Search Results (673)

Background/Objectives: To evaluate the association of preoperative morphometric and morphovolumetric parameters with post-endovascular aneurysm repair (EVAR) sac remodeling, endoleak development, and secondary interventions, and to assess the role of volumetric analysis in post-EVAR surveillance. Methods: This retrospective single-center study included 383 patients who underwent elective EVAR for infrarenal abdominal aortic aneurysm between 2016 and 2024, with available pre- and postoperative computed tomography angiography and at least 1 year of follow-up. Diameter- and volume-based sac dynamics were analyzed using standardized morphometric and 3-dimensional morphovolumetric measurements. Endoleak subtype distribution, risk factors, secondary interventions, and survival were assessed using regression and survival analyses. Results: Endoleaks were detected in 26.1% of patients (n = 100), with type II endoleak being the most frequent subtype (12.3%, n = 47), followed by type Ib (6.8%, n = 26), type III (5.5%, n = 21), type Ia (4.2%, n = 16), and 1 patient with type V endoleak in the revised manuscript framework. Secondary interventions were required in 14.1% of patients (n = 54), mainly for type I and III endoleaks, with a mean time to reintervention of 21.7 ± 10 months. Diameter and volume changes were strongly correlated; a 10% increase in aneurysm volume corresponded to an average 4 mm increase in diameter (R² = 0.72, p < 0.001). Significant predictors of overall endoleak included dual antiplatelet therapy, aneurysm length > 133 mm, elevated pre- and postoperative D-dimer levels, aneurysm diameter > 59 mm, aneurysm volume > 164 cm³, and thrombus volume > 89 cm³. Subtype-specific analyses identified distinct risk profiles for type Ia, Ib, II, and III endoleaks. Overall survival did not differ significantly between patients with and without endoleaks (p = 0.227), although worse survival was observed in type Ia and III endoleaks than in type II and Ib endoleaks. Conclusions: Preoperative morphovolumetric parameters are significant predictors of post-EVAR endoleaks and secondary interventions. Volumetric analysis may provide a complementary early signal of aneurysm sac remodeling beyond conventional diameter-based assessment, particularly in patients with type II endoleaks. However, the proposed volumetric thresholds remain exploratory and require prospective external validation before routine clinical adoption. Post-EVAR management should integrate endoleak subtype, sac behavior, and patient-specific morphovolumetric risk factors to improve surveillance and treatment selection. Full article

Antithrombotic therapy is central to the management of coronary artery disease (CAD), yet its optimal use requires a continuous balance between ischemic protection and bleeding risk. While aspirin has historically been the cornerstone of treatment, contemporary evidence supports a transition toward increasingly individualized strategies across the spectrum of disease. In primary prevention, the role of aspirin remains marginal and is limited to carefully selected high-risk individuals. Following percutaneous coronary intervention (PCI), dual antiplatelet therapy (DAPT) remains the standard of care; however, both its duration and composition are progressively tailored according to patient-specific ischemic and bleeding risk profiles. In chronic coronary syndromes, shorter DAPT followed by single antiplatelet therapy—particularly P2Y₁₂ inhibitor monotherapy—has emerged as an effective bleeding-avoidance strategy without compromising ischemic outcomes. In acute coronary syndromes, 12 months of DAPT remains the recommended approach, although de-escalation strategies may be considered in selected patients at lower ischemic risk. For long-term secondary prevention, emerging evidence suggests a potential advantage of clopidogrel over aspirin, while in patients with persistently high ischemic risk, intensified antithrombotic regimens may provide additional benefit. Special populations require tailored treatment strategies. Overall, contemporary evidence supports a paradigm shift toward a precision medicine approach in CAD, in which antithrombotic therapy is dynamically adapted to the individual balance between ischemic and bleeding risk to optimize long-term clinical outcomes. Full article

