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Contribution of Insulin-Like Growth Factor-I (IGF-I) and Its Binding Protein (IGFBP3) to Increased Left Ventricular Mass in Familial Hypertrophic Cardiomyopathy Caused by Distinct Sarcomeric Mutations
Sponsor study identifier
Secondary identifiers
observational
175
1 country
1
Study Start
February 1999
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
Not reported
Date not reportedStudy Completion
August 2002
Date type not reportedThis date has not been verified as actual or estimated.
The human heart is divided into four chambers. One of the four chambers, the left ventricle, is the chamber mainly responsible for pumping blood out of the heart into the circulation. There is an inherited condition affecting the heart, passed on through genetics, hypertrophic cardiomyopathy (HCM). HCM causes the left ventricle to become abnormally enlarged (left ventricular hypertrophy LVH). Some patients with the abnormal genes that may cause HCM do not have the characteristic LVH. Approximately 20 - 40% of patients with the genetic abnormality (missense mutation of genes encoding for sarcomeric protein) actually have an enlarged left ventricle. Because of this, researchers believe there may be other factors, along with the genetic abnormality that contribute to the development of HCM. Researchers are interested in learning more about several factors they suspect may play a role in the development of HCM. Specifically, researchers plan to study levels of a hormone and the protein it attaches to, which may contribute to the development of an abnormally enlarged heart. Insulin-like growth factor (IGF-1) and insulin-like growth factor binding protein (IGFBP) work together with growth hormone (GH) in the development and maturation of many organ systems. Previous studies have suggested that these hormones affect the development and function of the heart. Patients participating in this study will undergo a variety of tests including collection of blood samples, echocardiogram of the heart, treadmill exercise test, and continuous electrical monitoring of heart activity (Holter monitor).
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
August 2002
Date type not reportedThis date has not been verified as actual or estimated.
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Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
February 1999
Date type not reportedThis date has not been verified as actual or estimated.
November 3, 1999
Actual (reported)November 4, 1999
Actual (reported)August 2002
Date type not reportedThis date has not been verified as actual or estimated.
National Heart, Lung and Blood Institute (NHLBI)
Bethesda, Maryland, 20892, United States
Jarcho JA, McKenna W, Pare JA, Solomon SD, Holcombe RF, Dickie S, Levi T, Donis-Keller H, Seidman JG, Seidman CE. Mapping a gene for familial hypertrophic cardiomyopathy to chromosome 14q1. N Engl J Med. 1989 Nov 16;321(20):1372-8. doi: 10.1056/NEJM198911163212005.
Rayment I, Holden HM, Sellers JR, Fananapazir L, Epstein ND. Structural interpretation of the mutations in the beta-cardiac myosin that have been implicated in familial hypertrophic cardiomyopathy. Proc Natl Acad Sci U S A. 1995 Apr 25;92(9):3864-8. doi: 10.1073/pnas.92.9.3864.
First Submitted
November 3, 1999
First Posted
November 4, 1999
Study Start
February 1999
Date type not reportedThis date has not been verified as actual or estimated.
Study Completion
August 2002
Date type not reportedThis date has not been verified as actual or estimated.
Contact the study team to confirm eligibility.
Thierfelder L, Watkins H, MacRae C, Lamas R, McKenna W, Vosberg HP, Seidman JG, Seidman CE. Alpha-tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a disease of the sarcomere. Cell. 1994 Jun 3;77(5):701-12. doi: 10.1016/0092-8674(94)90054-x.
Last Updated
March 4, 2008
Record last verified: 2002-08
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