Background:Central obesity is strongly associated with cardiometabolic dysfunction and cardiovascular disease (CVD), yet CVD burden may vary by metabolic phenotype among affected adults. This study examined whether metabolically unhealthy central obesity (MUCO) is associated with higher CVD prevalence than metabolically healthy central obesity (MHCO), whether CVD increases in a dose-response manner with metabolic abnormality burden, and whether associations vary by age, sex, and race/ethnicity. Methods:We conducted a cross-sectional analysis of NHANES 2011-March 2020, including adults ≥20 years with central obesity (≥102 cm (40″) in men; ≥88 cm (35″) in women). Metabolic phenotype was defined by four abnormalities: elevated blood pressure (≥130/85 mmHg or antihypertensive use), dysglycemia (HbA1c ≥ 5.7%, self-reported diabetes, or diabetes medication use), low HDL cholesterol (<40 mg/dL in men or <50 mg/dL in women), and hypercholesterolemia (physician diagnosis or lipid-lowering therapy). Participants were classified as MHCO (0-1 abnormality) or MUCO (≥2 abnormalities); abnormalities were summed (0-4) to assess dose-response. The outcome was self-reported physician-diagnosed CVD (coronary heart disease, myocardial infarction, stroke, heart failure, or angina). Survey-weighted Poisson regression estimated adjusted prevalence ratios (PRs) and 95% confidence intervals (CIs). Results:Among 11,657 adults with central obesity, 6,997 were MHCO and 4,660 MUCO, representing 128.4 million U.S. adults. Weighted CVD prevalence was higher in MUCO than MHCO (15.7% vs 7.3%). After adjustment, MUCO was associated with higher CVD prevalence (PR 1.48; 95% CI 1.30-1.68; p < 0.001). Each additional metabolic abnormality increased CVD prevalence by 29% (PR 1.29; 95% CI 1.21-1.38; p < 0.001). The association was strongest among adults aged 20-39 years (PR 3.89; 95% CI 2.22-6.81), despite low absolute prevalence. Conclusions:Among U.S. adults with central obesity, metabolic dysfunction is associated with higher CVD prevalence, with a clear dose-response relationship. These findings support phenotype-based cardiovascular risk stratification beyond waist circumference and emphasize early identification and management of metabolic abnormalities, particularly in younger adults.
Background: Direct oral anticoagulants (DOACs) are widely used among hospitalized patients, yet real-world inpatient bleeding data remains relatively sparse. Most evidence derives from randomized trials enrolling ambulatory, clinically stable patients, or those being treated for a single specific indication such as acute venous thromboembolism (VTE), which may not reflect the risk profile of acutely ill inpatients with multimorbidity, procedural exposures, and fluctuating renal function. This study describes the incidence and types of bleeding events in a real-world inpatient cohort receiving apixaban or rivaroxaban at a single tertiary care center. Methods: We conducted a single-center, retrospective cohort study of 867 hospital encounters involving apixaban (n = 722, 83.3%) or rivaroxaban (n = 145, 16.7%) between 2019 and 2021. The primary outcome was a non-adjudicated, non-standardized composite of any documented bleeding (gastrointestinal bleeding, hematuria, intracranial hemorrhage, vaginal bleeding, or epistaxis) during the index hospitalization; International Society on Thrombosis and Haemostasis (ISTH) major bleeding or clinically relevant non-major (CRNM) bleeding definitions were not applied. Secondary outcomes included individual bleeding subtypes, hemoglobin drop ≥2 g/dL, transfusion requirement, ICU/CCU admission, vasopressor use, and bleeding-related mortality. All comparisons are unadjusted and descriptive. Between-group comparisons used Fisher’s exact test and the Mann–Whitney U test. Results: Bleeding was documented in 13 encounters (1.5% overall; apixaban 1.39%, rivaroxaban 2.07%); given reliance on clinical documentation rather than systematic adjudication, true incidence may be higher. The composite outcome was driven predominantly by gastrointestinal bleeding (n = 10, 76.9% of events). No hemoglobin drop ≥2 g/dL, transfusion, ICU/CCU admission, vasopressor use, or bleeding-related mortality occurred in either group. No statistically significant between-agent difference was observed (p = 0.47); all comparisons are unadjusted and descriptive. Median length of stay (LOS) differed between drug groups (8.6 vs. 6.2 days; p = 0.006), an exploratory finding confounded by patient class imbalance. Conclusions: In this single-center, retrospective cohort, bleeding was documented in 1.5% of encounters; ascertainment limitations mean true incidence may be higher. Non-adjudicated, non-standardized outcome definitions and the small number of events limit comparability with the literature and preclude definitive inference. The absence of a statistically significant between-agent difference should not be interpreted as evidence of equivalence. These findings are hypothesis-generating and should not be used for comparative inference. Prospective, multicenter studies using ISTH-standardized outcomes, indication-level data, and formal adjudication are needed.
