Saturday, September 02, 2006
Heart disease adds up to 40 years to your artery age
People suffering from the advanced stages of heart disease have arteries that are biologically up to 40 years older than their real age, research funded by the British Heart Foundation has found.
The more advanced the disease, the older the artery cells are.
“In early stages of heart disease, the arteries are between 5-15 years older than the person's real age,” says Professor Martin Bennett, BHF Professor of Cardiovascular Sciences, whose research group at the University of Cambridge led the research.
He added,“If you have mild heart disease and can limit your risk factors by stopping smoking, controlling hypertension and diabetes, and taking statins to lower cholesterol, you will slow this ageing process.
"If you do nothing, the cells can reach extreme old age very prematurely – and once it does that, the process cannot be reversed.”
The study, published in the journal Circulation Research, was a result of collaboration between Professor Bennett's team and surgeons and pathologists from Papworth Hospital. It is the first in-depth study to use human tissue from heart bypass and transplant patients to map artery cell ageing.
The researchers studied the smooth muscle cells of diseased blood vessels, and identified accelerated telomere damage, which is a biological marker of ageing in the DNA of the cells.
Cells in the body can only divide a limited number of times. In patients with heart disease, their artery cells divide 7-13 times more often than normal and the cells run out of divisions, resulting in premature ageing of the arteries.
Older artery cells cannot repair properly, so do not function as well as younger ones. This makes them less capable of preventing fatty deposits called atherosclerotic plaques from forming, which can narrow the arteries and cause heart attacks.
“This is the first study that has mapped the extent of ageing in the artery. It's like an archaeological dig. If you take a cross section of the artery, the further you dig down the more aged the cells are,” says Professor Bennett.
Researchers believe that the major risk factors that cause heart disease – high blood pressure, diabetes, high cholesterol, smoking, lack of exercise and poor diet – are responsible for the chemical damage that causes the premature ageing. “All these factors work through a final common pathway to prematurely age cells in the vessel wall,” says Professor Bennett.
Similar cell ageing may take place in the bloodstream. If so, it may be possible in future to use this to identify patients at high risk of heart disease.
Professor Peter Weissberg, medical director of the BHF says: “ One of the defining features of ageing tissues is an inability to repair themselves efficiently: the older the tissue, the less able it is to deal with physical or biochemical injury.
“This research suggests that if blood vessel cells could be prevented from ageing so quickly, then potentially heart attacks could be prevented. This opens up a new avenue of research aimed at preventing heart attacks.”
The more advanced the disease, the older the artery cells are.
“In early stages of heart disease, the arteries are between 5-15 years older than the person's real age,” says Professor Martin Bennett, BHF Professor of Cardiovascular Sciences, whose research group at the University of Cambridge led the research.
He added,“If you have mild heart disease and can limit your risk factors by stopping smoking, controlling hypertension and diabetes, and taking statins to lower cholesterol, you will slow this ageing process.
"If you do nothing, the cells can reach extreme old age very prematurely – and once it does that, the process cannot be reversed.”
The study, published in the journal Circulation Research, was a result of collaboration between Professor Bennett's team and surgeons and pathologists from Papworth Hospital. It is the first in-depth study to use human tissue from heart bypass and transplant patients to map artery cell ageing.
The researchers studied the smooth muscle cells of diseased blood vessels, and identified accelerated telomere damage, which is a biological marker of ageing in the DNA of the cells.
Cells in the body can only divide a limited number of times. In patients with heart disease, their artery cells divide 7-13 times more often than normal and the cells run out of divisions, resulting in premature ageing of the arteries.
Older artery cells cannot repair properly, so do not function as well as younger ones. This makes them less capable of preventing fatty deposits called atherosclerotic plaques from forming, which can narrow the arteries and cause heart attacks.
“This is the first study that has mapped the extent of ageing in the artery. It's like an archaeological dig. If you take a cross section of the artery, the further you dig down the more aged the cells are,” says Professor Bennett.
Researchers believe that the major risk factors that cause heart disease – high blood pressure, diabetes, high cholesterol, smoking, lack of exercise and poor diet – are responsible for the chemical damage that causes the premature ageing. “All these factors work through a final common pathway to prematurely age cells in the vessel wall,” says Professor Bennett.
Similar cell ageing may take place in the bloodstream. If so, it may be possible in future to use this to identify patients at high risk of heart disease.
Professor Peter Weissberg, medical director of the BHF says: “ One of the defining features of ageing tissues is an inability to repair themselves efficiently: the older the tissue, the less able it is to deal with physical or biochemical injury.
“This research suggests that if blood vessel cells could be prevented from ageing so quickly, then potentially heart attacks could be prevented. This opens up a new avenue of research aimed at preventing heart attacks.”
