Sept. 20, 2000 -- Having a parent who had an early heart attack is a well-known risk factor for heart disease, and researchers may now have a better understanding of why that is. It appears that hardening of the arteries begins very early for people who have a genetic predisposition, with significant damage often occurring before age 20.
But inheriting bad genes doesn't mean a person can do nothing to lessen the risk of heart attack or stroke. In fact, these are the people who benefit most from adopting a heart-healthy lifestyle, experts say.
"People with a family history of heart disease have a higher absolute risk, so they actually have a lot more to gain by reducing their risk with lifestyle changes and drug therapy. Someone with this history shouldn't even think about smoking, should make sure their blood pressure and cholesterol is under control, and should avoid obesity, which is strongly associated with diabetes and heart disease," American Heart Association spokesman Harlan Krumholz, MD, tells WebMD.
The cholesterol plaque build-up, which causes the hardening of the arteries known as atherosclerosis, generally occurs as people grow older, and is associated with both heart attack and stroke. Lifestyle influences, such as high blood pressure, high cholesterol, and smoking are critical risk factors in artery blockage, but genetic influences also play an important, but as-yet mysterious, role.
It has been suggested that the risk of heart attack death is as much as seven times higher for those with parents having attacks prior to age 60, compared with the general population.
"What we wanted to know was whether or not there are structural and functional changes in the arteries of the children of a parent who has had a premature heart attack," Gene Bond, PhD, of Wake Forest University School of Medicine in Winston-Salem, NC, tells WebMD. Bond and Wake Forest colleagues collaborated with researchers from the State University of New York at Buffalo and the Federico II University of Naples, Italy, to answer the question. They report their findings in the Sept. 21 issue of TheNew England Journal of Medicine.
Using ultrasound imaging, researchers measured the thickness and function of arteries, two indicators of early hardening of the arteries, in 40 healthy young people (age range six through 30) with a parent who suffered a heart attack before the age of 60; this was considered the high-risk group. They compared them with a low-risk group: 40 similar people with no parental history of heart disease.
On average, at the end of the study subjects' teenage years, the artery walls of the high-risk group were already 11% thicker, and their arteries were functionally about 55% less reactive than the low-risk group, according to Bond.
"This study is another piece of the puzzle which suggests a genetic influence at the level of the artery wall in the development of hardening of the arteries," he says.
Parental history was the only factor present in this group of young people that predicted artery hardening. There was no significant difference between the two groups in cholesterol levels or blood pressure.
"If increased arterial wall thickness and decreased artery reactivity can be identified in these high-risk young people, it means they can take special care to avoid other risk factors such as tobacco consumption and high fat and cholesterol diets," Bond says. "This kind of information could definitely save lives. If you took 100 people who will have a heart attack or stroke within the next five years and reduced their cholesterol by 35% with drugs or lifestyle changes, you could reduce those events by almost one-third."
Krumholz agreed, but said he does not believe ultrasound screening will be a useful tool in identifying young people at high risk for heart attacks because the degree of arterial damage measured in this study would not be easily detected in a routine clinical setting. And even if it could be, he would never tell a patient without such damage who had a family history of early heart attack that he or she was at low risk.
"You want to be aggressive with risk reduction for anyone who has a family member with premature disease, and you certainly can't modify that approach based on these test results," Krumholz says.