages, the anti-inflammatory effect of EMPA was mimicked by β-HB and abolished by Bdh1 knockdown, which was rescued by exogenous β-HB. In conclusion, EMPA attenuates maladaptive inflammation and confers cardioprotection after MI, potentially through a BDH1/β-HB/NF-κB pathway in macrophages. This ketone-mediated immunomodulatory axis, primarily defined in vitro, identifies a novel and potential pharmacological mechanism of SGLT2 inhibition in the context of post-MI inflammation.
Machine learning (ML) models integrating genetic and clinical data show promise for personalizing antiplatelet therapy after myocardial infarction (MI). This study aimed to develop an ML model using clinical features and CYP2C19 genotype to predict long-term major adverse cardiac events (MACEs) and guide P2Y12 inhibitor selection. In a prospective observational study of 218 MI patients undergoing percutaneous coronary intervention, with up to 9-year follow-up for MACEs, we trained and evaluated multiple models incorporating clinical, genetic, and angiographic variables. Uplift modeling principles were applied to assess treatment heterogeneity, and feature importance was analyzed using Shapley Additive Explanations (SHAP). The optimal model (CatBoost with SHAP-based feature selection) achieved an area under the receiver operating characteristic curve of 0.721. Discrimination remained stable under bootstrap resampling and across both infarction presentations. Key prognostic predictors included age, comorbidity index, number of significant coronary lesions, P2Y12 inhibitor type, stent type, and CYP2C19 loss-of-function/gain-of-function variants. Notably, CYP2C19 variants were significant MACE predictors, while drug-eluting stents and ticagrelor were associated with lower predicted long-term risk. These findings suggest that an ML framework incorporating CYP2C19 genotype can stratify long-term MACE risk. This data-driven approach points to the prognostic utility of genetic testing and supports the potential role of ticagrelor, particularly in genetically defined high-risk MI patients, for optimizing secondary prevention.
This retrospective multicenter cohort study compared the safety and efficacy of low- versus high-dose colchicine in adult patients with chronic kidney disease (CKD) treated for pericarditis between August 2015 and August 2024. CKD was identified using ICD codes and confirmed by an age- and sex-adjusted estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2. Patients with recurrent pericarditis or prior colchicine use before admission were excluded. Patients were categorized as receiving high-dose (≥0.6 mg/day) or low-dose (<0.6 mg/day) colchicine. The primary outcomes were colchicine-related adverse effects and a composite of dose reduction or discontinuation. Secondary outcomes included symptom improvement within 72 hours, recurrent pericarditis, and pericardial tamponade within 12 months. A total of 93 patients were included (53 high-dose and 40 low-dose). Idiopathic pericarditis was the most common etiology in both groups. End-stage kidney disease (57.5% vs. 15%) and dialysis (52.5% vs. 13%) were more common in the low-dose group. High-dose colchicine was associated with more gastrointestinal adverse events (39.6% vs. 12.5%, p=0.004), a higher rate of the composite outcome of dose reduction or discontinuation (41.5% vs. 20%, p=0.043), and more frequent dose reduction alone (30.2% vs. 7.5%, p=0.009), while discontinuation rates were similar. Symptom relief, recurrent pericarditis, and pericardial tamponade were comparable between groups. Initial colchicine doses of less than 0.6 mg daily were associated with improved tolerability in patients with CKD and pericarditis.
