Search Results (3,669)

Background: Whether the comparative effectiveness of a drug-coated balloon (DCB)-based versus drug-eluting stent (DES)-only percutaneous coronary intervention (PCI) strategy differs between stable angina (SA) and acute coronary syndrome (ACS) remains uncertain. Methods: In this observational, registry-based study, we analyzed 11,522 patients (4490 with SA and 7032 with ACS) from two multicenter registry sources who had undergone PCI in routine clinical practice; the treatment strategy was not assigned by a study protocol. Within each presentation, the DCB-based and DES-only strategies were compared using propensity-score overlap weighting. Complementary within-strategy analyses compared SA with ACS. The primary outcome was the 3-year rate of major adverse cardiac and cerebrovascular events (MACCE). Results: In both presentations, a DCB-based strategy was associated with a lower 3-year risk of MACCE than a DES-only strategy, with a stronger association in SA (overlap-weighted hazard ratio [HR], 0.33; 95% confidence interval [CI], 0.22–0.49) than in ACS (HR, 0.73; 95% CI, 0.59–0.91; p-for-interaction < 0.001). Within-strategy analyses localized this effect modification to the DCB-based group: SA was associated with a lower risk of MACCE than ACS (HR, 0.47; 95% CI, 0.31–0.69) in the DCB-based group, whereas this gradient was absent in the DES-only group. The incidence of major bleeding was lower with the DCB-based strategy in both presentations. Conclusions: A DCB-based PCI strategy was associated with lower 3-year event rates than a DES-only strategy in both SA and ACS, with the strongest relative association in SA. These observational findings are hypothesis-generating and warrant confirmation in randomized trials. Full article

Coronavirus disease 2019 (COVID-19) is increasingly recognized as a multisystem disorder associated with persistent metabolic complications extending beyond the acute phase of infection. Accumulating evidence suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may disrupt glucose homeostasis through mechanisms involving pancreatic β-cell dysfunction, insulin resistance, chronic inflammation, oxidative stress, mitochondrial dysfunction, and hypoxia-related signalling. This review summarizes current evidence regarding the molecular and cellular mechanisms linking SARS-CoV-2 infection to impaired insulin secretion and post-COVID metabolic disturbances. Particular emphasis is placed on the regulation of insulin secretion, β-cell compensation and failure, oxidative stress, inflammatory signalling, mitochondrial dysfunction, and the development of the post-COVID metabolic phenotype. Emerging evidence indicates that persistent metabolic abnormalities after COVID-19 may range from transient dysglycaemia to new-onset diabetes mellitus and metabolic syndrome. The review also discusses clinical implications, biomarkers, therapeutic perspectives, and unresolved questions regarding the reversibility of post-COVID β-cell dysfunction. A better understanding of the mechanisms underlying post-COVID metabolic dysfunction may improve risk stratification, facilitate early intervention, and support development of targeted therapeutic strategies aimed at preserving β-cell function and long-term metabolic health. Full article

Drug-coated balloon (DCB) PCI can avoid permanent metallic scaffolding in selected acute coronary syndrome (ACS) lesions, but interpretation depends on lesion preparation, procedural selection, and follow-up ascertainment. We analyzed a retrospective dual-center registry of 276 unique patients who underwent one index DCB-treated ACS procedure after operator-judged adequate lesion preparation. Presentations were NSTEMI in 174 patients (63.0%), STEMI in 90 (32.6%), and unstable angina in 12 (4.3%). Paclitaxel-coated DCBs were used in 262 patients (94.9%) and sirolimus/non-paclitaxel DCBs in 14 (5.1%). Thrombus aspiration and GP IIb/IIIa inhibitors were used selectively in 17 (6.2%) and 28 (10.1%) patients, respectively. Bail-out stenting was required in 13 patients (4.7%). Predominantly benign/non-flow-limiting angiographic dissection was recorded in 18 patients (6.5%). A follow-up of at least 365 days or death within 365 days was available for 274 patients (99.3%). Clinically driven TLR occurred in 18 patients (crude 18/274, 6.6%; Kaplan–Meier 365-day estimate, 6.8%; 95% CI, 4.3–10.5), all occurring between 3 and 9 months. All-cause death occurred in 12 patients (Kaplan–Meier estimate, 4.4%; 95% CI, 2.5–7.5). In selected ACS lesions that passed a preparation gate, DCB treatment was associated with feasible procedural results and acceptable 12-month clinically recorded outcomes. The findings do not estimate all-comer DCB eligibility and should not be interpreted in terms of the efficacy of DCBs compared with DESs. Full article

