Fibrin-Derived Peptide Reduces Cardiac Reperfusion Injury

A new study has shown that a fibrin-derived peptide is effective in preventing cardiac damage resulting from reperfusion therapy, a well-established treatment following a heart attack, which paradoxically causes additional damage to heart muscle.

Researchers from the University of Oslo (Oslo, Norway) and 25 other leading centers of interventional cardiology in Europe conducted a randomized, double blind, placebo-controlled study evaluating the effect of the peptide, FX06, on infarct size in 234 patients undergoing percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI) between October 2006 and March 2008. FX06 was administered intravenously to patients during reperfusion treatment, and the effect on heart muscle preservation was then assessed using cardiac magnetic resonance imaging (CMRI). The primary endpoint was reduction in infarct size at five days after myocardial infarction (MI).

The results of the study showed that at five days post-PCI, the necrotic zone of the infarct was significantly reduced by 58%, and the total affected zone of the left ventricle was reduced by 21%. This was accompanied by a reduction in markers of heart muscle cell necrosis. After four months, the resulting scar mass was reduced by 37%, suggesting that a reduction of reperfusion injury indeed may lead to decrease in scar tissue formation. The researchers added that major adverse cardiac events in the FX06 group were also lower compared to the placebo group, which may indicate an effect of the drug on adverse patient outcome after an infarction. The results of the study were presented at the European Society of Cardiology Congress, held during September 2008 in Munich (Germany).

"Reestablishment of blood flow, either by catheter-based balloon-intervention or by thrombolysis, is necessary and life-saving in the treatment of acute myocardial infarctions. However, such interventions can lead to further damage to the heart muscle due to blood vessel dysfunction and inflammation,” said the coordinating investigator of the FX06 in the Ischemia and REperfusion (FIRE) phase II clinical study, Prof. Dan Atar, M.D., of the division of cardiology. "FX06 has been shown to reduce damage to the heart muscle by inhibiting inflammation and protecting vascular function. We predict that FX06 may become a novel treatment for STEMI patients undergoing PCI, representing a major advance in acute cardiac care.”

FX06 is a peptide that binds to VE-cadherin, a target on the surface of endothelial cells in blood vessels, thereby preserving their function. This leads to reduced inflammation, reduced edema, and reduced infarct sizes.

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University of Oslo