Hypertrophic CardiomyopathyNCT00001878
Factors Contributing to Increased Left Ventricle Size in Patients With Abnormally Enlarged Hearts
An observational study of Hypertrophic Cardiomyopathy and Left Ventricular Hypertrophy, run by National Heart, Lung, and Blood Institute (NHLBI) at 1 site in United States.
Trial summary
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). Read more about this study
- Who is it for?
- Any age
- Conditions the study is for
- Hypertrophic Cardiomyopathy, Left Ventricular Hypertrophy
- How many people
- 175 participants
- Where
- 1 siteUnited States
- Study dates
- Feb 1999to Aug 2002
- Phase
- Observational
- 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 Any age
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
Who may be able to join
- HCM subjects 5 years or older, with distinct sarcomeric gene mutations and LV wall thickness greater than 15 mm in subjects older than 18 years, and greater than 2 SDs in subjects 18 years of age or younger, as assessed by MRI.
- Age- and gender-matched blood relatives with sarcomeric gene mutations but without LVH.
- Age- and gender-matched blood relatives without sarcomeric gene mutations.
Who cannot join
- History of hypertension (basal systolic and diastolic pressures above 170 mm Hg and 95 mm Hg, respectively) or another systemic or cardiac disease that may cause cardiac hypertrophy.
- History of recent acute illness or other chronic illness that might affect plasma levels of IGF-I and IGFBP3.
- History of thyrotoxicosis, diabetes mellitus or abnormally elevated fasting blood sugar.
- Any conditions which would exclude patients from undergoing MRI scan.
Trial locations and contacts
1 site in 1 country.
United States1 site
National Heart, Lung and Blood Institute (NHLBI)
Bethesda, Maryland, 20892
About this study
Official title: 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
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.
Read more
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).
Read the detailed description
Hypertrophic cardiomyopathy (HCM) is a genetic disease with an autosomal dominant pattern of inheritance which is characterized by left ventricular hypertrophy (LVH). HCM is often caused by missense mutations of genes that encode for sarcomeric proteins. The LVH varies markedly in patients with identical sarcomeric gene mutations, and notably, 20 to 40% of subjects with disease mutation do not have LVH as assessed by echocardiography. These findings suggest that other factors affect LV wall thickness in HCM. We wish (1) to investigate the potential role of IGF-I and its binding protein, IGFBP3, in determining increased LV mass in HCM caused by sarcomeric mutations; and (2) to assess myocardial ultrasound backscatter, exercise tolerance, and propensity to arrhythmias, in subjects who have inherited sarcomeric mutations but who do not have LVH.
- Keywords
- Growth Hormone, Cardiac Hypertrophy, Hypertrophic Cardiomyopathy, Sarcomeric Gene Mutations
- Medical subject headings
- Cardiomyopathy, Hypertrophic, Hypertrophy, Left Ventricular, Cardiomegaly
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 Nov 1999 (estimated)
- Study startFeb 1999
- Study completionAug 2002
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (3)Papers the sponsor has linked to this study.
- Other trials for Hypertrophic CardiomyopathyStudies of the same condition, open and under way.
- More trials run by National Heart, Lung, and Blood Institute (NHLBI)The sponsor's other registered studies.
- 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
- Observational
- Enrolment
- 175 participants
Sponsor and investigators
- Sponsor type
- US National Institutes of Health
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00001878
- Sponsor's protocol ID
- 990058
- Other IDs
- 99-H-0058
- Status last verified
- Aug 2002
- First submitted
- 3 Nov 1999
- Last updated
- 4 Mar 2008
- Results posted
- No
Publications
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.
PubMed 2811944Rayment 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.
PubMed 7731997Thierfelder 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.
PubMed 8205619
Study at a glance
From the registry record, last updated by the sponsor on 4 Mar 2008. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- 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
- ClinicalTrials.gov ID
- NCT00001878
- Acronym / sponsor ID
- 990058
- Keywords
- Growth Hormone, Cardiac Hypertrophy, Hypertrophic Cardiomyopathy, Sarcomeric Gene Mutations
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 175 participants
- Lead sponsor
- National Heart, Lung, and Blood Institute (NHLBI)US National Institutes of Health
- Study start
- Feb 1999
- Study completion
- Aug 2002
- First posted
- 4 Nov 1999 (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.
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).
Detailed description
Hypertrophic cardiomyopathy (HCM) is a genetic disease with an autosomal dominant pattern of inheritance which is characterized by left ventricular hypertrophy (LVH). HCM is often caused by missense mutations of genes that encode for sarcomeric proteins. The LVH varies markedly in patients with identical sarcomeric gene mutations, and notably, 20 to 40% of subjects with disease mutation do not have LVH as assessed by echocardiography. These findings suggest that other factors affect LV wall thickness in HCM. We wish (1) to investigate the potential role of IGF-I and its binding protein, IGFBP3, in determining increased LV mass in HCM caused by sarcomeric mutations; and (2) to assess myocardial ultrasound backscatter, exercise tolerance, and propensity to arrhythmias, in subjects who have inherited sarcomeric mutations but who do not have LVH.
Study design
Who may qualify
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
Key inclusion criteria (3 listed)
- HCM subjects 5 years or older, with distinct sarcomeric gene mutations and LV wall thickness greater than 15 mm in subjects older than 18 years, and greater than 2 SDs in subjects 18 years of age or younger, as assessed by MRI.
- Age- and gender-matched blood relatives with sarcomeric gene mutations but without LVH.
- Age- and gender-matched blood relatives without sarcomeric gene mutations.
Key exclusion criteria (4 listed)
- History of hypertension (basal systolic and diastolic pressures above 170 mm Hg and 95 mm Hg, respectively) or another systemic or cardiac disease that may cause cardiac hypertrophy.
- History of recent acute illness or other chronic illness that might affect plasma levels of IGF-I and IGFBP3.
- History of thyrotoxicosis, diabetes mellitus or abnormally elevated fasting blood sugar.
- Any conditions which would exclude patients from undergoing MRI scan.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 4 Mar 2008.
- Background: PubMed 2811944Jarcho 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.
- Background: PubMed 7731997Rayment 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.
- Background: PubMed 8205619Thierfelder 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.
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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.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Hypertrophic Cardiomyopathy and Left Ventricular Hypertrophy, run by National Heart, Lung, and Blood Institute (NHLBI) at 1 site in United States.
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 3 inclusion and 4 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: finished, as of the sponsor's last update on 4 Mar 2008. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
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.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
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.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00001878, which also lists 3 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 4 Mar 2008.