COlchicine for the Prevention of Post Electrical Cardioversion Recurrence of AF
NCT ID: NCT02582190
Last Updated: 2018-01-25
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
WITHDRAWN
Clinical Phase
PHASE3
Study Classification
INTERVENTIONAL
Study Start Date
2017-12-02
Study Completion Date
2018-09-02
Brief Summary
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There is substantial evidence linking inflammation to the initiation and perpetuation of AF. Although the precise mechanism by which inflammation contributes to the development of AF remains unclear, it has been proposed that inflammation may lead to "atrial myocarditis" with subsequent electrical and structural changes involving both atrial myocytes and extracellular matrix, leading finally to initiation and maintenance of AF. The high incidence of AF in post-operative cardiac surgeries, a state of intense inflammatory process, points out this association. Similarly, in non operative AF, inflammation appears to play a prominent role in both etiology and maintenance of AF. Indeed an increase of inflammatory markers to both paroxysmal and persistent AF was shown by numerous studies.
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Detailed Description
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In particular, CRP levels in patients with persistent AF are higher than in those with paroxysmal AF, and levels in both groups are higher than those in the control group. Moreover, hs-CRP and IL-6 levels have been reported as markers that may identify those patients with a higher risk of AF recurrence after successful electrical cardioversion (EC), providing prognostic information regarding the immediate and long-term success of EC.
CRP is an acute-phase protein and a reliable marker of systemic inflammation. CRP has been shown to specifically bind to phosphatidylcholine on the membranes of myocardial cells which inhibits the exchange of sodium and calcium ions in sarcolemma vesicles, promoting therefore AF development. CRP may also play a part in the structural remodeling; it may induce apoptotic loss of atrial myocytes because of calcium accumulation within atrial myocytes during AF participating also in the clearance of apoptotic atrial myocytes as an opsonin. Myocyte loss is typically accompanied by replacement fibrosis which provides substrate for AF development. IL-6 is one of the most important stimuli of CRP release. As the strongest stimuli of macrophage, TNF-α is in the upstream of this cascade by activating macrophage to release a number of cytokines including IL-6.
Whether inflammatory effects are a consequence of AF or the presence of a pre-existing systemic inflammatory status promotes AF development remains unclear. However, accumulative proofs have implied that both mechanisms may interrelate, suggesting that inflammatory markers are not only a consequence but also a cause.
Consequently, pharmacological interventions with pleiotropic/anti-inflammatory effects might be efficacious in the prevention of AF by modulating inflammatory pathways.(17) Keeping with this, several agents with anti inflammatotory properties as statins, fatty acids, oral glucocorticoids, nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors have been administered with controversial results.
Colchicine is a lipid-soluble drug classified as an anti-inflammatory agent. It exerts its anti-inflammatory action without involving the arachidonic acid pathway affected by NSAIDs and glucocorticosteroids. The anti-inflammatory effects of colchicine are attributed to its ability to disrupt the assembly of microtubules in immune-mediated cells. By inhibiting tubulin polymerization, colchicine prevents the activation, degranulation, and migration of neutrophils, which are known initiating factors in inflammatory process. It has also been found to increase leukocyte cyclic adenosine monophosphate levels, inhibit interleukin-1 (IL-1) production by activated neutrophils and down-regulate tumor necrosis factor alpha (TNFa) receptors in macrophages and endothelial cells.
Clinical evidence support that colchicine administration reduced significantly the incidence of AF post-cardiac surgery (POAF) or post-AF ablation and this effect was attributed to the drug anti-inflammatory action. Of note, this effect was accompanied by a significant decrease in inflammatory mediators, IL-6 and CRP as it was shown in post-AF ablation patients.(33) Additional mechanisms may play also a role in the reduction of POAF or post-ablation AF as in vitro or animal studies showed colchicine administration to exert electrophysiological effects related to cytoskeletal disruption.
All patients will undergo echocardiography and blood examination (including thyroid function, renal and liver function tests, lipid assessment, international normalized ratio and foul blood cell count) before EC. Blood samples for CRP, IL-6 and TNFa measurement will be obtained immediately before ECV (day 0), one day after successful ECV (day 1) and after 3 days of colchicine treatment (day 4). Anticoagulation therapy will be instituted according to the current guidelines. If there is indication for transesophageal echocardiography this will be performed prior to EC.
