Differential mononuclear cell activity and endothelial inflammation in coronary artery disease and cardiac syndrome X.
BACKGROUND
Circulating mononuclear cells could be activated with endothelial inflammation in patients with coronary artery disease (CAD). In some patients with normal coronary angiograms, myocardial ischemia could also present with coronary microvascular dysfunction (cardiac syndrome X). This study was undertaken to investigate whether mononuclear cell activation and endothelial inflammation can present in syndrome X patients.


METHODS
We evaluated the biochemical parameters, circulating soluble adhesion molecules, circulating superoxide free radicals, and mononuclear cell activity in 32 patients with syndrome X, 34 with angiographically documented CAD, and 17 age- and gender-matched healthy control subjects.


RESULTS
Compared to that in control subjects, plasma high-density lipoprotein was reduced (P<0.001) and insulin to glucose ratio increased (P=0.02) in CAD patients. Circulating level of soluble intracellular adhesion molecule-1 was significantly higher in both syndrome X and CAD patients than in control subjects (P<0.01), whereas the levels of soluble vascular cell adhesion molecule (P=0.02) and von Willebrand factor (P=0.01) were increased in CAD patients only. The peak (P<0.001) and total counts of superoxide free radicals in whole blood (P<0.001) was significantly higher in syndrome X patients than in the other two groups. However, phorbol-12-myristate-13-acetate-induced superoxide free radical generation of mononuclear cells was increased in CAD (10.5+/-4.6%, P=0.01) but not in syndrome X patients (8.7+/-2.0%) as compared with control subjects (7.7+/-0.5%).


CONCLUSIONS
The results indicated that the activity of mononuclear cells was increased with significant endothelial inflammation and injury in CAD patients. In syndrome X patients, though circulating superoxide free radicals were increased, there was minimal endothelial inflammation without mononuclear cell activation. The relatively preserved lipid and metabolic profiles might contribute to less vascular inflammation in syndrome X patients.
Department of Pathology, Taipei Veterans General Hospital, 201 Shih-Pai Road Section 2, Taipei, Taiwan 11217, ROC.
Chih-Pei
CP
Lin
Wen-Tsai
WT
Lin
Hsin-Bang
HB
Leu
Tao-Cheng
TC
Wu
Jaw-Wen
JW
Chen
D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000097:blood; D016009:Chi-Square Distribution; D003327:Coronary Disease / Q000097:blood*; D016207:Cytokines / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005609:Free Radicals / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008297:Male; D017566:Microvascular Angina / Q000097:blood*; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D018384:Oxidative Stress; D012044:Regression Analysis
D015415:Biomarkers; D015815:Cell Adhesion Molecules; D016207:Cytokines; D005609:Free Radicals; D009566:Nitrates; D009573:Nitrites