WEDNESDAY, Aug. 18, 2004 (HealthDayNews) -- For once, snake venom may be helping save lives rather than putting them in danger. Scientists say a protein in venom gives valuable insight as to why a group of new heart medications called integrin antagonists cause more harm than good in some patients.
The drugs are designed to prevent blood clots from forming and causing heart attack during angioplasty, where doctors use a balloon-like device to clear narrowed arteries. Intravenous versions of integrin antagonists used during angioplasty have proved effective in most patients.
Oral forms of these drugs were developed for use by patients after they were discharged from the hospital. But research trials on the oral versions were halted after early results found a 33 percent increase in patient deaths. No clear cause for the deaths could be found.
Integrin antagonists block the body's natural clotting mechanism by targeting integrin, a protein on blood platelets, which is essential to the clotting process. Clotting begins when integrin receptors combine with fibrinogen, a protein in the fluid part of the blood. This causes blood platelets to collect at the site of an injury to stop blood loss.
In this new study, led by Wake Forest University Baptist Medical Center, researchers used a protein found in snake venom that binds to the integrin and blocks fibrinogen.
The scientists found the snake venom protein blocks the integrin receptors, just like the integrin antagonist drugs. But after the snake venom protein is withdrawn, some of the integrin receptors remain activated, meaning it's still possible for clotting to occur.
"Likewise, the drugs are effective at blocking the receptor, but some of the newer drugs also cause the receptor to remain activated. The beneficial effects of these drugs seem to be inseparable from their side effects," principal investigator Roy Hantgan said in a prepared statement.
He and his colleagues tested several intravenous and oral integrin antagonists and found that all had the same response in varying degrees.
"This results suggests that no matter how good a drug you develop, you're going to have this problem in some patients. We believe that drugs that are designed to bind to intergrin receptors inside the platelet, rather than on the surface, might have a better chance of working," Hantgan said.
The study appears in the current online issue of the Journal of Molecular Biology.
The U.S. National Library of Medicine has more about angioplasty.