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Direct Thrombin Inhibitors Prevent Left Atrial Remodeling Associated With Heart Failure in Rats
Céline Jumeau1, Alain Rupin2, Pauline Chieng-Yane3
1Sorbonne University, Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche 1166, Institute of Cardiometabolism and Nutrition (ICAN), Paris, France; Servier Research Institute, Suresnes, France.
Insights
Direct oral anticoagulants, specifically direct thrombin inhibitors, were found to reduce left atrial remodeling and atrial fibrillation duration in a rat heart failure model. These findings suggest DTIs may slow the progression of the arrhythmogenic substrate.
Area of Science:
- Cardiology
- Pharmacology
- Biomedical Research
Background:
- Left atrial remodeling contributes to atrial fibrillation (AF) progression.
- Thrombin is hypothesized to play a role in left atrial remodeling.
- Direct oral anticoagulants (DTIs) are used to prevent thromboembolism in AF.
Approach:
- Utilized a rat model of heart failure with left atrial dilation.
- Administered chronic treatment with direct thrombin inhibitors (DTIs).
- Assessed the impact of DTIs on atrial remodeling, AF episode duration, myocardial hypertrophy, and fibrosis.
Key Points:
- Chronic DTI treatment significantly reduced atrial remodeling in the rat model.
- DTIs decreased the duration of burst pacing-induced atrial fibrillation episodes.
- Inhibition of myocardial hypertrophy and fibrosis by DTIs was observed.
Conclusions:
- Thrombin inhibition by DTIs effectively mitigates left atrial remodeling.
- DTIs show potential in slowing the progression of the arrhythmogenic substrate in AF.
- Beyond thromboembolism prevention, DTIs may offer therapeutic benefits for AF structural changes.
Abstract:
The present study tested the hypothesis that thrombin participates in formation of left atrial remodeling and that direct oral anticoagulants, such as direct thrombin inhibitors (DTIs), can prevent its progression. In a rat model of heart failure associated with left atrial dilation, we found that chronic treatment with DTIs reduces the atrial remodeling and the duration of atrial fibrillation (AF) episodes induced by burst pacing by inhibiting myocardial hypertrophy and fibrosis. In addition to the prevention of thromboembolism complicating AF, DTIs may be of interest to slow down the progression of the arrhythmogenic substrate.