The protocol of electrical cardioversion will be as follows: a shock will be delivered with external paddles positioned in the anterior-apex position connected to an external electrical cardioverter for biphasic external cardioversion. The first shock energy will be delivered at 200 J following a step-up protocol (to 300 J). In case of unsuccessful ECV, a second attempt in anteroposterior position could be made. ECV will be considered successful if sinus rhythm remains 24 hrs after the procedure.
Successfully cardioverted patients will be entered the maintenance phase of the study and treatment will be continued for up to 6 months
CRP is an acute-phase protein and a reliable marker of systemic inflammation. CRP has been shown to specifically bind to phosphatidylcholine on the membranes of myocardial cells which inhibits the exchange of sodium and calcium ions in sarcolemma vesicles, promoting therefore AF development. CRP may also play a part in the structural remodeling; it may induce apoptotic loss of atrial myocytes because of calcium accumulation within atrial myocytes during AF participating also in the clearance of apoptotic atrial myocytes as an opsonin. Myocyte loss is typically accompanied by replacement fibrosis which provides substrate for AF development. IL-6 is one of the most important stimuli of CRP release. As the strongest stimuli of macrophage, TNF-α is in the upstream of this cascade by activating macrophage to release a number of cytokines including IL-6.
Whether inflammatory effects are a consequence of AF or the presence of a pre-existing systemic inflammatory status promotes AF development remains unclear. However, accumulative proofs have implied that both mechanisms may interrelate, suggesting that inflammatory markers are not only a consequence but also a cause.
Consequently, pharmacological interventions with pleiotropic/anti-inflammatory effects might be efficacious in the prevention of AF by modulating inflammatory pathways.(17) Keeping with this, several agents with anti inflammatotory properties as statins, fatty acids, oral glucocorticoids, nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors have been administered with controversial results.
Colchicine is a lipid-soluble drug classified as an anti-inflammatory agent. It exerts its anti-inflammatory action without involving the arachidonic acid pathway affected by NSAIDs and glucocorticosteroids. The anti-inflammatory effects of colchicine are attributed to its ability to disrupt the assembly of microtubules in immune-mediated cells. By inhibiting tubulin polymerization, colchicine prevents the activation, degranulation, and migration of neutrophils, which are known initiating factors in inflammatory process. It has also been found to increase leukocyte cyclic adenosine monophosphate levels, inhibit interleukin-1 (IL-1) production by activated neutrophils and down-regulate tumor necrosis factor alpha (TNFa) receptors in macrophages and endothelial cells.
Clinical evidence support that colchicine administration reduced significantly the incidence of AF post-cardiac surgery (POAF) or post-AF ablation and this effect was attributed to the drug anti-inflammatory action. Of note, this effect was accompanied by a significant decrease in inflammatory mediators, IL-6 and CRP as it was shown in post-AF ablation patients.(33) Additional mechanisms may play also a role in the reduction of POAF or post-ablation AF as in vitro or animal studies showed colchicine administration to exert electrophysiological effects related to cytoskeletal disruption.
All patients will undergo echocardiography and blood examination (including thyroid function, renal and liver function tests, lipid assessment, international normalized ratio and foul blood cell count) before EC. Blood samples for CRP, IL-6 and TNFa measurement will be obtained immediately before ECV (day 0), one day after successful ECV (day 1) and after 3 days of colchicine treatment (day 4). Anticoagulation therapy will be instituted according to the current guidelines. If there is indication for transesophageal echocardiography this will be performed prior to EC.
The protocol of electrical cardioversion will be as follows: a shock will be delivered with external paddles positioned in the anterior-apex position connected to an external electrical cardioverter for biphasic external cardioversion. The first shock energy will be delivered at 200 J following a step-up protocol (to 300 J). In case of unsuccessful ECV, a second attempt in anteroposterior position could be made. ECV will be considered successful if sinus rhythm remains 24 hrs after the procedure.
