The Preventive Efficacy of Carvedilol on Cardiac Dysfunction in Duchenne Muscular Dystrophy
Primary Purpose
Duchenne Muscular Dystrophy, Cardiomyopathies
Status
Unknown status
Phase
Phase 4
Locations
Japan
Study Type
Interventional
Intervention
Carvedilol
Sponsored by
About this trial
This is an interventional prevention trial for Duchenne Muscular Dystrophy focused on measuring Adrenergic beta-Antagonists, Duchenne Muscular Dystrophy, Cardiomyopathies, Troponin I
Eligibility Criteria
Inclusion Criteria:
Male patients with Duchenne muscular dystrophy are required to meet the following criteria:
- Aged 8 to 45 years
- Positive plasma cardiac troponin I (0.06ng/mL) at least 4 blood measurement in every 3 month.
- Left ventricular ejection fraction >30% by echocardiography assessment
- Written informed consent
Exclusion Criteria:
Patients with the following conditions will be excluded from the study:
- Left ventricular ejection fraction <30%
- No plasma cTnI elevation
- beta-blocker is already administered without measurement of plasma cTnI
- Contraindication against treatment with β blockers
- Any other serious disease that could potentially complicate the management and follow-up protocols
Sites / Locations
- Suzuka HospialRecruiting
Arms of the Study
Arm 1
Arm 2
Arm Type
Experimental
No Intervention
Arm Label
Carvedilol
Control
Arm Description
Outcomes
Primary Outcome Measures
The suppression of minor cardiac damage indicated as elevation of plasma cTnI
Secondary Outcome Measures
Left ventricular function deterioration assessed by echocardiography In-hospital mortality for cardiac dysfunction In-hospital mortality for any cause Overall mortality
Full Information
NCT ID
NCT00606775
First Posted
January 22, 2008
Last Updated
February 4, 2008
Sponsor
Suzuka Hospital
Collaborators
Nagoya University
1. Study Identification
Unique Protocol Identification Number
NCT00606775
Brief Title
The Preventive Efficacy of Carvedilol on Cardiac Dysfunction in Duchenne Muscular Dystrophy
Official Title
Carvedilol for the Prevention of Minor Cardiac Damage and Cardiac Function in Duchenne Muscular Dystrophy
Study Type
Interventional
2. Study Status
Record Verification Date
December 2007
Overall Recruitment Status
Unknown status
Study Start Date
December 2007 (undefined)
Primary Completion Date
December 2008 (Anticipated)
Study Completion Date
December 2012 (Anticipated)
3. Sponsor/Collaborators
Name of the Sponsor
Suzuka Hospital
Collaborators
Nagoya University
4. Oversight
Data Monitoring Committee
Yes
5. Study Description
Brief Summary
Purpose This cardiac dysfunction in patients with Duchenne muscular dystrophy is associated with minor cardiac damage as indicated by elevation of plasma cardiac troponin I (cTnI). The purpose of this study is to investigate whether the administration of Carvedilol can suppress the minor cardiac damage and prevent deterioration of cardiac function.
Detailed Description
The life span in patients with Duchenne muscular dystrophy has been extending due to the development of artificial respiratory devices. According to that, the ratio of cardiac dysfunction as a cause of death has been increasing. This cardiac dysfunction was associated with minor cardiac damage as indicated by elevation of plasma cardiac troponin I (cTnI). Furthermore, and the detection rate of cTnI plasma as revealed to be correlated with the deterioration speed of LV dysfunction assessed by serial echocardiography measurements. Accordingly, if this minor cardiac damage is suppressed, it is postulated that the progression of cardiac dysfunction can be stopped. In the cases with ventricular arrhythmia and tachycardia, we found plasma cTnI became undetectable after administration of beta-blocker. Accordingly, we investigate whether administration of beta-blocker, carvedilol can persistently suppress the minor cardiac damage and lead to suppress the deterioration of LV function. Note that his study preventive study for preserved to moderate LV dysfunction and is not intended to the beta-blocker treatment for severe LV dysfunction. Because we assume that the mechanism of elevation of cTnI is different; spontaneous in preserved to mild LV dysfunction in patients but LV wall stress in severe LV dysfunction in patients with Duchenne muscular dystrophy.
6. Conditions and Keywords
Primary Disease or Condition Being Studied in the Trial, or the Focus of the Study
Duchenne Muscular Dystrophy, Cardiomyopathies
Keywords
Adrenergic beta-Antagonists, Duchenne Muscular Dystrophy, Cardiomyopathies, Troponin I
7. Study Design
Primary Purpose
Prevention
Study Phase
Phase 4
Interventional Study Model
Parallel Assignment
Masking
None (Open Label)
Allocation
Randomized
Enrollment
60 (Anticipated)
8. Arms, Groups, and Interventions
Arm Title
Carvedilol
Arm Type
Experimental
Arm Title
Control
Arm Type
No Intervention
Intervention Type
Drug
Intervention Name(s)
Carvedilol
Other Intervention Name(s)
Artist, Daich-Sankyo Co.Ltd
Intervention Description
2.5-5mg/day
Primary Outcome Measure Information:
Title
The suppression of minor cardiac damage indicated as elevation of plasma cTnI
Time Frame
2 years
Secondary Outcome Measure Information:
Title
Left ventricular function deterioration assessed by echocardiography In-hospital mortality for cardiac dysfunction In-hospital mortality for any cause Overall mortality
Time Frame
5 years
10. Eligibility
Sex
Male
Minimum Age & Unit of Time
8 Years
Maximum Age & Unit of Time
45 Years
Accepts Healthy Volunteers
No
Eligibility Criteria
Inclusion Criteria:
Male patients with Duchenne muscular dystrophy are required to meet the following criteria:
Aged 8 to 45 years
Positive plasma cardiac troponin I (0.06ng/mL) at least 4 blood measurement in every 3 month.