BACKGROUND:Corticosteroids are widely used in pericarditis despite guideline recommendations reserving them for select indications. Observational studies have reported inconsistent associations between corticosteroid use and pericarditis recurrence, and optimal dosing and tapering strategies remain unclear. We conducted a systematic review of oral corticosteroids for acute or recurrent pericarditis to characterize patterns of treatment and evaluate the association between corticosteroids and pericarditis recurrence across different disease contexts. METHODS:MEDLINE, EMBASE, CENTRAL, and Scopus were searched from inception to November 26, 2025. Studies enrolling adults with acute or recurrent pericarditis treated with oral corticosteroids were included. Randomized trials, cohort studies, and case-control studies reporting clinical outcomes were eligible. Risk of bias was assessed using the Newcastle-Ottawa Scale (NOS). Data were synthesized descriptively due to anticipated clinical and methodological heterogeneity. RESULTS:Ten studies (2 prospective, 8 retrospective) including 2632 patients (800 corticosteroid-treated) met inclusion criteria. Prednisone was most frequently studied, with heterogeneous dosing (0.25-1.0 mg/kg/day) and non-standardized tapering strategies. Follow-up ranged from 1 to 6.7 years, and overall risk of bias was moderate with limited adjustment for confounding. Findings on recurrence were inconsistent in acute idiopathic and post-procedure pericarditis, while most studies in recurrent pericarditis reported higher recurrence with corticosteroid exposure. CONCLUSIONS:Evidence evaluating oral corticosteroids in pericarditis is limited by heterogeneity, confounding, and inconsistent reporting of treatment strategies. Observational data show variable associations with recurrence across clinical contexts. High-quality randomized trials stratified by pericarditis etiology and acuity are needed to define the optimal use of corticosteroids in pericarditis.
Type 2 myocardial infarction (T2MI) results from myocardial oxygen supply-demand imbalance in the absence of acute atherothrombotic plaque rupture and is associated with substantial short- and long-term mortality. Although increasingly recognized with the widespread use of high-sensitivity cardiac troponin assays, optimal pharmacologic management of T2MI remains poorly defined. We performed a narrative review evaluating pharmacologic treatment patterns and outcomes in adults with adjudicated or clinically coded T2MI. Evidence consistently demonstrates a high prevalence of underlying coronary artery disease (CAD) in T2MI, with up to two-thirds of patients exhibiting significant coronary artery stenosis. Despite this overlap with ischemic heart disease, prescription rates of antiplatelet agents, statins, β-blockers, and renin-angiotensin-aldosterone system (RAAS) inhibitors are substantially lower in T2MI compared with T1MI. Observational data suggest that statins, β-blockers, RAAS inhibitors, and combination secondary prevention strategies may be associated with improved survival, whereas evidence supporting routine antiplatelet or anticoagulant therapy remains limited and inconsistent. Overall, T2MI represents a high-risk and underrecognized clinical entity for which pharmacologic management is largely extrapolated from T1MI and CAD. Prospective, T2MI-focused studies are urgently needed to define optimal secondary prevention strategies and improve clinical outcomes.
ABSTRACT:To identify potential agents associated with the development of valvular heart diseases (VHD), we used Mendelian randomization and colocalization analyses to pinpoint genes significantly linked to VHD. A total of 324 genes were found to be positively associated with VHD, among which AGK and TLE5 demonstrated evidence of colocalization. Then, transcriptome data of aortic and mitral valve diseases were retrieved from GEO database. Based on the expression levels of AGK and TLE5, sequencing data for aortic and mitral valve diseases were stratified into 2 subtypes, respectively. Differentially expressed genes between these subtypes underwent KEGG pathway enrichment analysis. Molecular docking revealed that ergotamine and fosfomycin exhibited the highest binding affinities to AGK and TLE5, respectively. Then, FDA Adverse Event Reporting System database was used to corroborate the associations between the identified drugs and aortic and mitral valve diseases. Analysis of the FDA Adverse Event Reporting System database indicated reporting odds ratios of 13.82 [95% confidence interval (CI): 5.17-36.94] for ergotamine and 2.14 (95% CI: 0.69-6.63) for fosfomycin. For further validation, naratriptan and aztreonam were used as control drugs. The adjusted odds ratios for ergotamine and fosfomycin were 8.31 (95% CI: 1.61-38.39) and 2.96 (95% CI: 0.84-18.75), respectively, when compared with the control drugs. Finally, human aortic and mitral interstitial cells were isolated and transfected with AGK plasmid. After adding Ly294002 (inhibitor of PI3K-Akt), the Western blot results showed that AGK promoted the fibrosis of aortic and mitral interstitial cells by PI3K-Akt signaling pathway. In conclusion, ergotamine may contribute to the development of aortic and mitral valve diseases through the activation of AGK.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are a key component of lipid-lowering therapies for atherosclerotic cardiovascular disease risk management in high-risk primary and secondary prevention populations. PCSK9 monoclonal antibodies such as evolocumab and alirocumab were the first agents approved and are the preferred agents given phase 3 trial data supporting improved cardiovascular outcomes. Subgroup analyses of these trials have highlighted high-risk populations that may especially benefit from PCSK9 inhibitor therapy, although demographic disparities persist regarding their implementation. Additional injectable agents with less-frequent dosing schedules have been developed, such as the small-interfering RNA inclisiran, though they lack data regarding cardiovascular outcomes. Oral agents are also in development, with promising data recently presented regarding enlicitide. Additionally, recent trials provide evidence supporting expanded indications for high-risk primary prevention. This review summarizes currently available and investigational PCSK9-targed therapies and examines evidence guiding their clinical implementation.