Introduction: The concomitant occurrence of myeloproliferative neoplasms (MPNs) and plasma cell dyscrasias is rare and presents significant diagnostic challenges. Accurate distinction between overlapping features is essential, particularly when bone marrow fibrosis (BMF) is present. Case Description: We report a 57-year-old female, with a 10-year history of thrombocytosis managed with antiplatelet therapy, who presented with anemia and severe lumbar pain. Bone marrow biopsy revealed marked fibrosis, and imaging revealed multiple vertebral lesions. Diagnostic workup identified features consistent with myelofibrosis (MF) and coexisting IgG-Kappa multiple myeloma (MM). Although the patient initially fulfilled WHO criteria for MF, the rapid resolution of fibrosis following first-line plasma-cell-directed therapy suggested a secondary, cytokine-mediated process rather than a true concomitant MPN. Conclusions: This case highlights the importance of an integrated diagnostic approach in patients with overlapping features of hematologic malignancies. Differentiating between MM-associated fibrosis and true concurrent MPN and MM is critical, as misclassification may alter both prognosis and therapeutic strategy. In triple-negative cases, the histologic response to plasma-cell-directed therapy can serve as a key discriminating criterion. Awareness of the potential association between MM with fibrosis and extramedullary disease is also essential for clinical management. This case underscores the importance of an integrated diagnostic approach in patients with overlapping hematologic features. Full article

Background: Optimal platelet inhibition is essential for minimizing both thrombotic and hemorrhagic complications in patients with coronary artery disease (CAD). Although high on-treatment platelet reactivity (HPR) has been consistently associated with adverse clinical outcomes, the relationship between platelet reactivity—measured as P2Y12 reaction units (PRU)—and cardiovascular mortality remains incompletely characterized. In particular, potential non-linear associations have not been adequately explored. Objective: We aimed to investigate the association between PRU and cardiovascular mortality in patients with CAD, with a specific focus on identifying potential non-linear relationships. Methods: We conducted a retrospective observational cohort study including 1000 patients with angiographically confirmed CAD treated at a tertiary cardiology center in Almaty, Kazakhstan, between 2024 and 2025. Platelet reactivity was assessed using the VerifyNow P2Y12 assay. Multivariable logistic regression models were used to identify independent predictors of cardiovascular mortality. To assess potential non-linear associations between PRU and mortality, restricted cubic spline regression was applied with predefined knot placement. Model performance was evaluated in terms of discrimination (C-statistic) and calibration (Hosmer-Lemeshow goodness-of-fit test). Results: In conventional linear regression models, PRU was not independently associated with cardiovascular mortality (odds ratio [OR] ~1.00; p > 0.05). However, spline-based analyses demonstrated a statistically significant non-linear (U-shaped) relationship between PRU and mortality risk (p for non-linearity = X). Both low and high PRU values were associated with increased mortality, whereas intermediate PRU levels corresponded to the lowest observed risk. Additional independent predictors of mortality included advanced age, diabetes mellitus, and elevated inflammatory markers. Conclusions: Our findings reveal a significant non-linear association between platelet reactivity and cardiovascular mortality in patients with CAD. Both insufficient and excessive platelet inhibition appear to confer increased risk, suggesting that optimal PRU targets may lie within an intermediate therapeutic range. These results support a paradigm shift toward more individualized antiplatelet therapy strategies guided by platelet function testing. Full article

Background/Objectives: While standardized guidelines have been established for the evaluation and management of blunt cerebrovascular injuries (BCVIs) in adults, there remains a paucity of standardized guidelines for BCVIs in pediatric populations. Shortcomings in treatment algorithms also persist as uncertainty remains about the optimal approach to manage these cases. A review of the literature was performed to compile the current evidence and provide recommendations based on current overarching trends. Methods: PubMed was queried for studies related to the diagnosis and management of BCVIs in the pediatric population. Prevalence, mechanism of injury (MOI), screening criteria, diagnostic modality, vascular injuries identified, associated injuries, treatment, and patient risk factors were analyzed. Results: The Utah and McGovern criteria were the first tools developed for screening BCVIs in pediatric patients. Among all screening tools, the high sensitivity and specificity of the McGovern criteria support its use as the optimal screening strategy to date for pediatric patients. Given the high prevalence of high-energy MOI, observation is the most common approach chosen due to contraindications to medical therapy. Antiplatelet agents showed no significant differences in stroke prevention or hemorrhagic complications compared to anticoagulation. Strokes represent the primary source of morbidity among pediatric patients with BCVIs. Conclusions: Pediatric BCVIs represent an uncommon but clinically significant consequence of blunt trauma, with a significant risk for ischemic stroke and neurologic morbidity. Early recognition through appropriate screening with pediatric-specific screening criteria, CTA imaging, and timely initiation of grade-based treatment can help mitigate injury progression and complications. Full article

