Comparison And Study Of Inflammatory Cytokynes And Coronary Lesions In Patients With Unstable Angina

Background: Growing evidence has shown that unstable angina(UA)was an important event of acute coronary syndromes(ACS), which wascaused by plaque disruption with superimposed thrombosis.Atherosclerosis vas a chronic inflammatory intimal disease.Inflamatory outburst lay in local and system played a pivotal rolein plaque rupture and ACS. Interleukin-lbeta(IL-1β) and tumornecrosis factor-alpha(TNF- α ) were two important proinflammatorycytokines, which played important roles in the initiation andprogression of atherosclerosis. C-reactive protein(CRP), as a serummaker of inflammation, has been demonstrated to be a reliable makerof prognosis of acute coronary events, and to reflect localinflammation. Angiographic morphology of coronary lesions and levelsof serum makers of inflammation were all associated with the stabilityof plaque.Objective: To observe the serum levels of CRP. IL-1β and TNF-a in patients with UA, and to examine the angiographic morphology ofcoronary lesions, and to compare the changes of the serum levels ofCRP. IL-1β and TNF- α in different angiographic morphology of coronarylesions, as well as to explore the role of inflammation in patientswith UA.Methods: Serum levels of CRP. IL-1β and TNF-αa were determinedin 30 patients with UA(UA group)and 35 patients with stable angina(SA group) by immunoturbidometry and radio-immuneassay, and data werecompared with 37 controls. Coronary andiography was performed in allpatients with UA and SA, and the severity of coronary stenoses wasevaluated by a quantitative method.Results: ① Serum levels of CRP, IL-1β and TNF- a weresignificantly higher in patients with UA than those in patients withSA (P<0. 05) and controls (P<0. 01 ), but no difference between the lattertwo groups (P>0. 05);②Type Ⅱ lesions were more frequently found inpatients with UA than those with SA (66. 67% vs 20%, P<0. 01);③Severcoronary stenoses occurred more cormon in patients with SA than thosewith UA(P<0. 05);④Patients with type Ⅱ lesions had significantlyhigher serum 1eve1s than those with other type lesions(P<0. 05), butno difference among different stenoses grades and numbers of lesions.Conlusions: The results demonstrated that there were activationof inflammatory cells and inflanunation in patients with UA, whichmight play an important role in the disruption and thrombosis of plaqueand the pathogenesis of UA.