Modulation of SERCA in Patients with Persistent Atrial Fibrillation Treated by Epicardial Thoracoscopic Ablation: The CAMAF Study.
SERCA
calcium channels
epicardial ablation
persistent atrial fibrillation
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
17 Feb 2020
17 Feb 2020
Historique:
received:
20
01
2020
revised:
13
02
2020
accepted:
14
02
2020
entrez:
22
2
2020
pubmed:
23
2
2020
medline:
23
2
2020
Statut:
epublish
Résumé
To evaluate atrial fibrillation (AF) recurrence and Sarcoplasmic Endoplasmic Reticulum Calcium ATPase (SERCA) levels in patients treated by epicardial thoracoscopic ablation for persistent AF. Reduced levels of SERCA have been reported in the peripheral blood cells of patients with AF. We hypothesize that SERCA levels can predict the response to epicardial ablation. We designed a prospective, multicenter, observational study to recruit, from October 2014 to June 2016, patients with persistent AF receiving an epicardial thoracoscopic pulmonary vein isolation. We enrolled 27 patients. Responders (n = 15) did not present AF recurrence after epicardial ablation at one-year follow-up; these patients displayed a marked remodeling of the left atrium, with a significant reduction of inflammatory cytokines, B type natriuretic peptide (BNP), and increased levels of SERCA compared to baseline and to nonresponders (p < 0.05). Furthermore, mean AF duration (Heart rate (HR) 1.235 (1.037-1.471), p < 0.05), Left atrium volume (LAV) (HR 1.755 (1.126-2.738), p < 0.05), BNP (HR 1.945 (1.895-1.999), p < 0.05), and SERCA (HR 1.763 (1.167-2.663), p < 0.05) were predictive of AF recurrence. Our data indicate for the first time that baseline values of SERCA in patients with persistent AF might be predictive of failure to epicardial ablative approach. Intriguingly, epicardial ablation was associated with increased levels of SERCA in responders. Therefore, SERCA might be an innovative therapeutic target to improve the response to epicardial ablative treatments.
Sections du résumé
OBJECTIVES
OBJECTIVE
To evaluate atrial fibrillation (AF) recurrence and Sarcoplasmic Endoplasmic Reticulum Calcium ATPase (SERCA) levels in patients treated by epicardial thoracoscopic ablation for persistent AF.
BACKGROUND
BACKGROUND
Reduced levels of SERCA have been reported in the peripheral blood cells of patients with AF. We hypothesize that SERCA levels can predict the response to epicardial ablation.
METHODS
METHODS
We designed a prospective, multicenter, observational study to recruit, from October 2014 to June 2016, patients with persistent AF receiving an epicardial thoracoscopic pulmonary vein isolation.
RESULTS
RESULTS
We enrolled 27 patients. Responders (n = 15) did not present AF recurrence after epicardial ablation at one-year follow-up; these patients displayed a marked remodeling of the left atrium, with a significant reduction of inflammatory cytokines, B type natriuretic peptide (BNP), and increased levels of SERCA compared to baseline and to nonresponders (p < 0.05). Furthermore, mean AF duration (Heart rate (HR) 1.235 (1.037-1.471), p < 0.05), Left atrium volume (LAV) (HR 1.755 (1.126-2.738), p < 0.05), BNP (HR 1.945 (1.895-1.999), p < 0.05), and SERCA (HR 1.763 (1.167-2.663), p < 0.05) were predictive of AF recurrence.
CONCLUSIONS
CONCLUSIONS
Our data indicate for the first time that baseline values of SERCA in patients with persistent AF might be predictive of failure to epicardial ablative approach. Intriguingly, epicardial ablation was associated with increased levels of SERCA in responders. Therefore, SERCA might be an innovative therapeutic target to improve the response to epicardial ablative treatments.
Identifiants
pubmed: 32079238
pii: jcm9020544
doi: 10.3390/jcm9020544
pmc: PMC7074346
pii:
doi:
Types de publication
Journal Article
Langues
eng
Déclaration de conflit d'intérêts
Authors declare no conflict of interests.
Références
J Cardiovasc Electrophysiol. 2016 Dec;27(12):1462-1471
pubmed: 27571932
J Cardiovasc Electrophysiol. 2013 Nov;24(11):1224-31
pubmed: 24020717
Pharmacogenomics. 2015 Nov;16(16):1863-77
pubmed: 26554530
Circulation. 2018 Sep 11;138(11):1144-1154
pubmed: 29593014
Can J Cardiol. 2012 Mar-Apr;28(2):245.e17; author reply 245.e17-8
pubmed: 22244772
Circulation. 2004 Sep 14;110(11):1358-63
pubmed: 15313939
Am J Cardiol. 2017 May 1;119(9):1382-1386
pubmed: 28258730
Ann Intern Med. 2019 Jul 16;171(2):JC10
pubmed: 31307071
J Am Coll Cardiol. 2011 Sep 27;58(14):1474-81
pubmed: 21939832
J Am Heart Assoc. 2019 Oct;8(19):e013294
pubmed: 31564186
Acta Physiol (Oxf). 2013 Feb;207(2):308-23
pubmed: 22958452
Circulation. 2014 Feb 25;129(8):837-47
pubmed: 24345399
Adv Exp Med Biol. 2018;1067:373-385
pubmed: 28956314
JAMA. 2014 Feb 5;311(5):498-506
pubmed: 24496537
Europace. 2012 Apr;14(4):528-606
pubmed: 22389422
Int Heart J. 2016;57(2):183-9
pubmed: 26973277
J Am Heart Assoc. 2013 Mar 18;2(2):e004549
pubmed: 23537812
Eur J Echocardiogr. 2010 Aug;11(7):577-83
pubmed: 20400765
Adv Exp Med Biol. 2017;982:191-202
pubmed: 28551788
Eur J Heart Fail. 2010 Jun;12(6):541-8
pubmed: 20388650
Circ J. 2002 Oct;66(10):913-6
pubmed: 12381084
Eur Heart J. 2016 Oct 7;37(38):2893-2962
pubmed: 27567408
Int J Clin Pract. 2016 Jul;70(7):569-76
pubmed: 27291327
Card Electrophysiol Clin. 2019 Dec;11(4):563-571
pubmed: 31706465
Eur J Cardiothorac Surg. 2013 Nov;44(5):919-23
pubmed: 23475587
Am J Cardiol. 2011 Apr 15;107(8):1125-30
pubmed: 21296320
Europace. 2009 Aug;11(8):1018-23
pubmed: 19556251
Circulation. 1997 Oct 7;96(7):2455-61
pubmed: 9337224
J Mol Cell Cardiol. 2001 May;33(5):1005-15
pubmed: 11343422
N Engl J Med. 1998 Sep 3;339(10):659-66
pubmed: 9725923