Previous research has shown that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have cardioprotective effects. However, their efficacy in acute myocardial infarction (AMI) is not yet well established. We conducted a systematic review and meta-analyses to assess the impact of GLP-1 RAs in AMI. We systematically searched major databases for studies in patients with ST-elevation (STEMI) or non-ST-elevation myocardial infarction (NSTEMI). These included MEDLINE (accessed via PubMed), Excerpta Medica dataBASE (Embase), Cochrane Central Register of Controlled Trials (CENTRAL), ClinicalTrials.gov, and Google Scholar from their inception through February 2026. PRISMA guidelines were used to conduct this review. Both randomized controlled trials (RCTs) and observational studies were included in the systematic review. However, only RCTs were included in the meta-analyses. The primary outcome was infarct size relative to the area at risk (AAR). Secondary outcomes included major adverse cardiovascular events (MACE) and safety outcomes (nausea, hypoglycemia, pancreatitis). The Cochrane Risk of Bias 2 (RoB 2) tool and Newcastle-Ottawa Scale (NOS) were used to assess risk of bias. We included eight studies with a total of 1,483 participants. GLP-1 RAs led to a smaller infarct size indexed to the AAR compared with placebo. The mean reduction was 10.14
Abstract Vasculidities involve complex interactions of immune dysregulation leading to inflammation of blood vessels resulting in tissue damage due to necrotizing granulomatous progression with multisystem involvement. A 24-year-old Mexican immigrant female without significant past medical history other than working at a pet store with intermittent exposure to birds, rodents, guinea pigs and ferrets presented to the ED with a 10 day history of progressive worsening of fever and productive cough despite antibiotic treatment. Recently referred to podiatry for painful purple nodules that progressed to ulceration, failed to improve with antibiotics. Denied night sweats, weight loss, hemoptysis, sick contacts, outside travel, IV drug misuse or TB exposure. Initial vital signs temperature 100.5 F, heart rate 144 bpm, respiratory rate 26 with 97% room air sat. Normal physical exam except for previously described nodules. ED workup with WBC 16.1 x 10*3/uL, CRP 250 mg/L, ESR 83 mm/hr. CT angiogram of the chest revealed thick walled cavitary masses with irregular inner margin, surrounded by ground-glass, involving the inferior aspect of the left upper lobe and the superior segment of the left lower lobe, multiple (largest being 7.5 cm x 5.6 cm). ID was consulted for concern of TB vs necrotizing pneumonia, broad spectrum antibiotics were started. ID work up for HIV, blood cultures, Influenza A, Influenza B, RSV, Aspergillus, AFB smear, Chlamydia psittaci, hepatitis B, C, Histoplasmosis, Blastomycosis and Cryptococcosis returned negative. Autoimmune work up Rheumatoid factor 162 U/mL, CCP IgG/IgA negative, ACE 32 U/L, Complement C3 88 mg/dL, C4 5 mg/dL, Anti- PR3 antibodies positive with 4.9 units, C-ANCA titers of 1:40 (normal <1:20 titer). WIth persistent symptoms and onset of hemoptysis, Pulmonology was consulted. Bronchoscopic evaluation was negative bacterial and fungal stain/culture PJP PCR, aspergillus antigen, Mycobacterium PCR and nocardia. Lung biopsy, brushing negative for granulomatous inflammation and malignancy. A right ankle ulcer biopsy revealed prominent vascular proliferation in the dermis, ulcer with fibrinoid necrosis and neutrophilic infiltrate suggestive of pyoderma gangrenosum. Given rapidly progressive thick walled cavitary nodules in multiple locations with surrounding ground glass opacities and tissue biopsy with pyoderma gangrenosum, elevated inflammatory markers, negative infectious disease work up and autoimmune workup revealing ACR/EULAR score 7, patient has been diagnosed with Granulomatosis with Polyangiitis. She was started on Prednisone 50 mg daily and Methotrexate 25 mg weekly achieving complete resolution of hemoptysis within 48 hrs. This abstract is funded by: None