Background: Risk profiles of premature coronary heart disease (PCHD, ≤45 years) among high-altitude acute coronary syndrome (ACS) populations remain poorly characterized. This study explored clinical features and independent predictors of early-onset ACS in Lhasa. Methods: We retrospectively enrolled 467 first-ACS patients (1 July 2022–30 June 2024). Patients were further dichotomized into PCHD and non-PCHD groups for comparison. Univariable and multivariable logistic regression identified PCHD risk factors. Results: Compared with non-PCHD patients, PCHD patients featured higher proportions of male non-Tibetans, higher smoking and alcohol consumption rates, lower prevalence of hypertension and diabetes, and elevated SpO₂ (all p < 0.05). They had significantly higher CHOL, TG, LDL-C, UA and Hb (all p < 0.05), accompanied by lower WBC, PLT and D-dimer (all p < 0.001). Multivariate regression confirmed diabetes mellitus (OR = 1.158, p = 0.014), TG (OR = 1.625, p < 0.001), WBC (OR = 1.995, p = 0.007), D-dimer (OR = 2.841, p = 0.043) and SpO₂ (OR = 0.937, p = 0.019) as independent predictors of PCHD. Conclusions: Integrated monitoring of glucose, lipids, hypoxia and thromboinflammatory biomarkers may supply preliminary auxiliary reference for early prevention of PCHD in local highland youth, while large multi-center verification is still needed to confirm its clinical value. Full article

Background/Objectives: Exacerbations of chronic obstructive pulmonary disease (COPD) are a common reason for emergency department (ED) attendance and hospital admission. Acute respiratory worsening is non-specific, and previous spirometric confirmation may be unavailable at presentation. We aimed to translate current recommendations into an ED-specific clinical pathway that standardizes safety-critical steps without replacing individualized clinical judgment. Methods: We performed a targeted synthesis of international and Spanish guidance and key studies relevant to ED diagnosis, severity assessment, pharmacological treatment, respiratory support, antimicrobial stewardship, and disposition. The evidence base was updated in June 2026, and the pathway was reviewed by a multidisciplinary clinical group. Results: The revised pathway comprises four stages: (1) verify previous COPD confirmation, identify an acute exacerbation-like syndrome, and assess alternative or concomitant diagnoses; (2) grade acute severity using point-of-care variables and separately assess patient vulnerability; (3) provide severity-adjusted treatment with early reassessment; and (4) determine disposition and follow-up. It incorporates controlled oxygen, individualized bronchodilator delivery, explicit criteria for systemic corticosteroids and antibiotics, assessment of risk for Pseudomonas aeruginosa, non-invasive ventilation (NIV), and a defined adjunctive role for high-flow nasal cannula (HFNC). Patients without previous post-bronchodilator spirometry are classified as having suspected COPD and require confirmation after recovery. Conclusions: This evidence-informed pathway is a preliminary clinical framework, not a diagnostic rule or validated decision instrument. It is intended to support, rather than replace, professional judgment. Feasibility, acceptability, diagnostic safety, and clinical impact require prospective evaluation, beginning with a pilot implementation study. Full article