Successfully cardioverted patients will be entered the maintenance phase of the study and treatment will be continued for up to 6 months
Conditions
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Atrial Fibrillation
Study Design
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Allocation Method
NA
Intervention Model
SINGLE_GROUP
Primary Study Purpose
TREATMENT
Blinding Strategy
NONE
Study Groups
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Colchicine group
Colchicine add on therapy in atrial fibrillation
Group Type
OTHER
Colchicine group
Intervention Type
DRUG
antiarrhythmic therapy plus colchicine \& antiarrhythmic therapy alone.
Interventions
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Colchicine group
antiarrhythmic therapy plus colchicine \& antiarrhythmic therapy alone.
Intervention Type
DRUG
Other Intervention Names
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Colchicine in atrial fibrillation
Eligibility Criteria
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Inclusion Criteria
* patients experiencing their first episode of AF of less than 3 months duration will be given no other antiarrhythmic drugs but b-blocker
* In case of recurrent episodes of AF or if AF duration is \>3 months patients on antiarrhythmic drugs of class IC or III as first choice.
* men and women
* 18 to 80 years of age
* with persistent AF (sustained for \> 7 days) for which electrical cardioversion was indicated.
* In case of recurrent episodes of AF or if AF duration is \>3 months patients on antiarrhythmic drugs of class IC or III as first choice.
* men and women
* 18 to 80 years of age
* with persistent AF (sustained for \> 7 days) for which electrical cardioversion was indicated.
Exclusion Criteria
* active inflammatory or infectious disease
* malignancy
* known autoimmune diseases
* corticosteroid or other immunosuppressive or immunomodulatory therapy
* drugs that inhibit CYP3A4 (clarithromycin, azithromycin, ketoconazole, ritonavir, verapamil, and diltiazem)
* moderate or severe hepatic impairment (Child-Pugh class B or C)
* moderate or severe renal failure (≤ 40 ml/min per 1.73 m2)
* acute coronary syndrome within a month before study enrollment
* known blood dyscrasias or gastrointestinal disease
* pregnant and lactating women
* women of childbearing potential not protected by a contraception method -
* patients with atrial flutter will be also excluded unless there is history of coexisting AF.
* malignancy
* known autoimmune diseases
* corticosteroid or other immunosuppressive or immunomodulatory therapy
* drugs that inhibit CYP3A4 (clarithromycin, azithromycin, ketoconazole, ritonavir, verapamil, and diltiazem)
* moderate or severe hepatic impairment (Child-Pugh class B or C)
* moderate or severe renal failure (≤ 40 ml/min per 1.73 m2)
* acute coronary syndrome within a month before study enrollment
* known blood dyscrasias or gastrointestinal disease
* pregnant and lactating women
* women of childbearing potential not protected by a contraception method -
* patients with atrial flutter will be also excluded unless there is history of coexisting AF.
Minimum Eligible Age
18 Years
Maximum Eligible Age
80 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
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Elpen Pharmaceutical Co. Inc.
INDUSTRY
Sponsor Role
lead
Responsible Party
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Responsibility Role
SPONSOR
Principal Investigators
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Nikolaos Fragakis, MD
Role: PRINCIPAL_INVESTIGATOR
Hippokrateion hospital of Thessaloniki
References
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Issac TT, Dokainish H, Lakkis NM. Role of inflammation in initiation and perpetuation of atrial fibrillation: a systematic review of the published data. J Am Coll Cardiol. 2007 Nov 20;50(21):2021-8. doi: 10.1016/j.jacc.2007.06.054. Epub 2007 Nov 5.
Reference Type
BACKGROUND
Aviles RJ, Martin DO, Apperson-Hansen C, Houghtaling PL, Rautaharju P, Kronmal RA, Tracy RP, Van Wagoner DR, Psaty BM, Lauer MS, Chung MK. Inflammation as a risk factor for atrial fibrillation. Circulation. 2003 Dec 16;108(24):3006-10. doi: 10.1161/01.CIR.0000103131.70301.4F. Epub 2003 Nov 17.
Reference Type
BACKGROUND
Frustaci A, Chimenti C, Bellocci F, Morgante E, Russo MA, Maseri A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation. 1997 Aug 19;96(4):1180-4. doi: 10.1161/01.cir.96.4.1180.