Background/Objectives: Blood platelets exhibit substantial functional heterogeneity, yet no established principles exist for distinguishing their subpopulations. The present study proposes a methodology for the evaluation of platelet reactivity and inhibitor sensitivity, with the aim of facilitating the expeditious identification of platelet phenotypes under standard laboratory conditions. Methods: The phenotyping of healthy subjects was based on the study of platelet aggregation in response to agonists and inhibitors of P2Y₁₂, PAR-1 and GPVI receptors. The classification of variants was conducted on the basis of the similarities and differences in EC₅₀/IC₅₀ values obtained for individual ligands. Subsequently, the values were subjected to two- and six-variable cluster analyses. Results: Two major clusters (variants) were identified with consistent reliability across the range of analytical strategies employed. Cluster 1 comprised individuals with low EC₅₀ values and moderate to high IC₅₀ values, indicating high agonist responsiveness and relatively low inhibitor sensitivity. Conversely, cluster 2 exhibited the inverse pattern, characterised by moderate to high EC₅₀ values and moderate to low IC₅₀ values. Cluster 1 constituted a significant proportion of individuals (29–78%, depending on the analysis). The study did not identify a “low responder group”. Conclusions: The proposed methodology is distinguished by two features: its flexibility and its accessibility. These characteristics enable the identification of any platelet phenotype associated with selected signalling pathway(s). The application of this approach has the potential to facilitate the identification of individuals at elevated cardiovascular risk, thereby informing personalised antiplatelet therapy in the context of primary prevention. Full article

Background: Asymptomatic intracranial atherosclerotic arterial stenosis (ICAS) is an underrecognized entity for which vascular risk-factor optimization is the primary management strategy, with no current indication for routine antiplatelet therapy or endovascular intervention for primary stroke prevention. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce major adverse cardiovascular events, including stroke, in high-risk cardiometabolic populations, but their association with outcomes in asymptomatic ICAS is yet to be evaluated. The present study aims to evaluate the association between GLP-1RA use and cerebrovascular outcomes in adults with asymptomatic ICAS. Materials and Methods: We used the TriNetX US Collaborative Network (71 healthcare organizations) to identify adults (≥18 years) with ICAS between 1 January 2016 and 31 December 2025, and excluded patients with prior cerebral infarction, intracranial hemorrhage, or cerebrovascular ischemic syndromes. Exposure was defined as initiation of any GLP-1 receptor agonist (lixisenatide, semaglutide, liraglutide, tirzepatide, dulaglutide) during the 6 months before or on the date of index ICAS diagnosis. Outcomes were assessed at 1 year, and included ischemic stroke, all-cause mortality, and a composite of ischemic stroke or mortality. Propensity-score matching (1:1) was performed, including demographics, vascular risk factors, comorbidities, antithrombotics, lipid/diabetes therapies, and cardiometabolic laboratory/physiologic measures. Results: Before matching, 1746 GLP-1RA users and 71,792 non-users met inclusion criteria; after matching, 1728 patients remained in each cohort. GLP-1RA use was associated with lower 1-year risk of ischemic stroke (4.40% vs. 6.10%; hazard ratio [HR] 0.70, 95% CI 0.52–0.95; p = 0.044), lower all-cause mortality (3.40% vs. 9.40%; HR 0.35, 95% CI 0.26–0.47; p < 0.001), and lower composite outcome risk (7.50% vs. 15.00%; HR 0.48, 95% CI 0.39–0.59; p < 0.001). Notably, these associations were observed despite matching for HbA1c, LDL cholesterol, BMI, and systolic blood pressure, suggesting potential effects beyond measured cardiometabolic risk profiles. Conclusions: In this large, propensity-matched cohort of adults with a-ICAS, GLP-1RA use was associated with lower ischemic stroke, all-cause mortality, and composite outcome at 1 year. These findings are hypothesis-generating and require further prospective studies to confirm this observation. Full article

