The synergistic mechanisms of oxidized phospholipids and lipoprotein-associated phospholipase A2 associated with Lp ( a ) in promoting atherosclerosis / 中华检验医学杂志

Lipoprotein ( a ) [ Lp ( a ) ] is considered a causal risk factor for the formation and development of atherosclerosis ( AS).High plasma levels of Lp ( a) is recognized as a predictor of coronary heart disease. However, the pathogenic mechanisms of Lp ( a ) are still unknown. Recent studies demonstrated that a key role in the proatherogenic effects of Lp ( a ) may be linked to its oxidized phospholipids ( OxPL) content.Lipoprotein-associated phospholipase A 2 ( Lp-PLA2 ) is another important factor in Lp( a) functionality.OxPL are hydrolyzed by Lp-PLA2 into lysophosphatidylcholine ( lyso-PC) and oxidized free fatty acid(OxFFA), which are important inflammatory factors on promoting the occurrence and development of AS.The present review article describes Lp-PLA2 hydrolyzing OxPL associated with Lp (a). The process induces inflammatory factors , which promote development of AS .OxPL and Lp-PLA2 can be used as new targets of cardiovascular diseases , which have clinical application value to predict potential cardiovascular diseases .

The correlation between the carotid atherosclerosis unstable plaque, lipoprotein (a) levels with acute cerebral infarction patients / 中国基层医药

Objective To explore the correlation between the carotid atherosclerosis unstable plaque lipoprotein(a) [ Lp(a)]levels with acute cerebral infarction patients.Methods 120 patients with acute cerebral infarction were selected as the research group,and at the same period,120 health cases were selected as the control group.The level of Lp(a) of the two groups was tested,and neck vascular color dopplar ultrasound examination was conducted.Results The incidence of atherosclerotic plaque in carotid artery and unstable plaques was 70.8％,51.7％,respectively,and significantly higher than that of the control group(25.8％,6- 7％ ) ( x2 =5.12,6.43,all P ＜0.05 ).The Lp(a) level of the research group[ (273.6 ± 221.7 )ag/L] was significantly higher than that of the control group[ ( 81.6 ± 64.9) mg/L ] ( t =6.53,P ＜ 0.05 ).Conclusion High level of LP(a) is the independent risk factor of cerebral infarction.The instability of carotid atherosclerotic plaques is the important cause of cerebral infarction.