Abstract
BackgroundSince soluble TRAIL exhibits anti-inflammatory and anti-atherosclerotic activities both in vitro and in animal models, this study was designed to assess the relationship between the serum levels of TRAIL and clinical outcomes in patients with acute myocardial infarction (AMI).Methodology/Principal FindingsLevels of TRAIL were measured by ELISA in serial serum samples obtained from 60 patients admitted for AMI, both during hospitalization and in a follow-up of 12 months, as well as in 60 healthy control subjects. Serum levels of TRAIL were significantly decreased in patients with AMI at baseline (within 24 hours from admission), compared with healthy controls, and showed a significant inverse correlation with a series of negative prognostic markers, such as CK, CK-MB and BNP. TRAIL serum levels progressively increased at discharge, but normalized only at 6–12 months after AMI. Of note, low TRAIL levels at the patient discharge were associated with increased incidence of cardiac death and heart failure in the 12-month follow-up, even after adjustment for demographic and clinical risk parameters (hazard ratio [HR] of 0.93 [95% CI, 0.89 to 0.97]; p = 0.001).Conclusions/SignificanceAlthough the number of patients studied was limited, our findings indicate for the first time that circulating TRAIL might represent an important predictor of cardiovascular events, independent of conventional risk markers.
Highlights
In the serum of patients affected by acute myocardial infarction (AMI) several cytokines, including those belonging to the TNF family members, are known to be elevated [1], only limited information is available on the role of TNF family members in modulating cell death after myocardial ischemia [2,3,4]
It has been suggested that the CD95 system might be involved in post-ischemic cell death in the heart [2], and it has been reported that the serum levels of TNF-related apoptosis inducing ligand (TRAIL) tend to be reduced in patients with coronary artery disease [5,6]
We have demonstrated that the serum levels of TRAIL were significantly decreased in the early time points after AMI and progressively increased in the follow-up (6–12 months later), reaching levels comparable to those observed in the healthy controls
Summary
In the serum of patients affected by acute myocardial infarction (AMI) several cytokines, including those belonging to the TNF family members, are known to be elevated [1], only limited information is available on the role of TNF family members in modulating cell death after myocardial ischemia [2,3,4]. In this context, it has been suggested that the CD95 system might be involved in post-ischemic cell death in the heart [2], and it has been reported that the serum levels of TNF-related apoptosis inducing ligand (TRAIL) tend to be reduced in patients with coronary artery disease [5,6]. Since soluble TRAIL exhibits anti-inflammatory and anti-atherosclerotic activities both in vitro and in animal models, this study was designed to assess the relationship between the serum levels of TRAIL and clinical outcomes in patients with acute myocardial infarction (AMI)
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