New research finds drug to prevent secondary damage after heart attack

CRUCIAL research has unlocked a new drug that can effectively prevent major secondary damage from a heart attack, with Melbourne’s Baker Heart and Diabetes Institute researchers developing the “totally new concept”.

MELBOURNE researchers have used a one-off dose of a new drug to effectively prevent major damage from a heart attack by stopping the chain reaction of damage leading to heart failure in 80 per cent of people after cardiac event.

This finding in preclinical studies paves the way for the development of the first treatment to protect patients from secondary heart damage.

About 95 per cent of people who receive early treatment to reopen blocked blood vessels following a cardiac event survive. But most patients experience progressive heart failure in subsequent weeks as the immune system works overtime in the damaged heart.

The Baker Heart and Diabetes Institute.

NEW SCREENING TOOL FOR HEART FAILURE TRIALLED

MELBOURNE SCIENTISTS USE MICROBUBBLES TO BUT CLOTS

SEARCH FOR RED FLAGS IN THE BLOOD

Baker Heart and Diabetes Institute deputy director Professor Karlheinz Peter said they had developed a “totally new concept” to show they could overcome the immune reaction that occurred after coronary artery blockage was removed in the cath lab upon immediate arrival at hospital.

“Evolution hasn’t really foreseen we’d have heart attacks, so it’s probably an overshooting of the immune system that tries to get rid of the dead cells, but clears up the surviving cells as well,” he said.

“The estimate is over half the size of a heart attack is produced by this immune attack.”

Prof Peter and his team developed an antibody drug that takes the therapy to the exact area where it is needed in the heart. It has anti-inflammatory properties to prevent the immune attack, but can also prevent clots forming in the reopened vessels.

They gave mice a one-off dose of this antibody drug at the same time the coronary artery was reopened an hour after its closure; the same time frame typically experienced by human patients.

They compared it against a control drug and no treatment in three groups of mice that all started with 60 per cent ejection fraction.

After a month, mice that received the antibody drug maintained their heart function while the other two groups lost 20 per cent of their ability to push out blood with each heartbeat, a classic measure of heart failure.

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