Inflammatory cell infiltration in left atrial appendageal tissues of patients with atrial fibrillation and sinus rhythm.
Aged
Antigens, CD20
/ immunology
Atrial Appendage
/ immunology
Atrial Fibrillation
/ immunology
B-Lymphocytes
/ immunology
CD3 Complex
/ immunology
Cardiac Surgical Procedures
/ methods
Female
Heart Atria
/ immunology
Humans
Immune System
/ immunology
Inflammation
/ immunology
Male
T-Lymphocytes
/ immunology
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
03 02 2020
03 02 2020
Historique:
received:
21
09
2019
accepted:
23
12
2019
entrez:
5
2
2020
pubmed:
6
2
2020
medline:
11
11
2020
Statut:
epublish
Résumé
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in clinical practice and is known to be associated with significant morbidity and mortality. Previous studies suggested a link between inflammation and AF by findings of increased inflammatory markers in AF patients. However, it has not been finally clarified whether inflammation is a systemic or a local phenomenon reflecting an active inflammatory process in the heart. To address this subject, human left atrial appendage tissues were obtained from 10 patients who underwent cardiac surgery and subjected to immunohistochemical analysis. The number of inflammatory CD3-positive T cells significantly increased from patients with sinus rhythm to paroxysmal AF and persistent AF, respectively. Interestingly, in patients with persistent AF, these cells were frequently arranged in small clusters. Subsequently, the number of inflammatory CD3-positive T cells decreased and was significantly lower in patients with permanent AF than in patients with persistent AF. Inflammatory CD20-positive B cells could only be detected very occasionally in all AF subgroups and were not locatable in patients with SR. Hence, our data emphasize the potential prominent role of the cellular component of the immune system in the development and perpetuation of AF.
Identifiants
pubmed: 32015492
doi: 10.1038/s41598-020-58797-8
pii: 10.1038/s41598-020-58797-8
pmc: PMC6997354
doi:
Substances chimiques
Antigens, CD20
0
CD3 Complex
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1685Références
Heeringa, J. et al. Prevalence, incidence and lifetime risk of atrial fibrillation: the Rotterdam study. Eur. Heart J. 27, 949–953 (2006).
doi: 10.1093/eurheartj/ehi825
Krijthe, B. P. et al. Projections on the number of individuals with atrial fibrillation in the European Union, from 2000 to 2060. Eur. Heart J. 34, 2746–2751 (2013).
doi: 10.1093/eurheartj/eht280
Kannel, W. B., Wolf, P. A., Benjamin, E. J. & Levy, D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am. J. Cardiol. 82, N2–9N (1998).
doi: 10.1016/S0002-9149(98)00583-9
Chen, L. Y. & Shen, W. K. Epidemiology of atrial fibrillation: a current perspective. Heart Rhythm. 4, S1–S6 (2007).
doi: 10.1016/j.hrthm.2006.12.018
Fuster, V. et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 114, e257-354 (2006).
Haïssaguerre, M. et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N. Engl. J. Med. 339, 659–666 (1998).
doi: 10.1056/NEJM199809033391003
Burstein, B. & Nattel, S. Atrial fibrosis: mechanisms and clinical relevance atrial fibrillation. J. Am. Coll. Cardiol. 51, 802–809 (2008).
doi: 10.1016/j.jacc.2007.09.064
Wakili, R., Voigt, N., Kaab, S., Dobrev, D. & Nattel, S. Recent advances in the molecular pathophysiology of atrial fibrillation. J. Clin. Invest. 121, 2955–2968 (2011).
doi: 10.1172/JCI46315
Engelmann, M. D. & Svendsen, J. H. Inflammation in the genesis and perpetuation of atrial fibrillation. Eur. Heart J. 26, 2083–2092 (2005).
doi: 10.1093/eurheartj/ehi350
Aviles, R. J. et al. Inflammation as a risk factor for atrial fibrillation. Circulation. 108, 3006–3010 (2003).
doi: 10.1161/01.CIR.0000103131.70301.4F
Psychari, S. N. et al. Relation of elevated C-reactive protein and interleukin-6 levels to left atrial size and duration of episodes in patients with atrial fibrillation. Am. J. Cardiol. 95, 764–767 (2005).
doi: 10.1016/j.amjcard.2004.11.032
Patel, P., Dokainish, H., Tsai, P. & Lakkis, N. Update on the association of inflammation and atrial fibrillation. J. Cardiovasc. Electrophysiol. 21, 1064–1070 (2010).
