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| ID | Type | Description | Link |
|---|---|---|---|
| 04-AG-N294 |
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The prevalence, incidence, and severity of atherosclerotic disease all markedly increase with age. Basic experimental and observational data demonstrate that aging magnifies the pathologic and clinical consequences of established risk factors and is the most potent individual risk factor for coronary atherosclerosis and for adverse outcomes following an ischemic event. These findings suggest that normal aging alters the vascular substrate so as to promote the development and progression of atherosclerosis. The age-associated changes in vascular structure and function include an increase in central vascular stiffness, intimal proliferation, and endothelial dysfunction. The major hypothesis is that the above alterations in vascular substrate (i.e. vascular age) are an important determinant of the age associated increased likelihood for the development and progression of coronary atherosclerotic disease.
This program will non-invasively characterize vascular age and atherosclerotic burden in BLSA participants and individuals with successful aging, i.e. those with no or minimal evidence of coronary atherosclerotic disease, and those with premature, clinically evident coronary artery disease. It will repeat measures of vascular age and atherosclerotic burden three years after the first assessment. By examining the impact of vascular age on the initial extent and the progression of atherosclerotic burden over a two to three-year period, it will test the hypothesis that vascular age is an important determinant of the ageassociated increase in atherosclerotic disease....
The prevalence, incidence, and severity of atherosclerotic disease all markedly increase with age. Basic experimental and observational data demonstrate that aging magnifies the pathologic and clinical consequences of established risk factors and is the most potent individual risk factor for coronary atherosclerosis and for adverse outcomes following an ischemic event. These findings suggest that normal aging alters the vascular substrate so as to promote the development and progression of atherosclerosis. The age-associated changes in vascular structure and function include an increase in central vascular stiffness, intimal proliferation, and endothelial dysfunction. The major hypothesis is that the above alterations in vascular substrate (i.e. vascular age) are an important determinant of the age associated increased likelihood for the development and progression of coronary atherosclerotic disease.
This protocol will non-invasively characterize vascular age and atherosclerotic burden in BLSA participants and individuals with successful aging, i.e. those with no or minimal evidence of coronary atherosclerotic disease, and those with premature, clinically evident coronary artery disease. It will repeat measures of vascular age and atherosclerotic burden three years after the first assessment. By examining the impact of vascular age on the initial extent and the progression of atherosclerotic burden over a two to three-year period, it will test the hypothesis that vascular age is an important determinant of the age-associated increase in atherosclerotic disease.
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| Measure | Description | Time Frame |
|---|---|---|
| Characterize vascular age relat-BLSA | Two-three years |
| Measure | Description | Time Frame |
|---|---|---|
| Characterize vascular age relat-other | Two-three years |
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For all groups:
For the second group:
1) Coronary artery calcium score of zero or less than 25th percentile of that expected based on age and gender.
For the third group:
1) Coronary artery calcium score which is greater than the 50th percentile of that computed based on age and gender, or known coronary disease on the basis of:
i. prior documented myocardial infarction or
ii. typical ischemic symptoms and catheterization documented stenosis of greater than or equal to 70% in at least one major coronary artery
If male, diagnosis was made under 50 years of age
If female, diagnosis was made under 60 years of age.
EXCLUSION CRITERIA
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| Name | Affiliation | Role |
|---|---|---|
| Edward G Lakatta, M.D. | National Institute on Aging (NIA) | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Johns Hopkins University | Baltimore | Maryland | 21205 | United States | ||
| National Institute of Aging, Clinical Research Unit |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 10323658 | Background | Lakatta EG. Cardiovascular aging research: the next horizons. J Am Geriatr Soc. 1999 May;47(5):613-25. doi: 10.1111/j.1532-5415.1999.tb02579.x. No abstract available. | |
| 11847204 | Background | Franklin SS, Wong ND, Larson MG, Kannel WB, Levy D. How important is pulse pressure as a predictor of cardiovascular risk? Hypertension. 2002 Feb;39(2):E12-3. No abstract available. |
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| ID | Term |
|---|---|
| D050197 | Atherosclerosis |
| D002318 | Cardiovascular Diseases |
| D014652 | Vascular Diseases |
| ID | Term |
|---|---|
| D001161 | Arteriosclerosis |
| D001157 | Arterial Occlusive Diseases |
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| Baltimore |
| Maryland |
| 21224 |
| United States |
| 11473737 | Background | Grundy SM. Coronary plaque as a replacement for age as a risk factor in global risk assessment. Am J Cardiol. 2001 Jul 19;88(2A):8E-11E. doi: 10.1016/s0002-9149(01)01712-x. |