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CLINCAL STUDY

Endothelial dysfunction of peripheral arteries in patients with immunohistologically confirmed myocardial inflammation correlates with endothelial expression of human leukocyte antigens and adhesion molecules in myocardial biopsies

^* Free University Berlin, Berlin, Germany

Manuscript received December 12, 2001; revised manuscript received April 10, 2002, accepted May 14, 2002.

^* Reprint requests and correspondence: Dr. Katja B. Vallbracht, University Hospital Benjamin Franklin, Department of Cardiology, Free University of Berlin, Hindenburgdamm 30, 12200 Berlin, Germany.
vallbrac{at}zedat.fu-berlin.de

OBJECTIVES: The aim of this study was to investigate whether myocardial inflammation (MC) and endothelial activation are associated with clinically detectable endothelial dysfunction.

BACKGROUND: In patients with MC, immunohistologic evaluation of myocardial biopsies demonstrates a cellular infiltrate of lymphocytes in the myocardium and endothelial activation, as indicated by enhanced expression of human leukocyte antigen (HLA)-1, HLA-DR and intercellular adhesion molecule (ICAM)-1. This chronic inflammatory process may be associated with endothelial dysfunction.

METHODS: In 65 patients with suspected MC, endothelial function of the radial artery was noninvasively assessed. By means of high-resolution ultrasound, diameter changes in response to reactive hyperemia (endothelium-dependent), as compared with glyceroltrinitrate (endothelium-independent), were analyzed. In the myocardial biopsies, MC was confirmed by immunohistology in 53 patients; 12 patients with normal myocardial biopsies served as controls. Endothelial expression of HLA-1, HLA-DR and ICAM-1 was semiquantitatively evaluated by immunohistology. To minimize other factors influencing endothelial function, patients with coronary artery disease, diabetes, severely impaired left ventricular function or more than one arteriosclerotic risk factor were excluded from this study.

RESULTS: Endothelial function, as determined by flow-mediated vasodilation (FMD), in patients with MC was impaired (FMD_MC 4.28%), as compared with controls (FMD_Co 10.10%). The severity of endothelial dysfunction in patients with MC correlated significantly with the extent of endothelial expression of HLA-1, HLA-DR and ICAM-1 in myocardial biopsies. Endothelium-independent vasodilation was not affected by MC or endothelial activation.

CONCLUSIONS: Myocardial inflammation is associated with endothelial dysfunction of peripheral arteries. The severity of endothelial dysfunction correlates with the extent of endothelial activation.

Abbreviations and Acronyms   CAM   cell adhesion molecule   Co   control group   ECG   electrocardiogram   EF   ejection fraction   FMD   flow-mediated vasodilation   GTN   glyceroltrinitrate   GTN-MD   glyceroltrinitrate-mediated vasodilation   HLA   human leukocyte antigen   ICAM   intercellular adhesion molecule   MC   myocardial inflammation

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