Supplement to the Evolution of Cardiovascular Risk with Normal Aging

Investigators
Gerald S. Berenson, MD, Principal Investigator
S. R. Srinivasan, PhD,Co-Investigator
Wei Chen, PhD, Co-Investigator

Funding Agent
National Institute on Aging, NIH

Participating Institutes
Tulane University

Description
The cardiovascular (C-V) system is one of the organ systems most affected by the aging process. In addition to intrinsic aging, the long-term burden of C-V risk factors underlies C-V structure-function changes, which eventually lead to morbidity and mortality in the general population. The supplemental project is an extension of the present grant AG-16592 “Evolution of C-V Risk with Normal Aging”. The study cohort includes 1,200 individuals born between 1959 and 1969 who were examined in the Bogalusa Heart at least four times since childhood and who are now entering middle age. The ongoing research is an attempt to characterize traits of intrinsic or “normal “ aging versus the long-term risk factor burden of a black-white population being followed over 25 to 30 years. An extensive database has been obtained since childhood related to the development of clinical C-V risk factors and silent, underlying C-V disease. The cohort is being examined for obesity measures, blood pressure, lipoprotein variables, glucose, insulin, and nontraditional risk factor variables such as homocysteine and C-reactive protein. Lifestyles and psychosocial variables under study include tobacco and alcohol use, physical activity, diet and life change events. Importantly, subclinical cardiac and carotid structure-function measures of cardiac and brachial and radial artery compliance are being measured. In addition, selected longevity-associated allele markers like apoE, are being examined. The proposed research of this supplement is directed to 1) evaluate the familial longevity trait among the elderly relatives (>84 years old) of the study cohort, 2) construct a “Health Family Tree” describing reported C-V- disease and risk factors on siblings, parents, aunts, uncles, and grandparents of the study cohort to compute a “Family Risk Score”, a measure of familial predisposition to C-V diseases and 3) link the above familial traits with the intermediate (C-V risk variables) and outcome (C-V structure-function) phenotypes as well as longevity-related candidate genes. This is not a departure from the original aims of the funded study. Incorporation of the familial traits data into the ongoing research as proposed is cost-effective by using existing facilities, and staff, but, importantly will help characterize the study cohort better. These observations will provide additional insight into predisposing factors that influence the subclinical C-V structure-function changes in normal aging. The major strengths of the study include a biracial, black-white population reaching middle age along with multiple observations obtained since childhood and in a relatively homogenous setting of a rural community. Understanding the evolution of C-V risk in normal aging will aid the development of more rational program to achieve successful aging and C-V disease prevention.