Background: Myeloid/lymphoid neoplasms with FGFR1 rearrangement (MLN-FGFR1), also known as 8p11 myeloproliferative syndrome, are rare and aggressive hematologic malignancies arising from pluripotent stem cells. The FGFR1::ZMYM2 fusion resulting from t(8;13)(p11.2;q12) characteristically co presents as T-lymphoblastic lymphoma in lymph nodes alongside a myeloproliferative neoplasm in the bone marrow. The disease is resistant to tyrosine kinase inhibitors and conventional chemotherapy, and carries a median survival of less than 12 months without allogeneic hematopoietic stem cell transplantation (allo-HSCT). Case Presentation: We report a 23-year-old female who presented with progressive cervical lymphadenopathy and hyperleukocytosis (WBC 186.6 K/μL). Excisional lymph node biopsy demonstrated T-cell acute lymphoblastic lymphoma (T-ALL) with eosinophilic infiltration; immunohistochemistry confirmed lymphoblasts positive for CD1a, CD2, CD3, CD4, CD5, CD7, CD8, and TdT. Concurrent bone marrow biopsy showed a myeloproliferative neoplasm without excess blasts. Chromosomal analysis confirmed t(8;13)(p11.2;q12) with FGFR1::ZMYM2 rearrangement, and NGS identified a concurrent CSF3R variant (Q741*). She received induction chemotherapy per the PEDS AALL1231 protocol (Arm A) followed by consolidation, with a course complicated by hyperleukocytosis, venous thromboembolism, E. coli bacteremia, and severe mucositis requiring PICU admission. Despite initial response, the disease progressed to acute myeloid leukemia (AML) with acquisition of a PTEN variant; the patient was offered but did not complete allo-HSCT and died of refractory AML approximately 10 months after diagnosis. Conclusions: This case highlights the aggressive clinical course and diagnostic challenges of MLN-FGFR1, a rare stem cell-derived myeloid/lymphoid neoplasm. To our knowledge, this appears to be the first reported case documenting sequential CSF3R and PTEN variant acquisition with complete follow-up through fatal AML transformation, and the first to describe treatment with a pediatric ALL induction protocol (PEDS AALL1231) in this setting. The characteristic histomorphologic pattern of eosinophil-rich T-ALL in lymph nodes with concurrent myeloproliferative neoplasm in bone marrow should prompt immediate molecular workup. Allo-HSCT must be pursued urgently at diagnosis, as complications rapidly narrow the transplant window and the disease is uniformly fatal without it. Full article

Background and Clinical Significance: Encephalitis is a rare neurological complication associated with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection. In rare cases, focal neuroinflammation can manifest as a mass-like parenchymal lesion, creating profound diagnostic and treatment dilemmas by mimicking primary central nervous system neoplasms. Case Presentation: A 34-year-old female presented with cephalalgia, nausea, confusion, facial palsy, and a new onset of focal impaired awareness seizures (FIAS). Brain magnetic resonance imaging (MRI) revealed a prominent hyperintense lesion within the left temporal lobe with associated vasogenic edema and focal leptomeningeal enhancement highly suspicious of a low-grade glial neoplasm. Although nasopharyngeal RT-PCT was negative, the presence of serum anti-SARS-CoV-2 IgM and IgG suggested recent subclinical SARS-CoV-2 infection. To resolve diagnostic ambiguity and avoid empiric oncological overtreatment, a stereotactic brain biopsy was performed. Histopathology revealed acute neuroinflammation characterized by reactive gliosis, microglial hyperplasia, and perivascular lymphatic cuffing, with no evidence of neoplastic presence. Quantitative tissue RT-PCR confirmed the presence of SARS-CoV-2 (Ct33). Follow-up imaging demonstrated complete resolution of the abnormalities following conservative treatment with corticosteroids and antiepileptics, though mild clinical symptoms persisted for 12 months thereafter. Conclusions: Encephalitis presents a rare yet critical manifestation of SARS-CoV-2. Establishing definitive etiology remains challenging. Stereotactic biopsy is a valuable tool to guide appropriate treatment in cases of ambiguous imaging and clinical findings. Radiographic resolution may precede complete clinical recovery. Full article

Background: Acute liver failure (ALF) is a rare, yet potentially fatal clinical syndrome characterized by the rapid deterioration of hepatic function in individuals without pre-existing liver disease, typically occurring over a period of days to weeks. It is associated with substantial morbidity and mortality, particularly in low-income settings, and is clinically defined by the presence of jaundice, coagulopathy, and hepatic encephalopathy. Among its various etiologies, acetaminophen (APAP) overdose is the leading cause of drug-induced liver injury and ALF, especially in industrialized countries such as the United States and the United Kingdom. In the present study, we compared two experimental approaches for inducing APAP-mediated ALF in mice: oral and intraperitoneal (IP) administration. Methods: While most studies reported in the literature rely on a single route of administration, this comparative analysis provides a more comprehensive evaluation of the advantages and limitations associated with each method, thereby enhancing the reproducibility and translational relevance of experimental ALF models. Results: Our results demonstrate that both administration routes effectively recapitulate key clinical and biochemical features of human ALF, including hepatic encephalopathy, marked elevations in serum transaminases, and high mortality rates. However, the effective APAP dose required to achieve these outcomes differed between the two routes, with 400 mg/kg for IP administration and 500 mg/kg for oral administration, as would be expected based on pharmacokinetic considerations. From a clinical assessment perspective, the use of adapted scoring systems, such as the O’Grady criteria, is essential for evaluating encephalopathy in animal models. Notably, oral administration via gastric gavage requires greater technical expertise, which may influence experimental consistency. Conclusions: Taken together, these findings underscore the importance of route selection in experimental design and highlight the value of comparative approaches for optimizing preclinical models of ALF. Full article

Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune astrocytopathy in which antibodies against the aquaporin-4 (AQP4) water channel produce a stereotyped group of syndromes determined by the anatomical distribution of AQP4 expression. Six core clinical presentations are recognized: optic neuritis, longitudinally extensive transverse myelitis, area postrema syndrome, acute brainstem syndrome, diencephalic syndrome, and cerebral syndrome. Because disability in NMOSD almost always accrues at discrete, treatable relapses rather than through insidious progression, early recognition, supported by prompt AQP4-IgG testing and pattern recognition on MRI, is essential to preserving vision, mobility, and independence. This review summarizes the pathophysiology, clinical and radiologic features, diagnostic evaluation, and differential diagnosis of each core syndrome and synthesizes contemporary evidence for relapse prevention. Over the past decade, the therapeutic landscape has been transformed: agents targeting complement (eculizumab, ravulizumab), the interleukin-6 receptor (satralizumab, tocilizumab), and B cells (rituximab, inebilizumab) now have randomized evidence of efficacy in seropositive disease, with complement inhibitors ranking highest across indirect treatment comparisons. Evidence in seronegative disease remains limited, no approved agents have been compared head-to-head, and the optimal role of early plasma exchange is unsettled. Emerging neuroprotective strategies and chimeric antigen receptor T-cell therapy, both of which remain experimental, may further expand options for refractory disease. Once uniformly disabling, AQP4-IgG NMOSD is now a highly treatable condition in which timely diagnosis and sustained immunotherapy can meaningfully alter long-term outcomes. Full article

Background: Emergency services in urban areas are overcrowded due to a rise in mild-to-moderate acuity consultations, and physician-led home visits are less common. In response, a home-based urgent care model in an urban setting (Docadom) was developed. Consultation requests via a dedicated mobile application or phone call are triaged by a trained emergency nurse. Physicians travel to the patient via an electric cargo bike that has storage for medical equipment. During home visits, physicians perform testing/diagnosis and advanced procedures (e.g., intravenous medication delivery) and prescribe treatment (if needed). This descriptive analysis reports activities during the first 12 months of Docadom. Methods: Data from all patients seen during the first 12 months of Docadom activity (1 May 2023–30 April 2024) were analysed. Outcomes analysed included: age, sex, diagnosis, and whether the patient was referred to the hospital. Patient satisfaction (from 1 [worst] to 5 [best]) is also reported. Each outcome was analysed in two subgroups based on patient age (<75 or ≥75 years) because the Swiss health insurance system distinguishes between these two age groups, using Wilcoxon or chi-square tests as appropriate. Results: A total of 1736 patients requested a consultation (66% female; median age 70 years [interquartile range 36, 84]; 43% aged ≥75 years). The five most frequent clinical presentations were: ear, nose and throat infection, epistaxis and bronchitis (25.7%); soft tissue trauma (7.8%); acute cervical or lower back pain syndrome (5.6%); gastroenteritis and dehydration (5.0%); and cancer and general decline in the elderly (4.6%). Only 4.7% of the patients were referred to the hospital. The mean satisfaction score was 4.97 (response rate: 207/422 patients [49%] who requested a consultation via the app). Conclusions: These data highlight the feasibility and acceptability of a home-based urgent care model in an urban setting. The service effectively addressed a wide range of acute conditions, especially in elderly patients. The low hospital referral rate and high patient satisfaction are encouraging, but as a single-arm descriptive analysis without post-consultation outcome data or a comparator group, this study cannot establish clinical safety or an effect on emergency department use; these questions require a future comparative study. Full article