Left ventricular ejection fraction >30% by echocardiography assessment
Written informed consent
Exclusion Criteria:
Patients with the following conditions will be excluded from the study:
Left ventricular ejection fraction <30%
No plasma cTnI elevation
beta-blocker is already administered without measurement of plasma cTnI
Contraindication against treatment with β blockers
Any other serious disease that could potentially complicate the management and follow-up protocols
Central Contact Person:
First Name & Middle Initial & Last Name or Official Title & Degree
Takao Nishizawa, MD,PhD
Phone
+81-52-744-2150
Email
nishizta@med.nagoya-u.ac.jp
First Name & Middle Initial & Last Name or Official Title & Degree
Fumihiko Yasuma, MD,PhD
Phone
+81-59-378-1321
Email
yasuma@suzuka.go.jp
Overall Study Officials:
First Name & Middle Initial & Last Name & Degree
Takao Nishizawa, MD, PhD
Organizational Affiliation
Department of Cardiology, Nagoya University Graduate School of Medicine
Official's Role
Principal Investigator
Facility Information:
Facility Name
Suzuka Hospial
City
Suzuka
State/Province
Mie
ZIP/Postal Code
513-8501
Country
Japan
Individual Site Status
Recruiting
Facility Contact:
First Name & Middle Initial & Last Name & Degree
Takao Nishizawa, MD. PhD
Phone
+81-52-744-2150
Email
nishizta@med.nagoya-u.ac.jp
First Name & Middle Initial & Last Name & Degree
Fumihiko Yasuma, MD. PhD
Phone
+81-593-78-0337
Email
yasuma@suzuka.go.jp
First Name & Middle Initial & Last Name & Degree
Fumihiko Yasuma, MD, PhD
First Name & Middle Initial & Last Name & Degree
Toshimitsu Mori, MD
First Name & Middle Initial & Last Name & Degree
Motoko Sakai, MD, PhD
First Name & Middle Initial & Last Name & Degree
Satoshi Kuru, MD, PhD
First Name & Middle Initial & Last Name & Degree
Seigo Kimura, MD
First Name & Middle Initial & Last Name & Degree
Takuya Tamura, MD
First Name & Middle Initial & Last Name & Degree
Kentaro Sahashi, MD
First Name & Middle Initial & Last Name & Degree
Rei Shibata, MD, PhD
First Name & Middle Initial & Last Name & Degree
Taiki Ohashi, MD
12. IPD Sharing Statement
Citations:
PubMed Identifier
11157687
Citation
Sato Y, Yamada T, Taniguchi R, Nagai K, Makiyama T, Okada H, Kataoka K, Ito H, Matsumori A, Sasayama S, Takatsu Y. Persistently increased serum concentrations of cardiac troponin t in patients with idiopathic dilated cardiomyopathy are predictive of adverse outcomes. Circulation. 2001 Jan 23;103(3):369-74. doi: 10.1161/01.cir.103.3.369.
Results Reference
background
PubMed Identifier
15336589
Citation
Yasuma F, Konagaya M, Sakai M, Kuru S, Kawamura T. A new lease on life for patients with Duchenne muscular dystrophy in Japan. Am J Med. 2004 Sep 1;117(5):363. doi: 10.1016/j.amjmed.2004.03.028. No abstract available.
Results Reference
background
PubMed Identifier
7114081
Citation
Hunsaker RH, Fulkerson PK, Barry FJ, Lewis RP, Leier CV, Unverferth DV. Cardiac function in Duchenne's muscular dystrophy. Results of 10-year follow-up study and noninvasive tests. Am J Med. 1982 Aug;73(2):235-8. doi: 10.1016/0002-9343(82)90184-x.
Results Reference
background
PubMed Identifier
16246949
Citation
Jefferies JL, Eidem BW, Belmont JW, Craigen WJ, Ware SM, Fernbach SD, Neish SR, Smith EO, Towbin JA. Genetic predictors and remodeling of dilated cardiomyopathy in muscular dystrophy. Circulation. 2005 Nov 1;112(18):2799-804. doi: 10.1161/CIRCULATIONAHA.104.528281. Epub 2005 Oct 24.
Results Reference
background
PubMed Identifier
10220639
Citation
Ishikawa Y, Bach JR, Minami R. Cardioprotection for Duchenne's muscular dystrophy. Am Heart J. 1999 May;137(5):895-902. doi: 10.1016/s0002-8703(99)70414-x.
Results Reference
background
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The Preventive Efficacy of Carvedilol on Cardiac Dysfunction in Duchenne Muscular Dystrophy
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