ABSTRACT:Postural orthostatic tachycardia syndrome (POTS) is a debilitating autonomic disorder characterized by excessive orthostatic tachycardia and significant functional impairment. Conventional therapies, including beta-blockers, often provide incomplete relief or are poorly tolerated. Ivabradine, a selective If channel inhibitor, reduces heart rate without affecting blood pressure or myocardial contractility, making it a promising option, particularly in post-COVID-19 POTS. This systematic review and meta-analysis evaluated the efficacy and safety of ivabradine in patients with POTS. PubMed, Embase, and the Cochrane Library were searched through August 2025 in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines (PROSPERO CRD420251073600). Eligible studies included randomized controlled trials, observational studies, and case series reporting ivabradine outcomes in POTS. Primary outcomes were changes in standing and supine heart rate; secondary outcomes included symptom burden, quality of life, and adverse events. A random-effects model was used, heterogeneity was assessed through sensitivity analyses, and certainty of evidence was evaluated using Grading of Recommendations, Assessment, Development, and Evaluation. Nine studies involving 245 patients were included. Ivabradine significantly reduced standing heart rate (-18.5 bpm; 95% confidence interval -23.3 to -13.8) and supine heart rate (-9.7 bpm; 95% confidence interval -13.4 to -6.1). Symptom improvement particularly palpitations, lightheadedness, and exercise intolerance was consistently reported across classic, pediatric, hyperadrenergic, and post-COVID-19 subgroups. Adverse events were infrequent and mild, most commonly transient visual disturbances, with no reports of severe bradycardia or hypotension. Heterogeneity was high, largely driven by pediatric and post-COVID-19 cohorts. In conclusion, ivabradine seems to provide meaningful heart rate reduction and symptomatic improvement in POTS with a favorable safety profile. However, evidence is limited by small, heterogeneous, predominantly observational studies, underscoring the need for large, multicenter randomized controlled trials.
Anthracyclines remain a cornerstone of cancer therapy but are associated with a spectrum of cardiovascular toxicity, ranging from subclinical myocardial injury to overt heart failure (HF). Despite strong biological rationale, the role of universal pharmacologic prophylaxis remains uncertain. In this context, the recent meta-analysis by Pizzi et al. provides a timely synthesis of randomized evidence evaluating angiotensin-converting enzyme inhibitors (ACEi) for the prevention of anthracycline-related cardiotoxicity. The analysis demonstrates a statistically significant attenuation of left ventricular ejection fraction decline with ACEi prophylaxis, although the absolute effect size is modest and accompanied by substantial heterogeneity. Importantly, the magnitude of benefit appears to be context-dependent, with more consistent effects observed in higher-risk settings, such as combined anthracycline and trastuzumab exposure or in patients with early markers of myocardial injury. Contemporary data suggest that declining event rates and improved supportive care may limit the ability of prophylaxis trials to detect clinically meaningful differences in low-risk populations. Furthermore, the absence of significant effects on clinical endpoints underscores the limitations of current surrogate markers and trial design. Emerging evidence supports a more nuanced, risk-adapted approach, integrating early detection strategies such as global longitudinal strain and biomarker-guided intervention. Within this framework, ACEi prophylaxis may be most appropriately targeted to patients with higher baseline risk or early evidence of myocardial injury, rather than applied universally. Future studies should prioritize risk enrichment, standardized imaging protocols, and clinically meaningful outcomes to better define the role of cardioprotective strategies in cardio-oncology.
