Objective: Platelet-derived growth factor (PDGF) induces matrix metalloproteinase (MMP), which is regarded as a biomarker of plaque rupture or vulnerability. The aim of this study is to investigate those interactions in human coronary arteries at the onset of ST-segment elevation myocardial infarction (STEMI). Methods: Thirty-two patients with STEMI who underwent primary percutaneous coronary intervention (PCI) were enrolled in this study. Plasma levels of PDGF-BB and MMP-9 were measured from infarct-related artery (IRA) and from femoral artery (FA) during PCI. Results: Plasma levels of PDGF-BB and MMP-9 in the IRA were significantly higher than those in the FA (PDGF-BB: median 3130 pg/ml, IQR (interquartile range): 2020 to 4375 pg/ml vs. median 2605 pg/ml, IQR: 1305 to 3290 pg/ml, p <0.01, MMP-9: median 49 ng/ml, IQR: 35 to 100 ng/ml vs. median 42 ng/ml, IQR: 27 to 78 ng/ml, p = 0.04, IRA and FA, respectively).
Conclusions:This in vivo study demonstrated that PDGF-BB with MMP-9 seems to play a role in coronary plaque instability in acute phase of STEMI.Keywords: platelet-derived mediator, coronary artery plaque, myocardial infarction (MMP), which is involved in a degradation of extracellular matrix proteins leading to the migration of SMC into the intima and to the rupture of plaques 1,2) has been reported in animal studies. However, those interactions in human in vivo studies have not been fully elucidated.Therefore, we have examined whether this concept from animal study may be extended to in vivo human study using biomarkers including PDGF-BB and MMP-9 in circulating blood samples from infarct-related coronary artery (IRA), which was occluded by massive thrombus after coronary plaque rupture, in acute phase of STsegment elevation myocardial infarction (STEMI).