Arteries in Children of Premature Heart-Attack Victims Show Stiffening, Thickening at an Early Age

By Lois Baker

Release Date: September 20, 2000

THIS STORY IS EMBARGOED UNTIL 5 P.M. ON WEDNESDAY, SEPTEMBER 20, 2000

BUFFFALO, N.Y. -- Researchers can see the future in the blood vessels of children with a parent who has had a premature heart attack and the picture is not pretty.

A study in this week's issue of the New England Journal of Medicine reports that ultrasound images showed structural and functional abnormalities known to lead to atherosclerosis in children as young as 6 years.

"The parent's MI was already reflected in the kids," said Maurizio Trevisan, M.D., senior author on the study and professor and chair in the Department of Social and Preventive Medicine at the University at Buffalo.

Results showed that participants with a parent who had a heart attack before the age of 60 had vessel layers that were 11 percent thicker, and their vessels were 55 percent less reactive, than blood vessels in children with no parental history of heart attack.

"This was not a measurement of clinical disease," Trevisan said. "These were noninvasive direct measurements of vessel structure and function. Our findings showed thickening in the interior layers of the carotid artery, and a malfunction of the endothelium, the lining of the vessel. Both these abnormalities are indicators of 'pre-clinical disease,' disease that doesn't yet have symptoms."

It has been known for some time that persons with a parental history of premature coronary disease are themselves at high risk. This research set out to determine if it was possible to see structural and functional changes in the arteries of these persons at an early age.

The study involved recruitment of children and young adults with and without parental history of myocardial infarction, and was conducted by Trevisan and colleagues in Naples, Italy.

Forty healthy subjects between the ages of 6 and 30 years with a parental history of premature heart attack were compared with 40 persons with no family history of heart disease, matched for age and gender.

Researchers took blood-pressure readings, fasting blood samples, high-resolution ultrasound images and a survey of lifestyle habits and family history of coronary artery disease of all participants.

Ultrasound images were recorded on videotape and were analyzed by one expert reader who was unaware of the participants' family histories.

Results showed no significant differences between the two groups in the traditional measures of heart disease risk: blood pressure, cholesterol levels, triglycerides and smoking. The participants with a parental history of heart disease had a worse blood lipid profile than those without such a history.

Analysis of the ultrasound images showed that offspring of coronary patients had decreased artery reactivity, assessed by measuring blood flow in the arm before and after using a blood-pressure cuff. Blood flow increases after the cuff is deflated in healthy arteries, because the arteries react quickly in an effort to restore normal flow. Decreased reactivity, a risk factor for hardening of the arteries, was noted in offspring of coronary patients but not in controls.

Ultrasound analysis also showed thickened carotid artery walls in offspring of coronary patients, but not in controls.

Trevisan said few studies have looked at the association between family history of heart disease and both blood vessel structure and function. "These results could have important clinical implications," he said, "and need to be further explored so we can better understand the causes and disease path of coronary heart disease, and plan early intervention strategies that may save lives."

A team of physicians from the A. Cardarelli Hospital, Federico II University and S. Maria di Loreto Hospital in Naples; and M. Gene Bond, Ph.D., director of the Division of Vascular Ultrasound Research at Wake Forest University Baptist Medical Center, were major contributors to this study.