ABSTRACT:Imipramine was one of the first antidepressant drugs that entered the clinic and is still used to this day. The antidepressant action of imipramine is, at least in part, because of an inhibition of noradrenaline and serotonin transport in the brain. Binding studies indicated that imipramine binds to H 1 -histamine receptors with high affinity. We have recently generated mice that overexpress the human H 1 -histamine receptor in the heart (H 1 -TG). On stimulation of these hearts with H 1 -histamine receptor agonists, a positive inotropic effect was observed which was reversed by mepyramine, a selective H 1 -histamine receptor antagonist. Moreover, we have recently described that stimulation of H 1 -histamine receptors in the human atrium also increases force of contraction which was similarly reversed by mepyramine. Consequently, we investigated whether these H 1 -histamine receptor-mediated increases of force in atria from H 1 -TG and human atrium could be reversed by imipramine. We stimulated H 1 -histamine receptors in atria from H 1 -TG and noted that imipramine, starting at 100 nM, reduced force of contraction. To study imipramine in the human heart, we obtained human right atrial muscle preparations from adult patients succumbing to cardiac bypass surgery. Such as in H 1 -TG, imipramine, starting at 300 nM, antagonized the positive inotropic effects of H 1 -histamine receptor stimulation in human atrial preparations. We conclude that imipramine can antagonize H 1 -histamine receptor mediated positive inotropic effects in the mammalian atrium in general and, of note, in the human atrium. This may explain cardiac side effects of imipramine.
OBJECTIVE:The aim of the study was to investigate the prognostic value of previously established ceramide-phospholipid risk score, CERT2, and its response to lipid-lowering treatments in patients with symptomatic or suspected coronary heart disease. APPROACH AND RESULTS:Selected ceramides and phospholipids were analyzed with a quantitative liquid chromatography-mass spectrometry-based method from plasma or serum samples obtained from the Angiography and Genes study (ANGES, N = 966), and placebo-controlled trials investigating atorvastatin and simvastatin (N = 44) and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor RG7652 (N = 78). In the ANGES, the adjusted hazard ratios (95% confidence interval) per SD for the CERT2 risk score were 1.71 (1.42-2.08) for cardiovascular disease death, 1.36 (1.13-1.64) for myocardial infarction, 1.40 (1.20-1.63) for heart failure, 1.23 (1.08-1.40) for atrial fibrillation, 1.09 (0.89-1.33) for stroke, and 1.52 (1.06-2.18) for venous thromboembolism. The median decrease of the CERT2 risk score was 2 points by statin treatment ( P ≤ 0.001) and 3 points by PCSK9 inhibition ( P < 0.001) on the 0-12 scale. CONCLUSIONS:The CERT2 risk score is a significant predictor of cardiovascular outcomes in all-comer patients with symptomatic or suspected coronary heart disease. Treatment with lipid-lowering medication significantly lowers the CERT2 risk score.
ABSTRACT:Highly protein-bound anticoagulants such as warfarin and rivaroxaban have increased therapeutic effects in the setting of hypoalbuminemia due to increased free concentrations in the drug which result in increased bleed risk. Apixaban is also heavily protein bound at 87% but bleeding in hypoalbuminemic patients receiving apixaban has largely been unevaluated. Therefore, this retrospective, cohort study of hospitalized adults who received apixaban and had a serum albumin level measured was conducted. Included patients were evaluated for bleeding events in accordance with International Society on Thrombosis and Hemostasis criteria. Patients were grouped by bleeding status (bleed vs. nonbleed) and multivariable logistic regression modeling was used to evaluate the relationship between albumin, covariables, and bleeding events. A total of 391 patients were included, 49 who bled and 342 who did not. Multivariable modeling determined a significant association between bleeding events and serum albumin level (adjusted odds ratio [OR] 2.10 for every 1 g/dL reduction in serum albumin, 95% confidence interval [CI]: 1.26-3.60), high-risk IMPROVE Bleeding scores (adjusted OR 2.17, CI: 1.127-4.181), and active gastroduodenal ulcer (adjusted OR 5.20, CI: 1.11-24.39). Consideration of serum albumin levels may be relevant when treating patients with highly protein-bound anticoagulants such as apixaban.
