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Sterile Pericarditis in Aachener Minipigs As a Model for Atrial Myopathy and Atrial Fibrillation
Published on: September 24, 2021
Atrial fibrillation-associated remodeling does not promote atrial thrombus formation in canine models
Kunihiro Nishida1, Katsuyoshi Chiba, Yu-Ki Iwasaki
1Department of Medicine and Research Center, Montreal Heart Institute and Université de Montréal, Quebec, Canada.
Insights
Atrial fibrillation (AF) remodeling does not increase atrial thrombus formation after radiofrequency ablation (RFA). This study found no evidence that AF-related changes enhance the risk of blood clots.
Area of Science:
- Cardiovascular Research
- Thrombosis and Hemostasis
- Electrophysiology
Background:
- Atrial fibrillation (AF) is a major risk factor for thromboembolic stroke.
- AF-related remodeling is suspected to contribute to atrial thrombogenesis, but this has not been directly tested.
- This study aimed to investigate the prothrombotic potential of AF-related remodeling.
Purpose of the Study:
- To assess the effect of AF-related remodeling on the atrial thrombogenic milieu.
- To determine if electrical and structural remodeling in AF enhances thrombus formation after radiofrequency ablation (RFA).
Main Methods:
- Canine models of atrial tachycardia remodeling (ATR), congestive heart failure (CHF), and chronic AF (CAF) were established.
- Radiofrequency ablation (RFA) lesions were created in the atria of all groups, including controls.
- Atrial thrombi were quantified using histomorphometry post-ablation.
Main Results:
- No significant differences in total thrombus volume or thrombus volume per lesion were observed among control, ATR, CHF, and CAF groups.
- Neither electrical nor structural remodeling indices predicted post-RFA thrombogenic potential.
- Burst-pacing-induced AF duration was greater in AF models, but this did not translate to increased thrombus formation.
Conclusions:
- AF-related remodeling, including sustained atrial tachycardia/AF, did not enhance post-RFA atrial thrombus formation.
- The study found no prothrombotic effects of AF-related remodeling.
- Current notions regarding AF remodeling and thrombogenesis require re-evaluation.
Background:
The most important complication of atrial fibrillation (AF) is thromboembolic stroke. Although AF-related remodeling is considered important in atrial thrombogenesis, its role never has been directly tested. This study assessed effects of AF-related remodeling on the atrial thrombogenic milieu by using radiofrequency ablation (RFA) to create a quantifiable prothrombotic nidus.
Methods And Results:
We studied normal control dogs (control, n=16) and 3 canine AF-models: (1) atrial tachycardia remodeling (ATR; n=16) induced by atrial tachypacing (400 bpm for 1 week, with atrioventricular block and ventricular pacing at 80 bpm); (2) congestive heart failure (CHF; n=14) attributable to ventricular tachypacing (240 bpm for 2 weeks); and (3) chronic AF (CAF; n=8) induced by atrial tachypacing (35±3 days) without atrioventricular block. CAF dogs had AF for 13±1 days until euthanization. After remodeling was established, RFA lesions were created in both atria. Half the ATR and CHF dogs were subjected to atrial tachypacing during 7-day post-RFA follow-up. Electrophysiological and echocardiographic studies were performed before RFA and 7 days after RFA, and then hearts were removed and atrial thrombi were quantified by histomorphometry. Burst-pacing-induced AF duration was significantly greater in ATR, CHF, and CAF groups versus control group. The atrial effective refractory period shortened in ATR and CAF groups. Left atrial diameter was significantly larger with CHF, but not with ATR. Neither total thrombus volume nor thrombus volume per lesion differed significantly among groups. Table.Properties of Ablation Lesions and Atrial Thrombi Experimental GroupControl (n=16)ATR (n=16)CHF (n=14)CAF (n=8)N of ablation lesions per dog6.9±0.36.6±0.27.2±0.26.9±0.4Ablation lesion area, mm(2)53.1±3.558.3±4.857.7±4.944.3±3.7Ablation lesion depth, mm5.2±0.25.1±0.35.3±0.25.2±0.2Ablation lesion volume, mm(3)205.2±17.8211.6±17.6231.5±29.0176.8±22.2N of thrombi per dog5.4±0.44.7±0.35.6±0.46.5±0.4Presence of thrombus, %80±572±577±695±3Mean thrombus volume in both atria, mm(3)20.8±3.414.9±2.212.2±2.622.5±5.6Mean thrombus volume in left atria, mm(3)8.2±1.54.0±0.95.5±1.68.1±3.3Mean thrombus volume in right atria, mm(3)30.1±5.422.7±4.317.9±4.132.8±8.3Total thrombus volume in both atria, mm(3)140.5±21.399.7±16.886.1±17.5131.1±22.7Total thrombus volume in left atria, mm(3)22.8±5.311.8±3.317.0±3.723.3±6.4Total thrombus volume in right atria, mm(3)117.7±21.587.8±17.269.1±16.1107.8±23.3Thrombus volume normalized to ablation lesion area in both atria, mm(3)/mm(2)0.5±0.10.4±0.11.5±1.10.8±0.3Thrombus volume normalized to ablation lesion volume in both atria0.2±0.10.1±0.00.5±0.40.3±0.1 ATR indicates atrial tachycardia remodeling; CAF, chronic atrial fibrillation; and CHF, congestive heart failure. There were no statistically significant differences for any groups vs control group for any of these variables studied.
Conclusions:
None of the AF substrates tested, including sustained atrial tachycardia/AF itself, enhanced post-RFA atrial thrombus formation. Indices of electrical and structural remodeling did not predict post-RFA thrombogenic potential. Contrary to widely held but previously untested notions, we were unable to demonstrate prothrombotic effects of AF-related remodeling.
