Prevalence of Transthyretin Amyloidosis in Hypertrophic Cardiomyopathy
NCT ID: NCT01623245
Last Updated: 2019-08-14
Study Results
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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COMPLETED
294 participants
OBSERVATIONAL
2012-06-30
2014-12-31
Brief Summary
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Detailed Description
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The detection of this disease is important because this disease is fatal and a new treatment to prevent the accumulation of TTR is now available (Tafamidis). This drug has proved effective in stabilizing neurological damage.
Depending on the number of patient with cardiac amyloidosis in TTR detected, the prospect will begin a clinical trial to test the effectiveness of a new treatment to prevent the increase in mass of the left ventricle wall objectified resonance nuclear Magnetic.
Conditions
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Study Design
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COHORT
PROSPECTIVE
Study Groups
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Hypertrophic Cardiomyopathy
In the population of Hypertrophic Cardiomyopathy patients, patients suffering from a cardiac amyloidosis
No interventions assigned to this group
Eligibility Criteria
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Inclusion Criteria
* Patients with a signed consent authorizing the specific blood test for genetic sequencing to look for abnormal TTR gene
Exclusion Criteria
* Significant aortic stenosis (≤ 1 cm ²)
18 Years
ALL
No
Sponsors
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Thibaud Damy
OTHER
Responsible Party
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Thibaud Damy
Assistant Professor
Principal Investigators
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Thibaud DAMY
Role: PRINCIPAL_INVESTIGATOR
Assistance Publique - Hôpitaux de Paris
Locations
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Henri Mondor Hospital
Créteil, , France
Countries
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References
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Christoph DC, Boese D, Johnson KT, Schlosser TW, Hunold P, Baba HA, Erbel R, Philipp S. Heart failure and cardiac involvement as isolated manifestation of familial form of transthyretin amyloidosis resulting from Val30Met mutation with no clinical signs of polyneuropathy. Circ Heart Fail. 2009 Sep;2(5):512-5. doi: 10.1161/CIRCHEARTFAILURE.109.853697. No abstract available.
Merlini G, Bellotti V. Molecular mechanisms of amyloidosis. N Engl J Med. 2003 Aug 7;349(6):583-96. doi: 10.1056/NEJMra023144. No abstract available.
Morner S, Hellman U, Suhr OB, Kazzam E, Waldenstrom A. Amyloid heart disease mimicking hypertrophic cardiomyopathy. J Intern Med. 2005 Sep;258(3):225-30. doi: 10.1111/j.1365-2796.2005.01522.x.
Jacobson DR, Pastore RD, Yaghoubian R, Kane I, Gallo G, Buck FS, Buxbaum JN. Variant-sequence transthyretin (isoleucine 122) in late-onset cardiac amyloidosis in black Americans. N Engl J Med. 1997 Feb 13;336(7):466-73. doi: 10.1056/NEJM199702133360703.
Plante-Bordeneuve V, Ferreira A, Lalu T, Zaros C, Lacroix C, Adams D, Said G. Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). Neurology. 2007 Aug 14;69(7):693-8. doi: 10.1212/01.wnl.0000267338.45673.f4.
Plante-Bordeneuve V. [The diagnosis and management of familial amyloid polyneuropathy]. Rev Neurol (Paris). 2006 Nov;162(11):1138-46. doi: 10.1016/s0035-3787(06)75130-x. French.
Rapezzi C, Merlini G, Quarta CC, Riva L, Longhi S, Leone O, Salvi F, Ciliberti P, Pastorelli F, Biagini E, Coccolo F, Cooke RM, Bacchi-Reggiani L, Sangiorgi D, Ferlini A, Cavo M, Zamagni E, Fonte ML, Palladini G, Salinaro F, Musca F, Obici L, Branzi A, Perlini S. Systemic cardiac amyloidoses: disease profiles and clinical courses of the 3 main types. Circulation. 2009 Sep 29;120(13):1203-12. doi: 10.1161/CIRCULATIONAHA.108.843334. Epub 2009 Sep 14.
Said G, Plante-Bordeneuve V. Familial amyloid polyneuropathy: a clinico-pathologic study. J Neurol Sci. 2009 Sep 15;284(1-2):149-54. doi: 10.1016/j.jns.2009.05.001. Epub 2009 May 24.
Saraiva MJ. Sporadic cases of hereditary systemic amyloidosis. N Engl J Med. 2002 Jun 6;346(23):1818-9. doi: 10.1056/NEJM200206063462312. No abstract available.
Other Identifiers
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11714
Identifier Type: -
Identifier Source: org_study_id
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