Background: Despite recent advances in reperfusion strategies, acute coronary syndrome (ACS) patients remain at high risk for recurrent major adverse cardiovascular events (MACE). This study aims to investigate the association between lipoprotein(a) (Lp(a)) and MACE in ACS patients, and to systematically evaluate its predictive performance, incremental prognostic value and clinical utility. Methods: This retrospective cohort study included 300 ACS patients with a 1-year follow-up. Serum Lp(a) levels were measured by immunoturbidimetry using fasting venous blood samples collected on the day of admission. Kaplan–Meier and Cox regression analyses were used to assess the association between Lp(a) and MACE. Subgroup and interaction analyses were performed to test the robustness of the findings. Incremental predictive value and net clinical benefit were evaluated using receiver operating characteristic (ROC) curves, the DeLong test, decision curve analysis (DCA) and the integrated discrimination improvement (IDI) index. Results: Baseline Lp(a) levels were significantly higher in the event group (p = 0.006). A significantly lower cumulative survival probability was found in patients with elevated Lp(a) (log-rank p = 0.0014). As a standalone predictor of MACE, Lp(a) yielded an AUC of 0.606 (p = 0.006). The AUC of the baseline model was 0.753 (95% CI: 0.694–0.812), which increased to 0.771 (95% CI: 0.712–0.831) after adding Lp(a). DCA showed that the Lp(a)-guided strategy provided higher net benefit than both the “treat-all” and “treat-none” strategies within a threshold probability range of 0–0.35. Conclusions: Although Lp(a) offers limited incremental value over traditional risk factors and the Gensini score in the low-to-moderate risk range (<0.35), it provides net clinical benefit as a complementary biomarker in ACS. Full article

Sepsis is a life-threatening syndrome characterized by severe immune dysregulation, frequently culminating in acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI). Current supportive therapies fail to reverse the underlying pathophysiological damage. However, mesenchymal stromal cells (MSCs) have emerged as a promising therapeutic frontier due to their robust immunomodulatory, anti-inflammatory, and tissue-regenerative properties. Despite compelling preclinical evidence, translating these benefits into consistent clinical efficacy remains a major challenge. This review critically examines the biological and anatomical barriers limiting the efficacy of MSCs, particularly the pulmonary first-pass effect, which restricts the systemic delivery of viable cells to distant organs such as the kidneys. To overcome these physical limitations, we highlight the recent paradigm shift toward nanoscale, cell-free therapies, specifically MSC-derived extracellular vesicles (MSC-EVs). EVs effectively bypass pulmonary sequestration and thromboembolic risks, exerting their potent therapeutic effects through the horizontal transfer of bioactive cargo, notably microRNAs, to reprogram cellular fate and restore immune homeostasis. We also discuss the critical need for rigorous clinical trial designs, scalable good manufacturing practice protocols, and the integration of a precision medicine approach. Ultimately, incorporating validated biomarkers for targeted patient stratification will be the decisive step in unlocking the full therapeutic potential of MSCs and their derivatives in critical care. Full article

Background/Objectives: A complex karyotype (CK) in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDSs) is defined as the presence of three or more unrelated chromosomal abnormalities in the absence of defining core-binding factor translocations. Losses/Deletions on chromosomes 5, 7 and 17 are frequently observed. It is heavily associated with TP53 mutations, with 70–80% of CK cases in MDS/AML harboring TP53 mutations. Methods: An extensive literature search of the studies carried out in the last two decades has shown a consistent development of experimental and clinical studies aiming to characterize the biological properties and clinical features of AML and MDS bearing CK and TP53 mutations. Results: These studies have greatly contributed to identifying as separate entities AML and MDS bearing CK and or TP53 alterations. Particularly, the improvement in the methods of detection of chromosome aberrations has contributed to defining the specific nature of the various chromosome abnormalities and to deciphering the mechanisms of catastrophic events leading to gene rearrangements. Two types of CK were identified in AML and MDS, one more frequently associated with TP53 mutations (with poor prognosis) and another less frequently without TP53 mutations (with relatively better prognosis). Conclusions: The treatment of AML and MDS with CK and/or TP53 mutations alterations remains extremely challenging, and the prognosis of these patients is dismal. The main aim of the various induction treatments explored in these patients is to bridge patients to allo-HSCT, the only therapeutic approach able to improve the survival of at least a part of these patients. Full article

