Dyslipidemia is a major modifiable risk factor for atherosclerotic cardiovascular disease, and many high-risk patients do not reach target low-density lipoprotein cholesterol (LDL-C) levels despite conventional therapy. Ongericimab is a humanized monoclonal antibody against proprotein convertase subtilisin/kexin type 9. We searched PubMed, Scopus, Web of Science, and Cochrane CENTRAL from inception to April 4, 2026 for randomized controlled trials comparing ongericimab with placebo in dyslipidemia, pooled data using random-effects models, and rated certainty with GRADE. Five double- blind trials (10 intervention-placebo comparisons; 1415 participants), all conducted in China, were included. Ongericimab reduced LDL-C at 12 weeks by 69.39 percentage points relative to placebo (95% confidence interval, -73.67 to -65.11), with sustained reductions at 24 weeks (-68.19; -73.67 to -62.71) and 52 weeks (-68.99; -78.33 to -59.65). At 12 weeks, it also reduced apolipoprotein B (-60.68), non-high-density lipoprotein cholesterol (-66.30), total cholesterol (-46.49), lipoprotein(a) (-45.74), and triglycerides (-25.89), and increased apolipoprotein A1 (8.15) and high-density lipoprotein cholesterol (10.33) (all P < 0.0001). Treatment-emergent adverse events (risk ratio 1.01; 0.90-1.14), serious adverse events (1.52; 0.30-7.58), injection-related adverse events (1.31; 0.45-3.78), and laboratory abnormalities did not differ from placebo.
The optimal strategy for long-term oral anticoagulation (OAC) after catheter ablation for atrial fibrillation (AF) remains uncertain. Although current guidelines recommend anticoagulation based on thromboembolic risk scores irrespective of rhythm status, this recommendation has not been validated by randomized controlled trials (RCTs). We included 3 RCTs, ODIn-AF (Prevention of Silent Cerebral Thromboembolism by Oral Anticoagulation With Dabigatran After Pulmonary Vein Isolation for Atrial Fibrillation), ALONE-AF (AnticoaguLation ONE Year After Ablation of Atrial Fibrillation in Patients With Atrial Fibrillation), and OCEAN (Optimal Anticoagulation for Higher-Risk Patients Post-Catheter Ablation for Atrial Fibrillation Trial), enrolling patients at least 6 months postablation with no recurrent atrial arrhythmias. Primary efficacy outcomes were all stroke and embolism (including cerebral emboli). The primary safety outcome was major bleeding. Secondary outcomes included clinically relevant nonmajor bleeding and other thromboembolic and bleeding events. Risk ratios (RR) with 95% confidence intervals (CI) were pooled using a random-effects model. In total, 2324 patients were included. Discontinuation of anticoagulation therapy did not significantly increase the risk of all stroke and embolism, at least 6 months postcatheter ablation [RR, 0.58 (0.11-3.12); I2 = 54%]. OAC discontinuation was associated with lower risk of major bleeding [RR, 0.33 (0.11-0.95); I2 = 0%] and clinically relevant nonmajor bleeding [RR, 0.40 (0.19-0.84); I2 = 0%]. No significant differences were observed for other thromboembolic and bleeding events. Sensitivity analyses using per-protocol populations were significant only for a reduction in clinically relevant nonmajor bleeding [RR, 0.33 (0.17-0.65); I2 = 0%]. In patients remaining arrhythmia-free for at least 6 months after AF ablation, discontinuation of OAC was associated with fewer bleeding events without a statistically significant increase in thromboembolic risk. These hypothesis-generating findings highlight the need for larger, well-powered RCTs to better inform postablation anticoagulation strategies.
While traditionally albuminuria has been considered a marker of glomerular injury and chronic kidney disease, recent evidence establishes it as a cardiorenal integration biomarker; a signal of systemic congestion, endothelial activation, and inadequate therapeutic control that may help identify patients who could benefit from intensive cardiorenal protective therapy, pending prospective validation. Initial management usually targets the achievement of euvolemia to address the albumin leakage caused by the increase in intraglomerular pressure due to increased central and renal venous pressures. Further management focuses on renin-angiotensin-aldosterone system inhibition and sodium-glucose cotransporter 2 inhibitors for the restoration of tubuloglomerular feedback and reduction of intraglomerular pressure. Urinary albumin is a readily accessible biomarker that enhances risk stratification and may guide the optimization of cardiorenal protective therapies in heart failure patients. Integration of routine urinary albumin-to-creatinine ratio monitoring into heart failure management is a promising frontier that requires validation.
Admission for acute heart failure (AHF) represents a critical therapeutic window for intervention. Conventional therapies centered on maintaining hemodynamic balance fail to improve patients' long-term prognosis. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) constitute a pivotal therapeutic agent for heart failure (HF), and the timing and dosing strategies for their early administration after hospitalization have become a major research focus. This review summarizes the evidence base, major controversies, and real-world clinical application regarding the early use of SGLT2is in patients with AHF. Our previous research demonstrated that early initiation of SGLT2i therapy following clinical stabilization significantly improves clinical outcomes and reduces HF readmission, representing an innovative therapeutic strategy. Prior work from our research group also indicated that kidney-tonifying and blood-activating prescriptions can ameliorate myocardial energy metabolism, alleviate inflammatory responses, and mitigate myocardial fibrosis, identifying a promising therapeutic target for HF treatment. Nevertheless, several debates persist in routine clinical practice, including the definition of the "early" initiation window, patient selection criteria (particularly assessment of hemodynamic stability), risks of hypovolemia, and diabetic ketoacidosis. Recent international guidelines recommend initiating SGLT2is promptly once patients with HF achieve clinical stability. Successful implementation relies on establishing a multidisciplinary in-hospital initiation pathway, enhancing patient education, and optimizing transitional care communication after hospital discharge. SGLT2i therapy yields substantial net clinical benefits when administered to patients with AHF. Future research priorities should include generating evidence for special populations such as elderly patients and those with multiple comorbidities, long-term evaluation of hard clinical endpoints, cost-effectiveness analyses, and the development of individualized precision diagnosis and treatment strategies.
