Platelet and monocyte activity markers and mediators of inflammation in Takotsubo cardiomyopathy |
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Authors: | Rainer?Pirzer Elif?Elmas Dariusch?Haghi Christiane?Lippert Stefan?Kralev Siegfried?Lang Martin?Borggrefe Email author" target="_blank">Thorsten?K?lschEmail author |
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Institution: | (1) 1st Department of Medicine (Cardiology), University Medical Centre Mannheim, Medical Faculty Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany; |
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Abstract: | Patients with Takotsubo cardiomyopathy (TC) often present with symptoms similar to those of myocardial infarction (MI). We
analyzed blood concentrations of mediators of inflammation and platelet- and monocyte-activity markers in patients with TC
and MI for significant differences. Clinical data of patients with TC (n = 16) and acute MI (n = 16) were obtained. Serial blood samples were taken at the time of hospital admission (t
0), after 2–4 days (t
1) and after 4–7 weeks (t
2), respectively. Plasma concentrations of interleukin (IL)-6, IL-7, soluble CD40 ligand (sCD40L), and monocyte chemotactic
protein 1 (MCP-1) were determined with an ELISA. Tissue factor binding on monocytes, platelet-activation marker CD62P, platelet CD40-ligand (CD40L), and platelet-monocyte aggregates were measured using flow
cytometry. Expression of CD62P on platelets and IL-6 plasma levels were significantly lower in patients with TC compared to
MI at the time of hospital admission. IL-7 plasma levels were significantly elevated in patients with TC compared to patients
with MI at 2–4 days after hospital admission. No significant differences were observed concerning sCD40L and MCP-1 plasma
levels, tissue factor binding on monocytes, CD40L expression on platelets, and platelet-monocyte aggregates at any point in
time. Our results indicate that inflammatory mediators and platelet-activity markers contribute to the differences in the
pathogenesis of MI and TC. |
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Keywords: | |
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