| Full text | |
| Author(s): |
de Oliveira, Italo Martins
[1, 2]
;
da Silva, Jr., Evilasio Leobino
[1, 2]
;
Martins, Yasmin de Oliveira
[3]
;
Lima Rocha, Hermano Alexandre
[4]
;
Scanavacca, Mauricio Ibrahim
[1]
;
Gutierrez, Paulo Sampaio
[1]
Total Authors: 6
|
| Affiliation: | [1] Univ Sao Paulo, Inst Coracao InCor, Hosp Clin, Fac Med, Sao Paulo, SP - Brazil
[2] Hosp Messejana Coracao & Pulmao Dr Carlos Alberto, Fortaleza, Ceara - Brazil
[3] Hosp Geral Fortaleza HGF, Fortaleza, Ceara - Brazil
[4] Harvard TH Chan Sch Publ Hlth, Boston, MA - USA
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | Arquivos Brasileiros de Cardiologia; v. 117, n. 5, p. 999-1007, 2021. |
| Web of Science Citations: | 0 |
| Abstract | |
Abstract Background The primary factors that originate and perpetuate atrial fibrillation (AF) are electrical and anatomical substrate alterations. However, the central mechanisms governing AF perpetuation have not been elucidated yet, which is reflected on the modest results of the treatment in patients with long persistent AF. Objective To evaluate if human intrinsic cardiac autonomic nervous system (ICANS) remodeling, including nervous system fibers and muscarinic and β-adrenergic receptors, play a role in permanent AF. Methods Heart necropsy samples from thirteen patients with heart disease and permanent AF and thirteen controls without AF were used. By using immunoperoxidase and histomorphometry quantification, we identified the following: the density of all fibers of the ICANS, sympathetic and parasympathetic fibers; and the percentage of myocardium positive for β-adrenergic receptors 1, 2 and 3; G protein-coupled receptor kinase-5 (GRK-5); and muscarinic receptors M1 to M5. The results were compared using ANOVA and nested ANOVA and were adjusted according to the left atrium volume for all variables, and β-blocker use to evaluate the expression of β-receptors and GRK-5. Results There was an overall increase in the density of fibers of the ICANS (p=0.006), especially in atrial sympathetic nerve fibers (p=0.017). Only M1 muscarinic receptors were increased (5.87 vs 2.35, p=0.032). For adrenergic receptors, the results were positive for increased expression of β-3 (37.41 vs 34.18, p=0.039) and GRK-5 (51.16 vs 47.66; p<0.001). β-blocker use had no impact on β-receptor expression. Conclusion Increased ICANS innervation and remodeling receptor expression in regions prone to triggering AF may play a role in permanent AF. (AU) | |