Poster Presentations: Tuesday, October 25, 2011 |

Decreased TSP-1 Levels in Patients After Myocardial Infarction and Stenting as a Risk Factor for Major Adverse Cardiac Events FREE TO VIEW

Ralf Kaiser, MD; Katharina Grotemeyer, MD; Heinrike Wilkens, PhD; Robert Bals, PhD; Elif Elmas, PhD
Chest. 2011;140(4_MeetingAbstracts):246A. doi:10.1378/chest.1118542
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PURPOSE: Thrombospondin-1 (TSP-1) is known as a protein synthesized by different cells, e.g. platelets, endothelium, smooth muscle cells, fibroblasts and cardiomyocytes. Though high concentrations are found in platelets, it is induced during myocardial ischemia or pathologically altered shearstress in endothelial cells. TSP-1 acts as a bridging molecule in platelet aggregation promoting adhesion to subendothelial layers in atherosclerotic lesions. In ischemia and reperfusion, TSP-1 might develop deleterious effects by disrupting both NO-signaling as well as VEGF-pathways by binding to its receptors CD47 and CD36 and therefore damaging local microcirculation. It was assumed that TSP-1 would be washed out after successful coronary reperfusion after myocardial infarction. In this study we examined circulating TSP-1 as a biomarker for adverse cardiac events after acute myocardial infarction.

METHODS: TSP-1 peptides levels in platelet poor serum were measured by colorimetric ELISA. TSP-1 levels were measured on the day of intervention, one to five days after intervention and more than two months later in 54 patients after myocardial infarction. Major adverse cardiac events (MACE: angina, re-intervention, arrhythmia, cardiac surgery, death) were monitored for 426 days.

RESULTS: Patients with decreased TSP levels after coronary stenting showed a significant higher risk for MACE than patient with higher TSP levels (TSP1[d0]: n=46, no MACE = 16,38+/-1,98mg/ml vs. MACE 7,11+/-1,54mg/ml; p=0,003); TSP1[d1-5]: n=38, no MACE 19,46+/-3,75mg/ml vs. MACE 8,59+/-1,37mg/ml; p<0,002). Logistic regression analysis showed TSP-1 after PCI as independent risk factor for MACE and ventricular fibrillation but not death. AUC of ROC for identification of patients at risk for MACE was 0,796. Kaplan-Meyer-analysis showed a trend to better outcome for the group above the median of 12,10mg/ml (p=0,07).

CONCLUSIONS: We were able to demonstrate the alteration of circulating TSP-1 levels after acute myocardial infarction followed by PCI. We then identified decreased levels of TSP-1 as an independent risk factor for major adverse cardiac events.

CLINICAL IMPLICATIONS: A low TSP-1 after PCI may be laboratory argument for an early re-PCI and continuation of monitoring. It might also alter the decision in favor of systemic or intracoronary application of biologicals to promote reperfusion.

DISCLOSURE: The following authors have nothing to disclose: Ralf Kaiser, Katharina Grotemeyer, Heinrike Wilkens, Robert Bals, Elif Elmas

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