血小板活化因子乙酰水解酶活性可独立于全身炎症和其他危险因素提示血管造影阳性冠状动脉疾病:Ludwigshafen风险和心血管健康状况研究

来源 :世界核心医学期刊文摘(心脏病学分册) | 被引量 : 0次 | 上传用户:shui__hen
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Background- Platelet- activating factor acetylhydrolase(PAFAH), also denoted as lipoprotein- associated phospholipase A2, is a lipoprotein- bound enzyme that is possibly involved in inflammation and atherosclerosis. This study investigates the relationship of PAF- AH activity to angiographic coronary artery disease(CAD), the use of cardiovascular drugs, and other established risk factors. Methods and Results- PAF- AH activity, lipoproteins, sensitive C- reactive protein(sCRP), fibrinogen, serum amyloid A, and white blood cell count were determined in 2454 subjects with angiographically confirmed CAD and in 694 control subjects. PAF- AH activity was highly correlated with LDL cholesterol(r=0.517), apolipoprotein B(r=0.644), and non- HDL cholesterol(r=0.648) but not with sCRP or fibrinogen. PAF- AH activity was lower in women than in men and was affected by the intake of lipid- lowering drugs(- 12% ;P< 0.001), aspirin(- 6% ; P< 0.001), β - blockers(- 6% ; P< 0.001), and digitalis(+ 7% ; P< 0.001). Unlike sCRP, fibrinogen, and serum amyloid A, PAF- AH activity was not elevated in unstable angina, non- ST- elevation myocardial infarction, or ST- elevation myocardial infarction. When nonusers of lipid- lowering drugs were examined, PAF- AH activity was associated with the severity of CAD and the number of coronary vessels with significant stenoses. In individuals not taking lipid- lowering drugs and after adjustment for use of aspirin, β - blocker, and digitalis, the odds ratio for CAD associated with increasing PAF- AH activity was 1.39(95% CI 1.26 to 1.54, P< 0.001), a finding that was robust against further adjustments. Conclusions- PAF- AH activity is not an indicator of the systemic inflammation that accompanies acute coronary syndromes. PAF- AH activity is affected by a number of cardiovascular drugs; however, after such medication use was accounted for, PAF- AH activity was associated with angiographic CAD, complementary to sCRP and independently of established risk factors such as LDL cholesterol.
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