Cardiac myosin-binding protein C (cMyBP-C) is a cardiac-restricted sarcomeric protein; after cardiomyocyte injury, circulating intact cMyBP-C and/or cMyBP-C fragments, collectively referred to here as the cMyC biomarker signal, appear rapidly in blood. In suspected acute coronary syndrome (ACS), its most important potential role is not as another marker of injury but as a decision-enhancing biomarker beyond symptoms, electrocardiography, cardiac troponin T and I concentrations measured with high-sensitivity assays (hs-cTnT and hs-cTnI), time from pain onset, and pre-test probability. This narrative review separates three clinical tasks frequently conflated in the biomarker literature: diagnosis of acute myocardial infarction, emergency-department triage, and prediction of short-term or post-infarction risk. We integrate cMyBP-C sarcomeric architecture, N-terminal regulatory biology, phosphorylation, proteolysis, circulating fragments, assay epitopes, analytical stability, diagnostic algorithms, point-of-care testing, ST-segment elevation myocardial infarction reperfusion biology, and major confounders including renal dysfunction, heart failure, age, sex, and chronic ventricular remodeling. Current evidence supports further evaluation of cMyC as an adjunct in early presenters and accelerated diagnostic pathways. However, diagnostic safety and efficacy have not been consistently reproduced across platforms and populations, and external validation—particularly of rule-out performance—remains insufficient for routine clinical use. Recurrent injury assessment and post-infarction risk phenotyping remain promising but incompletely validated applications. Before guideline adoption, cMyC needs phenotype-specific, multicenter implementation trials demonstrating incremental net benefit, cost-effectiveness, and patient-level safety compared with contemporary hs-cTnT- and hs-cTnI-based clinical decision algorithms. Full article

Background: The optimal duration of dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) of the left main coronary artery remains uncertain because this lesion involves a large myocardial territory and requires a careful balance between ischemic protection and bleeding risk. This review aimed to provide an updated, left-main-focused synthesis of the evidence on DAPT duration after PCI and to clarify how treatment should be individualized according to clinical presentation, lesion complexity, procedural strategy, intravascular imaging, and validated ischemic and bleeding risk scores. Methods: This narrative review with a structured literature search examined studies published from January 2010 through May 2026 in PubMed/MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, and Google Scholar. From 248 identified records, 62 studies met the eligibility criteria and were included in the qualitative synthesis, comprising 38 randomized controlled trials and 24 observational studies or pooled analyses. The review prioritized direct left-main-specific evidence while also incorporating broader PCI studies with left-main subgroups and indirect contextual evidence relevant to antiplatelet decision-making. Independent screening, duplicate data extraction, and qualitative risk-of-bias assessment were performed, but the review was not prospectively registered, and no meta-analysis was conducted. Results: The available evidence supports an individualized rather than fixed DAPT strategy after left main PCI. In stable patients with anatomically simple left main lesions and acceptable bleeding risk, 6–12 months of DAPT appears generally sufficient, whereas patients with acute coronary syndromes, two-stent distal bifurcation strategies, high thrombotic burden, or other high-ischemic-risk features may derive greater benefit from extending therapy beyond 12 months when bleeding risk is low. Contemporary guideline recommendations are broadly aligned with this risk-adapted approach, and recent trials further refine decision-making: PARTHENOPE provided randomized support for risk-score-guided personalization of DAPT duration, whereas NEO-MINDSET cautioned against immediate aspirin withdrawal after PCI in acute coronary syndromes. Intravascular imaging, especially IVUS and OCT, improves procedural optimization and may help contextualize post-PCI thrombotic risk, although current data do not validate imaging findings alone as a stand-alone criterion for abbreviated DAPT. Conclusions: DAPT duration after left main PCI should be individualized by integrating clinical presentation, lesion and procedural complexity, intravascular imaging, and validated ischemic and bleeding risk tools. A personalized, risk-adapted strategy currently offers the most appropriate framework for balancing ischemic benefit against bleeding harm in this high-risk population. Full article