The Relationship Between The Levels Of Plasma Thrombomodulin、E-selectin And Cardiac Syndrome X

Background and purpose In1967, Likoff etal.[1] reported one case of patients with exertional angina symptoms、the exercise challenge test positive and normal coronary angiography, Kemp named this syndrome as cardiac syndrome X.The CSX is defined as typical symptoms of exertional angina, ECG exercise test positive, coronary angiography revealed no significant coronary vascular occlusion or stenosis, except epicardial coronary spasm, valvular heart disease, congenital heart disease, hypertensive heart disease, pulmonary heart disease, myocarditis, various types of cardiomyopathy, left ventricular hypertrophy, diabetes and other metabolic and endocrine diseases. The chest pain symptoms of CSX is due to myocardial ischemia that caused by a small resistance coronary vascular dysfunction, also known as microvascular angina.Recently, with the development and popularization of Coronary angiography, the detection rate of CSX is increasing continuously,patients with coronary angiography due to angina,CSX accounted for15%to20%. Compared with the normal population,the patients of CSX were more likely to occur the acute myocardial infarction, arrhythmia, stroke,even sudden death, serious cardiovascular and cerebrovascular diseases, but the exact mechanism that how the CSX lead to serious cardiovascular and cerebrovascular disease, is not yet clear. Although the diagnosis rate of CSX is improved than before, many clinicians have not yet payed enough attention to the CSX, inadequated understanding of the coronary microcirculation and can not combine recurrent chest pain with the CSX, which thereby affect the patient’s condition adversely.Although many domestic and external scholars study the pathogenesis of CSX from endothelial dysfunction, decreased coronary flow reserve capacity, inflammation, hematological factors, estrogen deficiency, insulin resistance and other aspects, so far, it not yet form a unified doctrine to explain the etiology mechanism of CSX. Endothelial dysfunction is an important part in the incidence of multiple cardiovascular diseases and is related to angina pectoris,myocardial infarction, and various types of coronary heart disease.The role of Endothelial dysfunction in particular atherosclerosis has been confirmed by most scholars. The traditional view is that CSX result from cardiac insufficiency caused by coronary microvascular endothelial dysfunction, domestic and external scholars research the idea by plasma of vWF, ET-1and NO, hs-CRP and other factors,but few studies research the correlationship between CSX and the levels of plasma TM and Es.The thrombomodulin is a multi-segment transmembrane glycoprotein, distributed on the surface of endothelial cells, plays an important role in clear thrombin、activative the anticoagulant protein C、promote fibrinolysis, regulate the thrombosis and dissolved.The levels of plasma TM is increasing in the diseases of endothelial cell injury such as diabetes, acute respiratory distress syndrome, the heart and peripheral vascular occlusive diseases, glomerulonephritis, disseminated intravascular coagulation.Blann et al. believed TM is the gold standard of endothelial injury. E-selectin also known as endothelial-leukocyte adhesion molecule-1, belonging to the selectin family, that mediated neutrophils, eosinophils and monocyte adhesion on vascular endothelial.It expressed on activated endothelial cell surface, is a sign of endothelial cell damage. The purpose of this project is to study the correlationship between CSX and plasma TM, Es levels,and investigate the role of coronary microvascular endothelial dysfunction in the CSX process.Method Select forty patients with CSX in our hospital from Cctober2011to April2012, inclusion criteria:①Typical exertional angina;②Objective evidence of myocardial ischemia:resting electrocardiogram displays the myocardial ischemic or exercise challenge test positive (ST segment depression=0.1mv, lasted time=2min), radionuclide myocardial perfusion imaging displays myocardial ischemia;③normal coronary angiography;④left ventricular function is normal;⑤except epicardial coronary spasm, valvular heart disease, congenital heart disease, hypertensive heart disease, pulmonary heart disease, myocarditis, various types of cardiomyopathy, left ventricular hypertrophy, diabetes and other metabolic and endocrine diseases. The control group consisted with forty healthy subjects from the hospital examination center over the same period, who are no typical angina,ECG is normal, and no other organic diseases. Both groups have no significant differences in age, gender, hypertension, smoking, drinking, BMI, liver function, kidney function, blood lipids, blood glucose(P>0.05). Collected morning fasting and resting venous blood5mL, placed it in a biochemical tube, next put it into a low-speed refigerated centrifuge to separate plasma at3000/Per-minute for10minutes. The plasma samples were stored in freezer refrigerator at-80℃until the specimen collection is completed. Use the enzyme-linked immunosorbent assay method to test plasma TM, Es levels. The SPSS13.0for windows statistical software was used for statistical analysis, P<0.05was considered statistically significant.Result1. CSX and control groups have no significant differences in age, gender, history of hypertension, smoking, drinking, liver and kidney function, blood lipid, blood glucose,BMI.(P>0.05).2. Plasma TM and Es level of CSX patients were significantly higher than the control group[(7.69±1.47) ug/1VS (5.53±1.55) ug/1,(3.45±0.98) ng/ml VS (2.58±0.94)ng/ml, P=0.000].3-The Plasma TM and Es level of CSX patients was positively correlated (r=1.41, P=0.000).4. TM and Es are risk factors that affect CSX(OR,=1.69, P,=0.04, OR2=2.42, P2=0.03)Conclusion1. Compared with the control group, plasma TM level in CSX patients was higher, and plasma Es level was also significantly higher.2. The Plasma TM and Es level of CSX patients was positively correlated, TM and Es are risk factors of CSX.3. The coronary microvascular endothelial dysfunction plays an important role in the pathophysiological process of CSX.