Reference Type
BACKGROUND
Nakamura Y, Nakamura K, Fukushima-Kusano K, Ohta K, Matsubara H, Hamuro T, Yutani C, Ohe T. Tissue factor expression in atrial endothelia associated with nonvalvular atrial fibrillation: possible involvement in intracardiac thrombogenesis. Thromb Res. 2003;111(3):137-42. doi: 10.1016/s0049-3848(03)00405-5.
Reference Type
BACKGROUND
Bruins P, te Velthuis H, Yazdanbakhsh AP, Jansen PG, van Hardevelt FW, de Beaumont EM, Wildevuur CR, Eijsman L, Trouwborst A, Hack CE. Activation of the complement system during and after cardiopulmonary bypass surgery: postsurgery activation involves C-reactive protein and is associated with postoperative arrhythmia. Circulation. 1997 Nov 18;96(10):3542-8. doi: 10.1161/01.cir.96.10.3542.
Reference Type
BACKGROUND
Psychari SN, Apostolou TS, Sinos L, Hamodraka E, Liakos G, Kremastinos DT. 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. 2005 Mar 15;95(6):764-7. doi: 10.1016/j.amjcard.2004.11.032.
Reference Type
BACKGROUND
Chung MK, Martin DO, Sprecher D, Wazni O, Kanderian A, Carnes CA, Bauer JA, Tchou PJ, Niebauer MJ, Natale A, Van Wagoner DR. C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation. Circulation. 2001 Dec 11;104(24):2886-91. doi: 10.1161/hc4901.101760.
Reference Type
BACKGROUND
Liu T, Li G, Li L, Korantzopoulos P. Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion: a meta-analysis. J Am Coll Cardiol. 2007 Apr 17;49(15):1642-1648. doi: 10.1016/j.jacc.2006.12.042. Epub 2007 Apr 2.
Reference Type
BACKGROUND
Dernellis J, Panaretou M. Relationship between C-reactive protein concentrations during glucocorticoid therapy and recurrent atrial fibrillation. Eur Heart J. 2004 Jul;25(13):1100-7. doi: 10.1016/j.ehj.2004.04.025.
Reference Type
BACKGROUND
Conway DS, Buggins P, Hughes E, Lip GY. Predictive value of indexes of inflammation and hypercoagulability on success of cardioversion of persistent atrial fibrillation. Am J Cardiol. 2004 Aug 15;94(4):508-10. doi: 10.1016/j.amjcard.2004.04.070.
Reference Type
BACKGROUND
Malouf JF, Kanagala R, Al Atawi FO, Rosales AG, Davison DE, Murali NS, Tsang TS, Chandrasekaran K, Ammash NM, Friedman PA, Somers VK. High sensitivity C-reactive protein: a novel predictor for recurrence of atrial fibrillation after successful cardioversion. J Am Coll Cardiol. 2005 Oct 4;46(7):1284-7. doi: 10.1016/j.jacc.2005.06.053.
Reference Type
BACKGROUND
Wazni O, Martin DO, Marrouche NF, Shaaraoui M, Chung MK, Almahameed S, Schweikert RA, Saliba WI, Natale A. C reactive protein concentration and recurrence of atrial fibrillation after electrical cardioversion. Heart. 2005 Oct;91(10):1303-5. doi: 10.1136/hrt.2004.038661. Epub 2005 May 12.
Reference Type
BACKGROUND
Loricchio ML, Cianfrocca C, Pasceri V, Bianconi L, Auriti A, Calo L, Lamberti F, Castro A, Pandozi C, Palamara A, Santini M. Relation of C-reactive protein to long-term risk of recurrence of atrial fibrillation after electrical cardioversion. Am J Cardiol. 2007 May 15;99(10):1421-4. doi: 10.1016/j.amjcard.2006.12.074. Epub 2007 Apr 5.
Reference Type
BACKGROUND
Watanabe E, Arakawa T, Uchiyama T, Kodama I, Hishida H. High-sensitivity C-reactive protein is predictive of successful cardioversion for atrial fibrillation and maintenance of sinus rhythm after conversion. Int J Cardiol. 2006 Apr 14;108(3):346-53. doi: 10.1016/j.ijcard.2005.05.021. Epub 2005 Jun 17.
