PMID- 12142120
OWN - NLM
STAT- MEDLINE
DCOM- 20020830
LR  - 20190708
IS  - 0735-1097 (Print)
IS  - 0735-1097 (Linking)
VI  - 40
IP  - 3
DP  - 2002 Aug 7
TI  - 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.
PG  - 515-20
AB  - 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.
FAU - Vallbracht, Katja B
AU  - Vallbracht KB
AD  - University Hospital Benjamin Franklin, Department of Cardiology, Free University 
      Berlin, Berlin, Germany. vallbrac@zedat.fu-berlin.de
FAU - Schwimmbeck, Peter L
AU  - Schwimmbeck PL
FAU - Seeberg, Bettina
AU  - Seeberg B
FAU - Kuhl, Uwe
AU  - Kuhl U
FAU - Schultheiss, Heinz-Peter
AU  - Schultheiss HP
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
RN  - 0 (HLA Antigens)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Arteries/*physiopathology
MH  - Biopsy
MH  - Blood Pressure/physiology
MH  - Endothelium, Vascular/*physiopathology
MH  - Female
MH  - HLA Antigens/*biosynthesis
MH  - Humans
MH  - Immunohistochemistry
MH  - Intercellular Adhesion Molecule-1/*biosynthesis
MH  - Male
MH  - Middle Aged
MH  - Myocarditis/*diagnosis/metabolism
MH  - Myocardium/*pathology
MH  - Severity of Illness Index
MH  - Statistics as Topic
MH  - Stroke Volume/physiology
MH  - Vasodilation/physiology
MH  - Ventricular Function, Left/physiology
EDAT- 2002/07/27 10:00
MHDA- 2002/08/31 10:01
CRDT- 2002/07/27 10:00
PHST- 2002/07/27 10:00 [pubmed]
PHST- 2002/08/31 10:01 [medline]
PHST- 2002/07/27 10:00 [entrez]
AID - S0735109702019903 [pii]
AID - 10.1016/s0735-1097(02)01990-3 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 2002 Aug 7;40(3):515-20. doi: 10.1016/s0735-1097(02)01990-3.