University of Vermont

College of Medicine

Tracy Co-authors NEJM Study on Lifetime Risk for Cardiovascular Disease

Russell Tracey, Ph.D.
Russel Tracy, Ph.D., profesor of pathology and biochemistry at the University of Vermont College of Medicine. (Photo: Raj Chawla/UVM Medical Photography

February is American Heart Month and an opportunity to highlight some of the University of Vermont College of Medicine research and researchers that are making a difference in the field of cardiovascular disease and stroke.

In a study reported to be one of the largest-ever analyses of lifetime risks for cardiovascular disease (CVD), investigators associated with the Cardiovascular Lifetime Risk Pooling Project, including Russell Tracy, Ph.D., University of Vermont Professor of Pathology and Biochemistry, confirmed that a person’s cardiovascular risk-factor profile at middle age corresponds to lifetime CVD risk. The study was published in the January 26, 2012 New England Journal of Medicine.

The meta-analysis examined more than 250,000 participants, including black men and women and white men and women, whose risk factors for cardiovascular disease were measured at the ages of 45, 55, 65, and 75 years, across 18 longitudinal studies.

Tracy, whose lab at UVM’s Colchester Research Facility was responsible for the cholesterol measurements of about 10,000 participants in two of the 18 different population groups analyzed for the study, has a long-standing interest in “competing risks” – analyzing the different possible health events that can lead to death.

While the study’s findings – that health status at middle age informs future risk of CVD-related death – are not completely new, this research does provide some notable advances in the field, says Tracy, including the examination of data from not only a large number of studies, but studies performed over a long period of time.

“This study’s analysis of risk data by birth cohort – groups born in different time periods – is a unique feature,” says Tracy. “We could ask questions, such as, ‘does a 55-year-old man born before 1920 have the same risk of cardiovascular disease as a 55-year-old man born after 1920?’ This allowed us to consider trends like medication differences over time.”

In addition, Tracy points out, the study’s large size permitted the researchers to calculate risk separately by gender and race/ethnicity, which has been limited in other studies like the Framingham Heart Study, which primarily includes data on white males.

Another unique feature of the study is the calculation of risk of CVD for the participants’ lifetime versus just 10 years, the timeframe measure employed in the Framingham Risk Score. According to Tracy, accomplishing this approach requires a consideration of the competing risk of other diseases that could occur prior to CVD.

“If you don’t adjust for competing risks, the rates for a given disease such as CVD look higher than they actually are,” cautions Tracy. “To acquire the CVD events information, the participants had to be alive in order to develop CVD. When you adjust for competing risks such as cancer, accidents, etc., the CVD lifetime risk goes down; people who might have developed CVD can die from something else first.”

Because of its design, adds Tracy, the study was able to provide powerful confirmation that increased burden of traditional CVD risk factors – blood pressure, cholesterol, diabetes, smoking – is strongly associated with lifetime risk of CVD in both men and women and older and younger people, but more so for younger than older, and for people born within different birth cohorts. Men and women with an optimal CVD risk profile at 55 years of age had a 4.7 percent and 6.4 percent respectively of lifetime risk of death due to CVD, and participants of the same age with two or more risk factors had a much greater risk of death due to CVD by age 80 – 29.6 percent for men and 20.5 percent for women. However, the study determined that 45 year olds with several major risk factors had a greater than 30-fold increased risk of CVD compared to those with all optimal risk factors, while for 75 year olds it was about a two-fold increased risk.

“There has been a decline in CVD disease in the last 30 years, and this analysis is consistent with most of that decline being due to a decline in risk factors in younger populations, not the important, but relatively modest improvement in medications or other treatments of risk factors,” Tracy says. “The main finding is also true for blacks and whites – blacks have a higher burden of traditional risk factors than whites so their lifetime risk for CVD appears higher, but not after adjusting for competing risks, since their risks for other diseases are also higher.”

In a news release issued by the National Institutes of Health, Tracy’s colleague Donald M. Lloyd-Jones, M.D., principal investigator of the study and an associate professor and chair of preventive medicine at Northwestern University Feinberg School of Medicine in Chicago, said “These data have important implications for prevention. We need to get more serious about promoting healthy lifestyles in children and young adults, since even mild elevations in risk factors by middle age seem to have profound effects on the remaining lifetime risks for CVD.”

The study was supported by grants from the National Heart, Lung, and Blood Institute, by funding from the Dedman Family Scholar in Clinical Care endowment at University of Texas Southwestern Medical Center, and by an American Heart Association grant.