Background: Although guidelines emphasize proper insertion techniques and tip positioning, catheter-related thrombosis (CRT) remains a common and clinically significant complication of peripherally inserted central catheters (PICCs) and midline catheters (MCs). In this context, the use of pharmacological prophylaxis is still debated. This study aims to assess the incidence of CRT in patients receiving anticoagulant therapy (therapeutic or prophylactic) and antiplatelet therapy. Methods: This retrospective study was conducted at a tertiary care hospital and included adult patients from March 2021 to May 2023. Six potential confounders were analyzed: anticoagulation status (none, prophylaxis, therapeutic), antiplatelet therapy, tip position (PICCs vs. MCs), number of lumens, CRT risk factors, and drug infusion requiring central access. CRT was diagnosed in symptomatic patients using compression ultrasonography. Propensity score weighting and logistic regression were employed to estimate odds ratios (OR) and average treatment effects. Results: A total of 1431 patients were enrolled. PICCs and therapeutic anticoagulant therapy were highly protective against CRT (OR 0.068 [95% CI 0.013–0.2] and OR 0.007 [95% CI 0.001–0.046], respectively). Prophylactic anticoagulant therapy (OR 0.328 [95% CI 0.200–0.519]) and antiplatelet therapy (OR 0.342 [95% CI 0.182–0.595]) also showed protective effects. At the same time, neither the number of lumens, the presence of risk factors, nor the infusion of irritating drugs was independently associated with CRT. Conclusions: The use of anticoagulant drugs (both prophylactic and therapeutic), antiplatelet therapy, and PICC use significantly lowered the risk of CRT. The findings support personalized prevention strategies and underscore the need for a well-designed randomized controlled trial to validate these findings. Full article

The cardiovascular risk imposed by chronic kidney disease is significantly enhanced, and carotid atherosclerosis is an early indicator of systemic vascular damage. In this review, we summarize available data relative to primary prevention strategies for carotid atherosclerosis in chronic kidney disease (CKD) with a focus on risk-adapted and stage-specific management. We conducted a narrative review of the literature. A structured literature search was performed in major databases (PubMed, Scopus, Web of Science and Google Scholar), focusing on studies published between 2012 and 2025, including observational studies, randomized controlled trials, and international guideline recommendations. The review focuses on blood pressure management, lipid-lowering therapy, glycemic control, antiplatelet therapy, as well as lifestyle interventions and screening strategies in patients with CKD without a history of cerebrovascular events. CKD-specific processes, such as inflammation, endothelial dysfunction and vascular calcification, may influence the progression of carotid plaques, highlighting the need to improve traditional and non-traditional risk factor management. The focus of prevention continues to emphasize blood pressure (BP) and lipid control as well. At the same time, routine carotid screening and systematically implemented antiplatelet therapy have no known benefit, but the potential for elevated bleeding risk, especially in advanced CKD. Primary prevention should therefore focus on optimal medical treatment, as well as disease-specific strategies according to CKD stage. Additional CKD-specific studies with carotid endpoints are necessary. Full article

Background and Objectives: Cardiac implantable electronic device (CIED) infections remain among the most serious complications of pacemaker, implantable cardioverter-defibrillator, and cardiac resynchronization therapy procedures. They are associated with substantial morbidity, mortality, prolonged hospitalization, system extraction, long-term antimicrobial therapy, and increased healthcare costs. As most infections arise from perioperative contamination or procedure-related complications, prevention has become a major priority in contemporary electrophysiology practice. This review aimed to summarize current evidence on the prevention of CIED infections, with particular emphasis on modifiable risk factors and perioperative preventive measures. Materials and Methods: A focused narrative review was undertaken using targeted searches of PubMed/MEDLINE and Scopus, supplemented by major international guideline and consensus documents, with priority given to contemporary guidelines, randomised trials, meta-analyses, and major observational studies relevant to CIED infection prevention. Results: Prevention of CIED infection requires a structured, multifactorial approach spanning the entire procedural pathway. Key preventive strategies include careful reassessment of device indication, individualized device selection, correction of modifiable risk factors, postponement of elective implantation in the presence of active infection, appropriate perioperative antibiotic prophylaxis, and optimized management of anticoagulant and antiplatelet therapy to minimize pocket hematoma. Additional relevant measures include meticulous skin antisepsis, limitation of temporary invasive devices and unnecessary hardware, appropriate venous access selection, careful generator pocket creation and wound closure, and avoidance of early reintervention whenever feasible. Antibacterial envelopes may reduce major CIED infections in selected high-risk patients, whereas routine escalation of preventive measures without proven benefit is not supported. Conclusions: CIED infection prevention is inherently multifactorial and depends on the consistent application of evidence-based measures before, during, and after device implantation. Rigorous control of modifiable risk factors, prevention of pocket hematoma, appropriate antimicrobial prophylaxis, and meticulous procedural technique remain the cornerstones of effective infection prevention in patients undergoing CIED procedures. Full article

