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    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 12 ( 2003-06-27), p. 1359-1366
    Abstract: This study investigated whether the myocardium is involved in the acute inflammatory reaction associated with bursts of unstable angina (UA). We looked for the presence of activated DR + inflammatory cells and the expression patterns, localization, and immunostaining identification of genes for cytokines (IL-1β, TNF-α, IL-6, and IFN-γ), MCP-1, and iNOS in the left ventricle biopsies from 2-vessel disease anginal patients, 24 with UA and 12 with stable angina (SA), who underwent coronary bypass surgery. Biopsy specimens from 6 patients with mitral stenosis who underwent valve replacement were examined as control hearts (CHs). Plasma levels of IL-2 soluble receptor (sIL-2R) were measured as a marker of systemic immune reaction. In CHs, DR + cells were undetectable, and cytokine and iNOS mRNA expression were negligible. UA patients had higher sIL-2R levels than SA patients ( P 〈 0.01), and their biopsy specimens showed both numerous DR + cells identified as lymphocytes, macrophages, endothelial cells, and elevated expression levels of cytokine and iNOS genes (from 2.4- to 6.1-fold vs SA; P 〈 0.01). Cytokine and iNOS genes and proteins were localized in endothelial cells without involvement of myocytes. IL-1β and MCP-1 mRNAs were nearly undetectable. No significant differences were found in the number of DR + cells, levels of cytokine, and iNOS genes between potentially ischemic and nonischemic left ventricle areas. In SA specimens, DR + cells were very rare and only mRNAs for TNF-α and iNOS genes were overexpressed versus CHs. These results indicated that an acute immunomediated inflammatory reaction, essentially involving coronary microvessels, is demonstrable in UA patients.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1467838-X
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