2015
DOI: 10.1016/j.cyto.2015.01.026
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Serum levels of interleukin-2 predict the recurrence of atrial fibrillation after pulmonary vein ablation

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Cited by 27 publications
(19 citation statements)
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“…Gene expression of pro-inflammatory factors associated to inflammatory response (IFN-γ, transcription factor T-bet, GATA-3; FoxP3 and CTLA-4; IL-17 and IL-18) were upregulated in heart samples of chronic Chagasic patients [24] and its inflammatory environment has been reported as inductor of gene expression related with heart failure [25] and gap junction dysfunction during Chagas disease [26], possibly explaining this fact the electrical disturbances observed in patients. Interestingly and closely related with our results, IL-2 was able to induce in vitro the expression of SCN3B and sodium current density [27], increasing of atrial action potential duration [28] and IL-2 has been linked to prognosis for atrial fibrillation in patients [29]. Additionally, Cx43 gene expression, a key protein of gap junctions tightly related with action potential spreading onto the heart, has been reported as impaired in Chagasic cardiomyopathy, reinforcing the possible association between inflammation and altered electrical function in Chagasic patients [30] and its fact possibly explains the positive effect of amiodarone treatment during Chagas disease [31].…”
Section: Discussionsupporting
confidence: 78%
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“…Gene expression of pro-inflammatory factors associated to inflammatory response (IFN-γ, transcription factor T-bet, GATA-3; FoxP3 and CTLA-4; IL-17 and IL-18) were upregulated in heart samples of chronic Chagasic patients [24] and its inflammatory environment has been reported as inductor of gene expression related with heart failure [25] and gap junction dysfunction during Chagas disease [26], possibly explaining this fact the electrical disturbances observed in patients. Interestingly and closely related with our results, IL-2 was able to induce in vitro the expression of SCN3B and sodium current density [27], increasing of atrial action potential duration [28] and IL-2 has been linked to prognosis for atrial fibrillation in patients [29]. Additionally, Cx43 gene expression, a key protein of gap junctions tightly related with action potential spreading onto the heart, has been reported as impaired in Chagasic cardiomyopathy, reinforcing the possible association between inflammation and altered electrical function in Chagasic patients [30] and its fact possibly explains the positive effect of amiodarone treatment during Chagas disease [31].…”
Section: Discussionsupporting
confidence: 78%
“…Although this data does not allow itself to state that the increasing nor decreasing of IL-2 levels are associated to any outcome, high IL-2 serum levels have been reported as an atrial fibrillation predictor [29, 37] and low levels have been associated with therapeutic success of amiodarone treatment in atrial fibrillation [38]. Further studies are necessary for elucidating the molecular mechanisms associated to the heart microenvironment during chronic Chagas disease.…”
Section: Discussionmentioning
confidence: 99%
“…In recent years, inflammation has been implicated in the pathogenesis of AF . Inflammatory markers such tumor necrosis factor α, interleukin 6, interleukin 2, and C‐reactive protein were all found to be elevated in patients with AF . Although data are not consistent, several authors have reported decreased levels of tumor necrosis factor α, interleukin 6, C‐reactive protein, and other proinflammatory cytokines after TRT .…”
Section: Discussionmentioning
confidence: 99%
“…In a cohort with preserved ejection fraction and permanent AF, patients with LV fibrosis had an exceptionally high rate of AF recurrence following catheter ablation; the 1‐year procedural success rate in those with extensive fibrosis and LV hypertrophy was only 7% . Even in patients with paroxysmal AF, the diagnosis of HFpEF or biomarkers of systemic inflammation presages a high rate of AF recurrence . These observations suggest that patients with latent or overt HFpEF have an underlying atrial myopathy that is the primary determinant of the development of AF; that substrate is highly resistant to therapeutic efforts to suppress or abolish the arrhythmia, especially when it is longstanding.…”
Section: Therapeutic Challenges In Patients With a Metabolic Disordermentioning
confidence: 99%