Coronary artery bypass grafting (CABG) using the autologous saphenous vein (SV) remains widely performed for obstructive atherosclerosis; however, vein graft disease drives recurrent ischaemia through early thrombosis and progressive intimal hyperplasia, and accelerated atherosclerosis developing within the grafts. Extracellular vesicles (EVs) are membrane-bound particles that transfer proteins, lipids, and microRNAs between cells. They modulate endothelial dysfunction, vascular smooth muscle cell phenotypic switching, inflammation, and coagulation, which are core processes in vein graft remodelling. Arterialisation exposes the vein to abrupt rises in shear stress, cyclic stretch, and intraluminal pressure. These forces increase EV release and reshape EV cargo in experimental systems, suggesting a potential mechanism for amplifying early graft injury which warrants direct investigation in vein tissue. This review synthesises current evidence for cell-specific EV contributions from ECs, vascular smooth muscle cells, platelets, and macrophages, and appraises EV-associated microRNAs with biomarker potential relevant to graft failure pathways. We also review therapeutic strategies that may modulate EV signalling including antiplatelet therapy, statins, KCa3.1 inhibition, and pro-reparative mesenchymal stromal cell-derived EVs. No published clinical studies evaluate EV-based biomarkers specifically for saphenous vein graft patency, and none prospectively predict saphenous graft failure. CABG provides a well-defined time zero event that enables longitudinal sampling and risk stratification. Prospective studies linking EV phenotypes and miRNA signatures to imaging-defined graft outcomes are needed to support clinical translation. Full article

Objective: Peripheral arterial occlusive disease (PAOD) is characterized by impaired tissue perfusion, chronic ischemia, and increased platelet reactivity. Hyperbaric oxygen therapy (HBOT) is used as adjunctive treatment in advanced PAOD, but its effect on platelet function remains insufficiently studied. This study examined the association between HBOT and platelet aggregation. Methods: This prospective observational study included 90 patients with Fontaine stage IV PAOD and chronic ulceration, assigned to an HBOT group (n = 60) or waiting-list control group (n = 30). Patients were predominantly male; mean age was 66.82 ± 9.42 years in the study group and 63.00 ± 8.31 years in controls, and diabetes mellitus was present in 55.0% and 63.3%, respectively. Prior revascularization included open surgery in 33.3% and 30.0%, endovascular treatment in 36.7% and 43.3%, and no option for revascularization in 30.0% and 26.7%, respectively. HBOT was administered over 4 weeks (20 sessions, 2.0–2.5 ATA). Platelet aggregation was measured by impedance aggregometry using arachidonic-acid-induced aggregation (ASPI), adenosine-diphosphate-induced aggregation (ADP), and thrombin-receptor-activating peptide-induced aggregation (TRAP) agonists. Changes were analyzed using generalized estimating equation models adjusted for antiplatelet therapy, diabetes mellitus, smoking, and C-reactive protein (CRP). Results: Significant group × time interactions were observed for all platelet activation pathways, indicating greater reductions in the HBOT group than controls: ASPI (β = −290.5; p < 0.001), ADP (β = −243.6; p < 0.001), and TRAP (β = −330.9; p < 0.001). No significant change was observed in controls. HBOT was associated with reduced pain intensity, while CRP and platelet-to-lymphocyte ratio (PLR) remained stable. Ulcer size showed no significant change after 4 weeks. Conclusions: In patients with PAOD, HBOT was associated with reduced platelet reactivity independent of antiplatelet therapy. Further randomized studies are needed to determine its clinical significance. Full article