doi: 10.1111/j.1540-8167.2010.01774.x
Dernellis, J. & Panaretou, M. Relationship between C-reactive protein concentrations during glucocorticoid therapy and recurrent atrial fibrillation. Eur. Heart J. 25, 1100–1107 (2004).
doi: 10.1016/j.ehj.2004.04.025
Young-Xu, Y. et al. Usefulness of statin drugs in protecting against atrial fibrillation in patients with coronary artery disease. Am. J. Cardiol. 92, 1379–1383 (2003).
doi: 10.1016/j.amjcard.2003.08.040
Pfister, R. et al. Plasma vitamin C and risk of hospitalisation with diagnosis of atrial fibrillation in men and women in EPIC-Norfolk prospective study. Int. J. Cardiol. 177, 830–835 (2014).
doi: 10.1016/j.ijcard.2014.11.016
Hemilä, H. & Suonsyrjä, T. Vitamin C for preventing atrial fibrillation in high risk patients: a systematic review and meta-analysis. BMC Cardiovasc. Disord. 17, 49 (2017).
doi: 10.1186/s12872-017-0478-5
Smorodinova, N. et al. Analysis of immune cell populations in atrial myocardium of patients with atrial fibrillation or sinus rhythm. PLoS One. 12, e0172691 (2017).
doi: 10.1371/journal.pone.0172691
Yamashita, T. et al. Recruitment of immune cells across atrial endocardium in human atrial fibrillation. Circ. J. 74, 262–270 (2010).
doi: 10.1253/circj.CJ-09-0644
Chen, M. C. et al. Increased inflammatory cell infiltration in the atrial myocardium of patients with atrial fibrillation. Am. J. Cardiol. 102, 861–865 (2008).
doi: 10.1016/j.amjcard.2008.05.038
Liu, L. et al. Activation of peripheral blood CD3(+) T-lymphocytes in patients with atrial fibrillation. Int. Heart J. 53, 221–224 (2012).
doi: 10.1536/ihj.53.221
Guo, Y., Lip, G. Y. & Apostolakis, S. Inflammation in atrial fibrillation. J. Am. Coll. Cardiol. 60, 2263–2270 (2012).
doi: 10.1016/j.jacc.2012.04.063
Chung, M. K. et al. C-reactive protein elevation in patients with atrial arrhythmias: Inflammatory mechanisms and persistence of atrial fibrillation. Circulation. 104, 2886–2891 (2001).
doi: 10.1161/hc4901.101760
Marcus, G. M. et al. Intracardiac and extracardiac markers of inflammation during atrial fibrillation. Heart Rhythm. 7, 149–154 (2010).
doi: 10.1016/j.hrthm.2009.10.004
Gollob, M. H. Atrial fibrillation as an autoimmune disease? Heart Rhythm. 10, 442–443 (2013).
doi: 10.1016/j.hrthm.2013.01.023
Chen, P. S. et al. Role of the autonomic nervous system in atrial fibrillation: pathophysiology and therapy. Circ. Res. 114, 1500–1515 (2014).
doi: 10.1161/CIRCRESAHA.114.303772
Mandal, K. et al. Association of anti-heat shock protein 65 antibodies with development of postoperative atrial fibrillation. Circulation. 110, 2588–2590 (2004).
doi: 10.1161/01.CIR.0000136825.96029.A5
Kornej, J. et al. Response of circulating heat shock protein 70 and anti-heat shock 70 antibodies to catheter ablation of atrial fibrillation. J. Transl. Med. 11, 49 (2013).
doi: 10.1186/1479-5876-11-49
Baek, Y. S. et al. Prevalence and the clinical outcome of atrial fibrillation in patients with Autoimmune Rheumatic disease. Int. J. Cardiol. 214, 4–9 (2016).
doi: 10.1016/j.ijcard.2016.03.083
Gurses, K. M. et al. M2-muscarinic acetylcholine receptor autoantibody levels predict left atrial fibrosis severity in paroxysmal lone atrial fibrillation patients undergoing cryoablation. Europace. 17, 239–246 (2015).
doi: 10.1093/europace/euu228
Baumgart, D. C. et al. Prospective randomized open-label multicenter phase I/II dose escalation trial of visilizumab (HuM291) in severe steroid-refractory ulcerative colitis. Inflamm. Bowel Dis. 16, 620–629 (2010).
doi: 10.1002/ibd.21084