Finally, we investigated the impact of circulating sCD93 levels on clinical outcomes in acute MI patients. In addition, monocytes isolated from acute MI Cryptochlorogenic-acid patients show increased shedding of CD93 upon inflammatory stimulation, suggesting possible mechanism for the elevated sCD93 in these patients. Finally, we also showed that elevated levels of sCD93 were associated with adverse clinical outcomes in patients with acute MI. The relationship between CD93 and CAD has been documented in previous genetic association studies. Ma��larstig et al. reported on the relationship between plasma levels of sCD93 and the risks of both premature MI and CAD in two independent cohorts. However, this study was a cross-sectional association study without prognostic implication. The present study is important because it is the first study to demonstrate the association between increased levels of sCD93 and clinical outcomes in patients with acute MI. We observed an early divergence of the Kaplan-Meier curves shortly after the diagnosis of acute MI. Activation of chronic inflammation might be related with early adverse event after the acute MI, however the cause and effect relationship between inflammation and early adverse prognosis is not clear yet. There are no known relevant biomarkers of immune activation in atherosclerotic plaque rupture. hsCRP is the most extensively studied biomarker of inflammation in cardiovascular diseases. However, the prognostic value of hsCRP in patients with acute MI is controversial. Some studies have found that serum hsCRP predicts the risk of 30-day or long-term mortality after an MI. However, other reports have found no such relationship. In this study, we have shown that the predictive prognostic value of sCD93 was independent of hsCRP in patients with acute MI. Relationship between increased levels of sCD93 and adverse clinical outcomes in patients with 
acute MI might be explained by the underlying pathophysiology of atherosclerosis. Monocyte plays a key role from the beginning of the atherosclerotic plaque development to the final plaque rupture eliciting an acute MI. Circulating monocytes are recruited into the activated endothelium of artery and then differentiate into macrophage, which comprises major cellular component of atherosclerotic plaque. With the progression of atherosclerotic plaque, activated macrophage produces various pro-inflammatory Ursolic-acid cytokines, proteases, free oxygen radicals and vasoactive molecules that can destabilize the lesions. All these molecules might induce the activation and rupture of atherosclerotic plaque, thrombosis, and subsequently an acute MI. A recent study showed that sCD93 induced differentiation of monocytes to macrophage like cells, as evidenced by activated cell adhesion and increased phagocytic activities. In addition, this differentiation resulted in increased pro-inflammatory cytokine production. The link between sCD93 and monocyte activation has been implicated in inflammation and circulating levels of sCD93 can be a maker of monocyte activation. In this study, we have demonstrated that circulating sCD93, novel monocyte inflammatory marker, are elevated in patients with acute MI and their levels were associated with adverse clinical outcomes.