Aspirin has been the default backbone of antiplatelet therapy after percutaneous coronary intervention (PCI) for over two decades, anchored by landmark trials that established 12-month dual antiplatelet therapy (DAPT) as the standard of care. Three developments have prompted reassessment of this paradigm: the markedly lower thrombotic risk of contemporary drug-eluting stents, the greater potency and consistency of potent P2Y₁₂ inhibitors (ticagrelor, prasugrel), and increasing recognition that major bleeding independently worsens outcomes after PCI. Recent randomised trials have systematically tested aspirin withdrawal at varying time points. Immediate aspirin-free strategies (NEO-MINDSET, STOPDAPT-3) demonstrated an early signal of excess ischaemic events in the ACS component of enrolled populations, suggesting that aspirin remains important during the earliest post-PCI period in ACS. One-month strategies (T-PASS, ULTIMATE-DAPT, TARGET-FIRST) and three-month strategies (TWILIGHT, TICO, DUAL-ACS) showed that transition to P2Y₁₂ monotherapy after an initial DAPT period significantly reduces bleeding without increasing ischaemic events in selected populations. Beyond one year, long-term randomised trials including the HOST-EXAM 10-year follow-up (Lancet 2026) and the STOPDAPT-2 5-year landmark analysis (Circ Cardiovasc Interv 2026), together with study-level meta-analyses (PANTHER) and recent individual patient data meta-analyses, provide converging evidence that clopidogrel monotherapy outperforms aspirin for chronic secondary prevention without excess bleeding. The choice of P2Y₁₂ agent is critical: clopidogrel monotherapy in ACS during the first post-procedural year carries excess thrombotic risk owing to CYP2C19 pharmacogenomic variability, whereas ticagrelor and prasugrel provide more reliable protection. This review synthesises the mechanistic rationale, trial evidence across all time points, special clinical contexts (oral anticoagulation, coronary artery bypass grafting, high bleeding risk), guideline evolution, and methodological considerations, providing a practical framework for individualising post-PCI antiplatelet therapy. Full article

Background: Femoral pseudoaneurysms are clinically heterogeneous, with substantial variability in anatomical features and patient-related bleeding risk. Standard treatment algorithms may be inadequate, particularly in patients receiving anticoagulation or presenting with altered coagulation profiles. A personalized, risk-adapted interventional strategy may optimize outcomes while preserving procedural safety. This study compares ultrasound-guided compression with endovascular and percutaneous therapies and evaluates the safety of minimally invasive approaches across different risk profiles to support individualized management. Methods: This single-center retrospective cohort study included 65 consecutive patients treated for femoral pseudoaneurysms between January 2019 and May 2025. Treatment modalities comprised ultrasound-guided compression, endovascular embolization (coils, covered stents, NBCA–Lipiodol), percutaneous glue injection, and hybrid approaches. Primary endpoints were technical and clinical success. Safety was assessed using pre- and post-procedural INR, platelet count, and hemoglobin levels. High-risk status was defined as ongoing anticoagulation or antiplatelet therapy, INR > 1.5, or platelet count <50 × 10⁹/L. Results: Endovascular and percutaneous approaches achieved significantly higher technical (100% vs. 68.5%, p = 0.006) and clinical success rates (100% vs. 77.8%, p = 0.009) compared with ultrasound-guided compression. In minimally invasive cohorts, INR and platelet counts remained stable after treatment, while hemoglobin showed an expected post-procedural decrease (p < 0.001). High-risk patients demonstrated technical success rates comparable to standard-risk patients, with no significant differences in laboratory trends. Favorable outcomes were observed across different embolic materials. Conclusions: Endovascular and percutaneous therapies provide superior effectiveness compared with ultrasound-guided compression while maintaining a reassuring safety profile, even in patients at increased bleeding risk. These findings support a personalized, patient-tailored interventional approach based on individual anatomical and clinical characteristics. Full article

Bleeding risk assessment is a critical component of the management of patients with ST-segment elevation myocardial infarction (STEMI), yet the optimal approach to risk stratification remains controversial. Although several bleeding risk scores have been developed, their predictive performance in STEMI populations is still evolving. Importantly, bleeding risk in STEMI is dynamic and influenced by clinical status, procedural factors, and antithrombotic strategies, underscoring the need for continuous reassessment throughout hospitalization. Bleeding avoidance measures—including radial access, judicious use of anticoagulation, and individualized antiplatelet therapy—play a pivotal role in reducing complications. Balancing ischemic and hemorrhagic risks is particularly challenging in patients with concomitantly high thrombotic and bleeding risks, requiring tailored management strategies. As bleeding remains a major determinant of prognosis, refining risk stratification tools and integrating evidence-based bleeding prevention strategies into clinical practice are essential. This narrative review summarizes the current evidence regarding the identification of high bleeding risk in hospitalized patients with STEMI and discusses its clinical implications. Also, this review proposes a dynamic, phase-specific framework for in-hospital bleeding risk assessment and management in patients with STEMI. Full article