Determinants of Coronary Disease in High Risk Families

This study has been completed.
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00005508
First received: May 25, 2000
Last updated: February 17, 2016
Last verified: August 2004

May 25, 2000
February 17, 2016
August 1998
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Complete list of historical versions of study NCT00005508 on ClinicalTrials.gov Archive Site
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Determinants of Coronary Disease in High Risk Families
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To define factors contributing to coronary heart disease (CHD) in high risk families.

DESIGN NARRATIVE:

The study followed healthy siblings of patients diagnosed with CHD before age 60. All siblings underwent comprehensive risk factor screening and exercise thallium tomography to identify occult CHD. Follow-up was performed from 6-15 years after entry (mean 8.7 years) to determine the incidence of (1) acute coronary events (sudden death, myocardial infarction, and unstable angina) and (2) progression of occult CHD (repeat exercise thallium tomography). Blood was obtained for genomic DNA, which was tested for polymorphisms of candidate genes which may be associated with premature thrombotic CHD events (platelet proteins GPIIB/IIIa[PlA1/A2 and Baka/b] and GPIbB, endothelial nitric oxide synthase, angiotensin converting enzyme, angiotensinogen, D-fibrinogen, plasminogen activator-1, and methylenetetrahydrofolate reductase). Plasma levels of proteins implicated in the pathogenesis of atherosclerosis and thrombotic CHD events were measured (fibrinogen, plasminogen activator inhibitor-1, tissue plasminogen activator, homocysteine, lipoprotein (a), and apo(a) isoform size). DNA was also obtained from living probands and affected siblings to use for genetic linkage studies using affected and unaffectedsibling pairs. Statistical analyses examined (1) whether selected genetic polymorphisms were linked to the occurrence of acute CHD events, and (2) to what extent traditional sociodemographic and biological coronary risk factors or new genetic polymorphisms explained the progression of occult CHD, or the transition from occult to symptomatic CHD events in families with premature CHD.

The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.

Observational
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  • Cardiovascular Diseases
  • Coronary Disease
  • Heart Diseases
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
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June 2003
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No eligibility criteria
Both
up to 100 Years   (Child, Adult, Senior)
No
Contact information is only displayed when the study is recruiting subjects
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NCT00005508
5026, R01HL059684
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National Heart, Lung, and Blood Institute (NHLBI)
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Investigator: Lewis Becker Johns Hopkins University
National Heart, Lung, and Blood Institute (NHLBI)
August 2004

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP