"‘Disbelief’ over discovery that could cut heart-attack damage April 21, 2011
Debra Black STAFF REPORTER
William Schwaeble, a professor of immunology at the University of Leicester, couldn’t believe what he had found: an antibody that could lessen the damage from the inflammation often caused by heart attacks and strokes.
“At first it was disbelief,” he explained in a telephone interview with the Star. “When data looks too nice, you always become critical.”
So he got researchers at three universities – Kings College London, the Medical University of Fukushima in Japan, and the State University of New York – to take a look.
Initially, they were skeptical, but the results and data won them over. And the researchers are now co-authors of a report in the Early Online Edition of the Proceedings of the National Academy of Sciences.
Schwaeble and his fellow researchers may be responsible for a significant development in the treatment of heart and stroke victims. “It certainly will have a significant protective effect on heart and stroke victims,” he said. “We anticipate there will be a dramatically reduced tissue loss and thereby a dramatically improved outcome.”
Initially, Schwaeble and his research team created a mouse strain that knocked out the gene for MASP-2, which is responsible for causing inflammation after a heart attack or stroke.
“This made resistant mice that was the proof of the principle. But we said ‘We can’t knock out the MASP-2 enzyme in humans.’ So we had to find an inhibitor.”
“We have developed a recombinant antibody which is safe enough to be used in humans,” Schwaeble said.
Schwaeble and his team of researchers have been working with Omeros Corporation from Seattle, Wash., for the past seven years on the therapeutic antibody.
The company has started manufacturing the inhibitor and is scaling up its production, Schwaeble said. It has secured worldwide intellectual property rights for the MASP-2 technology.
“The significance is you now have a tool in your hand that can limit the inflammation following the temporary loss of oxygen to tissues.”
But there are still a couple of steps before the inhibitor will be part of a regular emergency room or a paramedic’s tools for dealing with heart attacks or strokes.
Toxicity trails must first take place. In about 24 months, clinical trails will get underway at Glenfield Hospital, University Hospitals of Leicester.
The inhibitor must be administered nine to 12 hours after a heart attack or stroke, Schwaeble said. It will also save lives and improve survival rates, Schwaeble said.
For example, whether 30 per cent of your heart is destroyed or only 5 per cent of your heart is destroyed could mean the difference between life and death, he said.
“Think of the heart as a muscle. If you take 30 per cent of that electrical instrument out by making a big scar that will interfere with the electricity of the heard, that can lead to cardiac failure and death.”
But if the damage is limited to only 5 per cent of the heart, the impact won’t be as much. "