Effects of Sacubitril/Valsartan on the Expression of CaMKII/Ca1.2 in Atrial Fibrillation Stimulation Rabbit Model.

Methods: Overall, 18 rabbits were randomly divided into control, pacing (600 beats/min), and pacing+sac/val groups. The rabbits in the pacing+sac/val cohort received oral sac/val (10 mg/kg twice daily) across the 21-day investigation period. After three weeks, the atrial effective refractory period (AERP) and AF induction rate were compared.

Detection of circRNA Biomarker for Acute Myocardial Infarction Based on System Biological Analysis of RNA Expression.

Acute myocardial infarction (AMI) is myocardial necrosis caused by the persistent interruption of myocardial blood supply, which has high incidence rate and high mortality in middle-aged and elderly people in the worldwide. Biomarkers play an important role in the early diagnosis and treatment of AMI. Recently, more and more researches confirmed that circRNA may be a potential diagnostic biomarker and therapeutic target for cardiovascular diseases.

Hydroxychloroquine use and progression or prognosis of COVID-19: a systematic review and meta-analysis.

Hydroxychloroquine (HCQ) has been implicated in antiviral activity in vitro against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, there is still controversy about whether HCQ should be used for coronavirus disease 2019 (COVID-19) patients due to the conflicting results in different clinical trials. To systematically assess the benefits and harms of HCQ for the treatment of COVID-19.

Sacubitril/valsartan attenuates atrial electrical and structural remodelling in a rabbit model of atrial fibrillation.

Atrial structural and electrical remodelling play important roles in atrial fibrillation (AF). Sacubitril/valsartan attenuates cardiac remodelling in heart failure. However, the effect of sacubitril/valsartan on AF is unclear.

Chronic B-Type Natriuretic Peptide Therapy Prevents Atrial Electrical Remodeling in a Rabbit Model of Atrial Fibrillation.

Background: Atrial fibrillation (AF) is an important and growing clinical problem. Current pharmacological treatments are unsatisfactory. Electrical remodeling has been identified as one of the principal pathophysiological mechanisms that promote AF, but there are no effective therapies to prevent or correct electrical remodeling in patients with AF.

Qiliqiangxin attenuates atrial structural remodeling in prolonged pacing-induced atrial fibrillation in rabbits.

Qiliqiangxin (QL) can attenuate myocardial remodeling and improve cardiac function in some cardiac diseases, including heart failure and hypertension. This study was to explore the effects and mechanism of QL on atrial structural remodeling in atrial fibrillation (AF). Twenty-one rabbits were randomly divided into a sham-operation group, pacing group (pacing with 600 beats per minute for 4 weeks), and treatment group (2.