Why is early-onset atrial fibrillation uncommon in patients with Duchenne muscular dystrophy? Insights from the mdx mouse.
My-Nhan NguyenCharlotte HooperMatilde StefaniniBesarte VrellakuRicardo Carnicer HijazoMatthew J WoodJillian N SimonBarabara CasadeiPublished in: Cardiovascular research (2024)
Dystrophin depletion is not associated with atrial miR-31 up-regulation, reduced NOS activity, or increased AF susceptibility in the mdx mouse. Compared with the skeletal muscle, the milder atrial biochemical phenotype may explain why patients with DMD do not exhibit a higher prevalence of atrial arrhythmias despite a reduction in NOS1 content.
Keyphrases
- duchenne muscular dystrophy
- atrial fibrillation
- early onset
- catheter ablation
- left atrial
- skeletal muscle
- oral anticoagulants
- left atrial appendage
- late onset
- direct oral anticoagulants
- nitric oxide synthase
- muscular dystrophy
- heart failure
- cell proliferation
- long non coding rna
- percutaneous coronary intervention
- risk factors
- insulin resistance
- long noncoding rna
- nitric oxide
- type diabetes
- coronary artery disease
- adipose tissue
- acute coronary syndrome
- venous thromboembolism