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Accelerated cellular aging observed in CAD patients

המידע באדיבות medicontext.co.il
Last Updated: 2001-08-10 15:25:23 EDT (Reuters Health)

By Karla Gale

LONDON (Reuters Health) – Patients with severe coronary artery disease exhibit leucocytic telomere shortening, according to the results of a pilot study conducted in the UK. This novel finding, an indicator of accelerated cell aging, "could have major implications for how atherosclerosis may occur," according to Dr. Nilesh J. Samani of the University of Leicester.

Dr. Samani and colleagues measured the lengths of terminal restriction fragments of leucocytes isolated from 10 patients with triple-vessel CAD involving >75% stenosis, and from 20 individuals with normal arteries on angiography. Their findings appear in the August 11th issue of The Lancet.

Patients with CAD had mean terminal restriction fragment lengths significantly shorter than did control subjects (p = 0.002). Based on the researchers' estimate that telomere lengths decrease by about 35 base pairs per year, the cells of patients with CAD appeared to be, on average, 8.6 years older than those of their counterparts.

"This may be an effect of risk factors that predispose one to atherosclerosis," Dr. Samani told Reuters Health. "In that case, we think telomere shortening in white blood cells may be an epiphenomenon of risk factors' effects on the body and on vessel walls." He noted that his group is currently examining larger numbers of patients to see if risk factors for CAD affect telomere shortening.

"What excites us is knowing there's a strong genetic component to telomere length," Dr. Samani continued. "If one is unlucky to be born with shorter telomeres to start with," he said, then the risk for atherosclerosis may be increased.

He also suggested that his team's findings might support the "Barker hypothesis"–the theory that, "if one is born small, the catchup growth in the first few years of life causes replicative stress," resulting in shorter telomeres and earlier senescence.

Lancet 2001;358:472-473.

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