2012 年 19 巻 4 号 p. 357-368
Aim: Increasing evidence indicates that antimicrobial peptides, human neutrophil peptide-1, -2, and -3 (HNP1-3) and human antimicrobial peptide LL-37 are involved in the pathophysiology of atherosclerosis; however, little is known about their circulating protein levels in acute myocardial infarction (AMI). We therefore investigated whether their plasma levels are associated with stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI).
Methods: Systemic or local (culprit artery) blood samples were obtained from 112 consecutive male subjects including no CAD (n = 31) controls, stable CAD (n = 44) and STEMI (n = 47). Plasma HNP1-3 and LL-37 levels were measured by the ready-to-use solid-phase enzyme-linked immunosorbent assay (ELISA) based on the sandwich principle.
Results: Systemic HNP1-3 in STEMI was increased compared with no CAD (p = 0.000) and stable CAD (p = 0.008), and systemic HNP1-3 in stable CAD was higher than in no CAD (p = 0.004). Systemic LL-37 in STEMI was decreased compared with no CAD (p = 0.009) and stable CAD (p =0.001) and restored within 1 day following STEMI (p = 0.000). Local LL-37 levels in STEMI were higher than systemic levels (p = 0.013). The areas under the ROC curve of systemic HNP1-3 and LL-37 for STEMI were 0.717 (95% CI: 0.624, 0.811; p = 0.000) and 0.702 (95% CI: 0.609, 0.795; p = 0.000), respectively. In addition, ischemia time in the STEMI group correlated with systemic and local levels of HNP1-3 (rs = −0.360, p = 0.013; rs = 0.608, p = 0.000, respectively), and was also associated with systemic and local levels of hs-CRP (rs = 0.408, p = 0.004; rs = 0.425, p = 0.003, respectively), but not with those of LL-37 (all p > 0.05).
Conclusion: STEMI was associated with transiently decreased LL-37, but persistently increased HNP1-3 in the systemic circulation and the diagnostic accuracy for STEMI were moderate. Future studies should pay more attention to their prognostic values for myocardial infarction.
