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- Title
Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model.
- Authors
Cheng, Wen-Han; Lugtu, Isaiah C.; Chang, Shih-Lin; Liu, Shin-Huei; Chen, Shih-Ann; Lo, Li-Wei
- Abstract
Purpose: Left atrial appendage (LAA) closure decreases atrial natriuretic peptide (ANP) levels, which indirectly increases the risk of arrhythmogenicity. We aimed to determine the effect of a combined angiotensin receptor-neprilysin inhibitor (ARNi) on arrhythmogenicity following LAA closure in an animal model. Methods: Twenty-four rabbits were randomized into four groups: (1) control, (2) LAA closure (LAAC), (3) heart failure (HF)-LAAC, and (4) HF-LAAC with sacubitril/valsartan (+ARNi). HF models were developed in the HF-LAAC and HF-LAAC+ARNi groups. Epicardial LAA exclusion was performed in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups. ANP levels were measured. An electrophysiological study was performed. The myocardium was harvested for histopathological analysis. Results: The ANP level decreased in the LAAC group (785 ± 103 pg/mL, p = 0.03), failed to increase in the HF-LAAC group (917 ± 172 pg/mL, p = 0.3), and increased in the HF-LAAC+ARNi group (1524 ± 126 pg/mL, p < 0.01) compared to that in the control group (1014 ± 56 pg/mL). The atrial effective refractory period (ERP) was prolonged in the HF-LAAC group and restored to baseline in the HF-LAAC+ARNi group. Ventricular ERP was the longest in the HF-LAAC group. The atrial fibrillation window of vulnerability (AF WOV) was elevated in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups, with the latter group having lower AF WOV than the two former groups. Ventricular fibrillation (VF) inducibility was the highest in the HF-LAAC group (51 ± 5%, p < 0.001), followed by the LAAC group (30 ± 4%, p = 0.006) and the HF-LAAC+ARNi group (25 ± 5%, p = 0.11) when compared to the control group (18 ± 4%). Atrial and ventricular fibrosis were noted in all groups except the control group. Conclusion: LAA closure decreased ANP, which in turn increased AF and VF inducibility. Atrial and ventricular arrhythmogenicity was suppressed by ARNi.
- Subjects
LEFT heart atrium; ANGIOTENSINS; HEART failure; VENTRICULAR fibrillation; ANIMAL models in research; EVOKED potentials (Electrophysiology)
- Publication
Cardiovascular Drugs & Therapy, 2021, Vol 35, Issue 4, p759
- ISSN
0920-3206
- Publication type
Article
- DOI
10.1007/s10557-021-07174-2