| BackgroundAs the development of the society, the morbidity of Coronary Heart Disease hasincreased year by year due to the profound change of people’s diet and life style andthe intensified aged trendency of population. Epidemiological research revealed thatCHD has become one of the most deadly diseases of21th century including Cancerand Cerebrovascular Disease. Atherosclerosis is a pathological change that underliesseveral important cardiac-cerebral vascular diseases including Coronary HeartDisease, Myocardial Infarction and Peripheral Arterial Disease. AS mainly involveslarge and middle sized artery, especially in organs such as heart, brain and kidney.The basic pathology of AS contains lipid deposition in endarterium, fibrosis ofintima and formation of atheromatous plaque, resulting in sclerosis of aterial wall,stenosis of lumen and eventually a series of secondary ischemic change.The pathogenesis of AS is complicated and many mediators, including growthfactors and cytokines, are involved. The mechanism of AS is not well understood.Such has been demonstrated in the research that one of the key processes is oxidative modification of lipid, especially LDL. Oxidized LDL directly injuries endotheliumproducing a variety of cytokines which induce the adherence and migration ofmonocytes. As increasing monocytes adhere to endothelium, monocytes infiltrate theendothelium, differentiate into macrophages and can be then loaded with oxidizedLDL that is taken up by “scavenger receptors”. This process leads to the formationof foam cells, inducing nascent AS lesions. Under the further influence of cytokines,the fibrosis of the nascent lesions is accomplished and gives rise to the formation ofadvanced lesions.Platelet-activating factor is an endogenous synthesized phospholipid compoundwhich is proved to be1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine and consistsof a variety of molecules. PAF has various biological activities and is a potentinflammatory mediator, which shows its effect at very low concentrations（10-5~10-10mol/l）. PAF can be produced by a wide variety of isolated human cellsmainly via two pathways：Remodeling Pathway and De novo Pathway. PAF can beproduced by endothelial cells in response to oxidant injury and can serve as anintercellular messager. Recent researches have proved that PAF may get directlyinvolved in the initiate and development of AS and plays a significant role in theformation of CHD. There is, however, rare report about the expression of PAF indifferent types of CHD and the relationship between it and the Coronary GensiniScore.ObjectiveTo investigate the expression of the level of human plasma PAF in different typesof CHD and the correlation between PAF and coronary Gensini Score.Methods140subjects with suspected CHD were divided into groups including32normalhealthy control subjects and108patients with CHD which was further divided into subgroups including30patients with Acute Myocardial Infarction (AMI),41Unstable Angina Pectoris (UAP),37Stable Angina Pectoris(SAP). The plasma PAFconcentrations were determined by ELASA and the degree of coronary stenosis wasillustrated by Gensini Score, and then the concentrations were compared between thegroups and the relationship between the concentrations and Gensini Score wasanalyzed.Results1. Plasma concentrations of PAF were higher in patients with CHD (12.26±2.02)ng/ml than those in normal healthy control group (6.27±1.35)ng/ml (P <0.01).2. Plasma concentrations of PAF were higher in AMI group (13.31±1.36)ng/mland UAP group (13.01±1.48) ng/ml than in SAP group (10.61±1.97)ng/ml (P <0.01).3. Strong positive correlations existed between the plasma PAF concentrations andGensini Score(r=0.642,P＜0.01）, and differences are statistically significant.ConclusionHuman Plasma PAF concentrations were diverse in different types of CHD andwere correlated with coronary Gensini Score, which suggests that PAF may serve asan available index for CHD. |
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