Novel technique reduces restenosis

IF YOU guessed that women, particularly in the pre-menopause stage, are generally less prone to heart attacks as compared to men and post-menopause women then you are probably right. Medical evidence has proved this long ago. The agent responsible for this selective protection has been identified as estrogen - the female hormone naturally found in pre-menopause women.

This hormonal protection generally renders pre-menopause women a longer period of protection (nearly ten years) as compared to men. However, the estrogen level gradually tapers below therapeutic level after menopause thereby putting post-menopause women at equal risk like men to heart attacks.

This knowledge has been used by Dr. B. Chandrasekar, Consultant Interventional Cardiologist of Vijaya Hospital, Chennai, to reduce restenosis after angioplasty in animal studies. Though using estrogen to reduce restenosis (fresh tissue growth) is nothing new, the mode of presentation of estrogen by Dr. Chandrasekar is indeed one.

"Conventional estrogen therapy to reduce restenosis is through prolonged systemic treatment. But my procedure delivers estrogen at the specific site in the artery," Dr. Chandrasekar said. The advantages of such a procedure are aplenty. For one, it makes prolonged systemic estrogen treatment redundant. This is particularly significant in the case of men as estrogen is a female hormone and any prolonged exposure to it leads to breast enlargement. Men do not have more than 50 piccograms/millilitre of estrogen circulating in their body at any point of time.

Since it delivers estrogen at the specific site the quantity of estrogen used is only about 30 piccograms/millilitre. And most importantly, the estrogen is delivered just once when angioplasty is done. The significance of the dosage and one time delivery is that the estrogen gets metabolised within 24 hours and is flushed out of the body making the procedure relatively safe as compared to the conventional therapy. Easy metabolisation and the very small percentage of estrogen that reaches the site of restenosis are the very reasons for prolonged treatment in the case of conventional systemic estrogen therapy.

Animal studies have further shown that only a small fraction of 17b estradiol - the circulating form of estrogen in pre-menopause women - used by Dr. Chandrasekar for reducing restenosis actually enters the vessel wall. The highlight of the experimental studies was that the 17b was found to reduce the area of restenosis through neointima formation (new tissue growth) by 50 per cent. Restenosis through neointima formation is predominant when a stent is used and negative remodelling (shrinking of the artery) when balloon angioplasty is done.

"Large reduction in restenosis and the very small quantity of estrogen used makes this therapy attractive compared to the conventional one," he said. More importantly it uses a substance naturally found in humans.

The large reduction in restenosis is because the 17b estrogen unit truncates the restenosis triggering mechanism. But its one time exposure limits its ability to completely prevent restenosis. A longer period of treatment is required to achieve this but it negates the very advantage of this procedure.

"An ideal dose is yet to be found and more importantly it has to be proved effective in human trials too," he said. "Further animal studies have to be done using stents coated with 17b estrogen unit and finally the quantity of 17b unit actually entering the vessel has to be determined." The experimental work may get a boost and become available for regular therapy if the patent filed by Dr. Chandrasekar in Canada is approved.

R. Prasad

in Chennai

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