Abstract
BackgroundInflammation plays a key role in the pathogenesis of acute myocardial infarction (MI). However, it is unclear whether marker of immune activation will provide prognostic information in these patients. We hypothesized that circulating levels of soluble CD93 (sCD93), a soluble form of transmembrane glycoprotein CD93, is increased in acute MI patients and its level would be associated with clinical outcomes in patients with acute MI.MethodsWe measured circulating levels of sCD93 in 120 patients with acute MI (63±13 yrs, M∶F = 85∶35) and in 120 age, sex-matched control subjects. In patients with acute MI, clinical characteristics, echocardiographic and laboratory findings were assessed at the time of initial enrollment. The primary outcome was defined as all-cause and cardiovascular death.ResultsCirculating sCD93 levels were significantly higher in patients with acute MI than in control subjects (552.1±293.7 vs. 429.8±114.2 ng/mL, p<0.0001). Upon in vitro inflammatory stimulation, increased CD93 shedding was demonstrated in acute MI patients but not in control subjects. During follow up period (median 208 days, 3-1058 days), the primary outcome occurred in 18 (15%) patients (9 cardiovascular deaths). Circulating levels of sCD93 were associated with all cause (p<0.0001) and cardiovascular (p<0.0001) mortality in patients with acute MI. Multivariate Cox regression analysis revealed that initial sCD93 level was found to be an independent predictor of all cause (p = 0.002) and cardiovascular mortality (p = 0.033) when controlled for age and left ventricular ejection fraction.ConclusionsCirculating levels of sCD93 are elevated in patients with acute MI and their levels were associated with adverse clinical outcomes.
Highlights
Myocardial infarction (MI) is defined as a clinical event caused by coronary thrombosis, and subsequent myocardial ischemia in which there is evidence of myocardial injury or necrosis [1]
Circulating soluble CD93 (sCD93) levels in acute myocardial infarction (MI) patients Baseline clinical characteristics and laboratory findings are summarized in table 1 and detailed characteristics of acute MI patients are summarized in table 2
We showed that elevated levels of sCD93 were associated with adverse clinical outcomes in patients with acute MI
Summary
Myocardial infarction (MI) is defined as a clinical event caused by coronary thrombosis, and subsequent myocardial ischemia in which there is evidence of myocardial injury or necrosis [1]. Two major causes of coronary thrombosis are plaque rupture and endothelial erosion [2,3]. Recent studies have shown that inflammation plays a key role in the pathogenesis of both plaque rupture and endothelial erosion. Because inflammation plays a key role in the pathogenesis of acute MI, a relevant biomarker of immune activation may provide novel prognostic information in these patients. It has been shown that sCD93 induces the differentiation of monocytes into macrophage-like cells that have increased phagocytic activities and enhanced cell adhesion, and it has been implicated in inflammation and inflammatory diseases such as rheumatoid arthritis [6]. Inflammation plays a key role in the pathogenesis of acute myocardial infarction (MI) It is unclear whether marker of immune activation will provide prognostic information in these patients. We hypothesized that circulating levels of soluble CD93 (sCD93), a soluble form of transmembrane glycoprotein CD93, is increased in acute MI patients and its level would be associated with clinical outcomes in patients with acute MI
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
