Atrial FibrillationPhase 3COPPER-AFNCT02582190
COlchicine for the Prevention of Post Electrical Cardioversion Recurrence of AF
A Phase 3 study testing Colchicine group in people with Atrial Fibrillation, run by Elpen Pharmaceutical Co. Inc..
Trial summary
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… Read more about this study
- Who is it for?
- Ages 18 to 80 years
- Conditions the study is for
- Atrial Fibrillation
- What is being tested?
- Colchicine group
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 0 participants
- Where
- No sites listed yet
- Study dates
- 2 Dec 2017to 2 Sep 2018
- Phase
- Phase 3
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 80 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- 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.
Who cannot join
- 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)
Show all 12Show fewer
- 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.
About this study
Official title: Colchicine for the Prevention of Atrial Fibrillation Recurrence After Electrical Cardioversion of Persistent Atrial Fibrillation.
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.
Read the detailed description
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
- Conditions
- Atrial Fibrillation
- Being tested
- Colchicine group
- Keywords
- electrical cardioversion, persistent atrial fibrillation
- Medical subject headings
- Atrial Fibrillation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Colchicine groupDrug
Also called Colchicine in atrial fibrillation
antiarrhythmic therapy plus colchicine \& antiarrhythmic therapy alone.
| Study group | Role | What they receive |
|---|---|---|
| Colchicine group | Other | Colchicine add on therapy in atrial fibrillation Receives: Drug: Colchicine group |
What is being measured
The primary outcome is the main question the study is designed to answer.
Number of patients with AF recurrence
Change in AF recurrence from baseline to 180 days
Measured: 180 days
Secondary outcomes (1)
Number of adverse events
Change in adverse events incidence from baseline to 180 days
Measured: 180 days
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted21 Oct 2015 (estimated)
- Study start2 Dec 2017 (estimated)
- Primary completion2 Sep 2018 (estimated)
- Study completion2 Sep 2018 (estimated)
Why it stopped: Investigational Medicinal Product Supplies
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (36)Papers the sponsor has linked to this study.
- Other trials for Atrial FibrillationStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 3
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 0 participants (actual)
Sponsor and investigators
- Lead sponsor
- Elpen Pharmaceutical Co. Inc.
- Sponsor type
- Industry (pharma, biotech, devices)
- Responsible party
- Sponsor
- Investigators
- Nikolaos Fragakis, MD, Principal investigator, Hippokrateion hospital of Thessaloniki
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02582190
- Sponsor's protocol ID
- 2015-IIS-GR-COL
- Acronym
- COPPER-AF
- Status last verified
- May 2017
- First submitted
- 9 Oct 2015
- Last updated
- 25 Jan 2018
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
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.
PubMed 18021867Aviles 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.
PubMed 14623805Frustaci 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.
PubMed 9286947Nakamura 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.
PubMed 14678810Bruins 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.
PubMed 9396453Psychari 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.
PubMed 15757607Chung 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.
PubMed 11739301Liu 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.
PubMed 17433956Dernellis 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.
PubMed 15231367Conway 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.
PubMed 15325942Malouf 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.
PubMed 16198844Wazni 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.
PubMed 15890767Loricchio 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.
PubMed 17493472Watanabe 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.
PubMed 15964643Korantzopoulos 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.
PubMed 18811807
Study at a glance
From the registry record, last updated by the sponsor on 25 Jan 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Colchicine for the Prevention of Atrial Fibrillation Recurrence After Electrical Cardioversion of Persistent Atrial Fibrillation.
- ClinicalTrials.gov ID
- NCT02582190
- Acronym / sponsor ID
- COPPER-AF / 2015-IIS-GR-COL
- Conditions
- Atrial Fibrillation
- Keywords
- electrical cardioversion, persistent atrial fibrillation
- Phase
- Phase 3
- Study type
- Interventional
- Recruitment status
- WithdrawnReason stopped: Investigational Medicinal Product Supplies
- Enrolment
- 0 participants (actual)
- Lead sponsor
- Elpen Pharmaceutical Co. Inc.Industry (pharma, biotech, devices)
- Study start
- 2 Dec 2017 (estimated)
- Primary completion
- 2 Sep 2018 (estimated)
- Study completion
- 2 Sep 2018 (estimated)
- First posted
- 21 Oct 2015 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Detailed description
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
Study design
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Colchicine group | Other | Drug: Colchicine groupColchicine add on therapy in atrial fibrillation |
Who may qualify
- Ages
- 18 to 80 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- 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.
Key exclusion criteria (12 listed)
- 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)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Colchicine groupAlso: Colchicine in atrial fibrillationantiarrhythmic therapy plus colchicine \& antiarrhythmic therapy alone. | Drug | Colchicine group |
Primary outcome
Number of patients with AF recurrence
Time frame: 180 days
Change in AF recurrence from baseline to 180 days
1 secondary outcome
Number of adverse events
Time frame: 180 days
Results and safety
The study was withdrawn before enrolling participants, so there are no results.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 25 Jan 2018.
- Background: PubMed 18021867Issac 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.
- Background: PubMed 14623805Aviles 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.
- Background: PubMed 9286947Frustaci 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.
- Background: PubMed 14678810Nakamura 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.
- Background: PubMed 9396453Bruins 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.
- Background: PubMed 15757607Psychari 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.
- Background: PubMed 11739301Chung 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.
- Background: PubMed 17433956Liu 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.
- Background: PubMed 15231367Dernellis 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.
- Background: PubMed 15325942Conway 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.
- Background: PubMed 16198844Malouf 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.
- Background: PubMed 15890767Wazni 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.
- Individual participant dataSharing planned: No
Related trials for Atrial Fibrillation
Active, not recruiting
Horizon 360 Protocol for the Treatment of Paroxysmal Atrial Fibrillation With the Sphere-360™ Catheter and Affera™ Mapping and Ablation System (Horizon 360)
Paroxysmal AF
Active, not recruitingObservational study
Concomitant Left Atrial Appendage Closure and Pulsed Field Ablation-Asia
Concomitant Procedures, Atrial Fibrillation
Active, not recruiting
CONVERGE Post-Approval Study (PAS)
Chronic Atrial Fibrillation
Recruiting
Early Closure of Left Atrial Appendage for Patients With Atrial Fibrillation and Ischemic Stroke Despite Anticoagulation Therapy
Ischemic Stroke, Atrial Fibrillation
RecruitingPhase 2
Safety in Adult Participants With Atrial Fibrillation Who Are Treated With Anticoagulation
Atrial Fibrillation (AF)
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Nikolaos Fragakis, MD principal investigator
Hippokrateion hospital of Thessaloniki
Questions about this trial
What is this clinical trial studying?
A Phase 3 study testing Colchicine group in people with Atrial Fibrillation, run by Elpen Pharmaceutical Co. Inc..
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 12 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: withdrawn, as of the sponsor's last update on 25 Jan 2018. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 3 studies compare the treatment with the current standard treatment or a placebo in a large group, to confirm how well it works and watch for side effects.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study was withdrawn before enrolling participants, so there are no results.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Number of patients with AF recurrence (time frame: 180 days). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02582190, which also lists 36 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 25 Jan 2018; AzTrials last refreshed its copy on 6 Nov 2026.