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
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
COMPLETED
OBSERVATIONAL
1998-08-31
2003-06-30
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
Cardiovascular Risk Factors in United States Adolescents and Adults
NCT00005171
Genetic Epidemiology of Change in CVD Risk Factors
NCT00037440
Precursors of CVD Risk Factors--Project Heartbeat
NCT00005478
Age, Risk Factors for CVD and Cognitive Functioning
NCT00007397
Prospective Study of Diet and Cardiovascular Disease
NCT00005519
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
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.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
100 Years
ALL
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
National Heart, Lung, and Blood Institute (NHLBI)
NIH
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
Lewis Becker
Role:
Johns Hopkins University
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
5026
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.