Reference Type
BACKGROUND
Korantzopoulos P, Kalantzi K, Siogas K, Goudevenos JA. Long-term prognostic value of baseline C-reactive protein in predicting recurrence of atrial fibrillation after electrical cardioversion. Pacing Clin Electrophysiol. 2008 Oct;31(10):1272-6. doi: 10.1111/j.1540-8159.2008.01177.x.
Reference Type
BACKGROUND
Smit MD, Maass AH, De Jong AM, Muller Kobold AC, Van Veldhuisen DJ, Van Gelder IC. Role of inflammation in early atrial fibrillation recurrence. Europace. 2012 Jun;14(6):810-7. doi: 10.1093/europace/eur402. Epub 2012 Jan 10.
Reference Type
BACKGROUND
Van Wagoner DR. Oxidative stress and inflammation in atrial fibrillation: role in pathogenesis and potential as a therapeutic target. J Cardiovasc Pharmacol. 2008 Oct;52(4):306-13. doi: 10.1097/FJC.0b013e31817f9398.
Reference Type
BACKGROUND
Kallergis EM, Manios EG, Kanoupakis EM, Mavrakis HE, Kolyvaki SG, Lyrarakis GM, Chlouverakis GI, Vardas PE. The role of the post-cardioversion time course of hs-CRP levels in clarifying the relationship between inflammation and persistence of atrial fibrillation. Heart. 2008 Feb;94(2):200-4. doi: 10.1136/hrt.2006.108688. Epub 2007 Jun 17.
Reference Type
BACKGROUND
Wu N, Xu B, Xiang Y, Wu L, Zhang Y, Ma X, Tong S, Shu M, Song Z, Li Y, Zhong L. Association of inflammatory factors with occurrence and recurrence of atrial fibrillation: a meta-analysis. Int J Cardiol. 2013 Oct 25;169(1):62-72. doi: 10.1016/j.ijcard.2013.08.078. Epub 2013 Sep 8.
Reference Type
BACKGROUND
Wu J, Corr PB. Influence of long-chain acylcarnitines on voltage-dependent calcium current in adult ventricular myocytes. Am J Physiol. 1992 Aug;263(2 Pt 2):H410-7. doi: 10.1152/ajpheart.1992.263.2.H410.
Reference Type
BACKGROUND
Nattel S. New ideas about atrial fibrillation 50 years on. Nature. 2002 Jan 10;415(6868):219-26. doi: 10.1038/415219a.
Reference Type
BACKGROUND
Liu J, Fang PH, Dibs S, Hou Y, Li XF, Zhang S. High-sensitivity C-reactive protein as a predictor of atrial fibrillation recurrence after primary circumferential pulmonary vein isolation. Pacing Clin Electrophysiol. 2011 Apr;34(4):398-406. doi: 10.1111/j.1540-8159.2010.02978.x. Epub 2010 Nov 22.
Reference Type
BACKGROUND
Rader DJ. Inflammatory markers of coronary risk. N Engl J Med. 2000 Oct 19;343(16):1179-82. doi: 10.1056/NEJM200010193431609. No abstract available.
Reference Type
BACKGROUND
Cheruku KK, Ghani A, Ahmad F, Pappas P, Silverman PR, Zelinger A, Silver MA. Efficacy of nonsteroidal anti-inflammatory medications for prevention of atrial fibrillation following coronary artery bypass graft surgery. Prev Cardiol. 2004 Winter;7(1):13-8. doi: 10.1111/j.1520-037x.2004.3117.x.
Reference Type
BACKGROUND
Calo L, Bianconi L, Colivicchi F, Lamberti F, Loricchio ML, de Ruvo E, Meo A, Pandozi C, Staibano M, Santini M. N-3 Fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery: a randomized, controlled trial. J Am Coll Cardiol. 2005 May 17;45(10):1723-8. doi: 10.1016/j.jacc.2005.02.079.
Reference Type
BACKGROUND
Young-Xu Y, Jabbour S, Goldberg R, Blatt CM, Graboys T, Bilchik B, Ravid S. Usefulness of statin drugs in protecting against atrial fibrillation in patients with coronary artery disease. Am J Cardiol. 2003 Dec 15;92(12):1379-83. doi: 10.1016/j.amjcard.2003.08.040.
