Hepatocyte growth factor (HGF), a growth factor originally thought to be important in cellular growth and development, possesses characteristics that underscore a potential purpose in ACS. In the context of acute plaque rupture and thrombosis, there appears to be a relationship between thrombus formation and release of HGF. This appears to be dependent on the presence of mast cells as an intermediary. Perhaps, through activation of the thrombin receptor on mast cells, release of heparin leads to elevated HGF release from the extracellular matrix.
Clinically, significantly higher levels of HGF were demonstrated in patients with chest pain and evidence of acute thrombosis (from ACS, aortic dissection, or acute pulmonary emboli) compared with those without evidence of thrombosis.31 Similar findings were noted in patients who presented with cerebral infarction and unstable angina. It has been suggested that elevated levels of HGF may be protective in the ACS setting. Although HGF release may be a direct response to acute thrombosis and subsequent myocardial injury, larger studies are needed to validate these findings and to determine whether any relationship exists between levels of HGF and clinical prognosis.
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