Platelet and monocyte activity markers and mediators of inflammation in Takotsubo cardiomyopathy

被引:26
作者
Pirzer, Rainer [1 ]
Elmas, Elif [1 ]
Haghi, Dariusch [1 ]
Lippert, Christiane [1 ]
Kralev, Stefan [1 ]
Lang, Siegfried [1 ]
Borggrefe, Martin [1 ]
Kaelsch, Thorsten [1 ]
机构
[1] Univ Heidelberg, Univ Med Ctr Mannheim, Med Fac Mannheim, Dept Med Cardiol 1, D-68167 Mannheim, Germany
关键词
Platelets; Inflammation; Takotsubo cardiomyopathy; Stress; ACUTE MYOCARDIAL-INFARCTION; APICAL BALLOONING SYNDROME; CD40; LIGAND; UNSTABLE ANGINA; ENDOTHELIAL-CELLS; P-SELECTIN; INTERLEUKIN-6; STRESS; EXPRESSION; HYPERCHOLESTEROLEMIA;
D O I
10.1007/s00380-011-0132-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:186 / 192
页数:7
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