Reference Type
BACKGROUND
Siu CW, Lau CP, Tse HF. Prevention of atrial fibrillation recurrence by statin therapy in patients with lone atrial fibrillation after successful cardioversion. Am J Cardiol. 2003 Dec 1;92(11):1343-5. doi: 10.1016/j.amjcard.2003.08.023.
Reference Type
BACKGROUND
Madrid AH, Bueno MG, Rebollo JM, Marin I, Pena G, Bernal E, Rodriguez A, Cano L, Cano JM, Cabeza P, Moro C. Use of irbesartan to maintain sinus rhythm in patients with long-lasting persistent atrial fibrillation: a prospective and randomized study. Circulation. 2002 Jul 16;106(3):331-6. doi: 10.1161/01.cir.0000022665.18619.83.
Reference Type
BACKGROUND
Tveit A, Seljeflot I, Grundvold I, Abdelnoor M, Smith P, Arnesen H. Effect of candesartan and various inflammatory markers on maintenance of sinus rhythm after electrical cardioversion for atrial fibrillation. Am J Cardiol. 2007 Jun 1;99(11):1544-8. doi: 10.1016/j.amjcard.2007.01.030. Epub 2007 Apr 16.
Reference Type
BACKGROUND
Ferron GM, Rochdi M, Jusko WJ, Scherrmann JM. Oral absorption characteristics and pharmacokinetics of colchicine in healthy volunteers after single and multiple doses. J Clin Pharmacol. 1996 Oct;36(10):874-83. doi: 10.1002/j.1552-4604.1996.tb04753.x.
Reference Type
BACKGROUND
Terkeltaub RA. Colchicine update: 2008. Semin Arthritis Rheum. 2009 Jun;38(6):411-9. doi: 10.1016/j.semarthrit.2008.08.006. Epub 2008 Oct 29.
Reference Type
BACKGROUND
Van Wagoner DR. Colchicine for the prevention of postoperative atrial fibrillation: a new indication for a very old drug? Circulation. 2011 Nov 22;124(21):2281-2. doi: 10.1161/CIRCULATIONAHA.111.057075. No abstract available.
Reference Type
BACKGROUND
Deftereos S, Giannopoulos G, Kossyvakis C, Efremidis M, Panagopoulou V, Kaoukis A, Raisakis K, Bouras G, Angelidis C, Theodorakis A, Driva M, Doudoumis K, Pyrgakis V, Stefanadis C. Colchicine for prevention of early atrial fibrillation recurrence after pulmonary vein isolation: a randomized controlled study. J Am Coll Cardiol. 2012 Oct 30;60(18):1790-6. doi: 10.1016/j.jacc.2012.07.031. Epub 2012 Oct 3.
Reference Type
BACKGROUND
Kamkin A, Kiseleva I, Wagner KD, Scholz H, Theres H, Kazanski V, Lozinsky I, Gunther J, Isenberg G. Mechanically induced potentials in rat atrial fibroblasts depend on actin and tubulin polymerisation. Pflugers Arch. 2001 Jul;442(4):487-97. doi: 10.1007/s004240100564.
Reference Type
BACKGROUND
Climent V, Marin F, Mainar L, Roldan V, Garcia A, Martinez JG, Lip GY. Influence of electrical cardioversion on inflammation and indexes of structural remodeling, in persistent atrial fibrillation. Int J Cardiol. 2009 Feb 20;132(2):227-32. doi: 10.1016/j.ijcard.2007.11.044. Epub 2008 Jan 30.
Reference Type
BACKGROUND
Nichol G, McAlister F, Pham B, Laupacis A, Shea B, Green M, Tang A, Wells G. Meta-analysis of randomised controlled trials of the effectiveness of antiarrhythmic agents at promoting sinus rhythm in patients with atrial fibrillation. Heart. 2002 Jun;87(6):535-43. doi: 10.1136/heart.87.6.535.
Reference Type
BACKGROUND
Other Identifiers
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2015-IIS-GR-COL
Identifier Type: -
Identifier Source: org_study_id
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