Abstract：Objective: To investigate the changes of serum LTB4 level and its correlation with susceptibility in acute coronary syndrome (ACS) patients; and to explore its potential clinical significance. Methods: Serum LTB4 level was measured by enzyme linked immunosorbent assay in 403 patients with ACS and 132 subjects with chest pain who were free from coronary heart disease (CHD) by coronarography(control group). Results: LTB4 level was significant higher in patients with ACS[(477.97/370.52 pg/ml)in acute myocardial infarction (AMI) patients and (352.52/255.48 pg/ml)in unstable angina pectoris (UAP) patients respectively] than in control group (200.57/236.65 pg/ml)(P<0.001), and with the higher level in AMI than in UAP(P<0.001). Serum LTB4 level was significantly positive correlated with smoking(P<0.05), unrelated with the sex, age, hypertention, diabetes and hyperlipidemia(P>0.05)in ACS patients. Conclusion: Serum LTB4 level was significant higher and was positively correlated with the smoking in patients with ACS.
［1］ Werz O,Steinhilber D. Therapeutic options for 5 lipoxygenase inhibitors[J]. Pharmacol Ther, 2006,112(3):701-718.［2］ Mehrabian M, Allayee H. 5-lipoxygenase and atherosclerosis[J]. Curr Opin Lipidol， 2003,14(5):447-457.［3］ Chen MS, Bhatt DL. Highlights of the 2002 update to 2000 American College of Cardiology/American Heart Association acute coronary syndrome guidelines[J]. Cardio Rev,2003,11(3):113-121.［4］ Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis[J]. Circulation, 2002, 105(9): 1135-1143.［5］ Mueller C, Buettner HJ, Hodgson JM, et al. Inflammation and long-termmortality after non-ST-elevation acute coronary syndrome treated with a very early invasive st rategy in 1042 consecutive patients[J]. Circulation, 2002, 105(12): 1412-1415.［6］ Back M. Inflammatory signaling through leukotriene receptors in atherosclerosis[J]. Curr Atheroscler Rep, 2008,10(3):244-251.［7］ Back M. Leukotriene signaling in atherosclerosis and ischemia[J]. Cardiovasc Drugs Ther, 2009, 23(1): 41-48.［8］ Hakonarson H. Role of FLAP and PDE4D in myocardial infarction and stroke: target discovery and future treatment options[J]. Curr Treat Options Cardiovasc Med, 2006,8(3) :183-192.［9］ Zhao L, Moos MP, Grbner R, et al.The 5-lipoxygenase pathway promotes pathogenesis of hyperlipidemia-dependent aortic aneurysm[J]. Nat Med, 2004, 10(9): 966-973.［10］ Ahluwalia N, Lin AY,Tager AM, et al. Inhibited aortic aneurysm formation in BLT1-deficient mice[J]. J Immunol, 2007, 179(1): 691-697.［11］ Back M,Bu DX, Branstrom R, et al. Leukotriene B4 signaling through NF-kappaB-dependent BLT1 receptors on vascular smooth muscle cells in atherosclerosis and intimal hyperplasia[J]. Proc Natl Acad Sci USA, 2005, 102 (48):17501-17506.［12］ 许莎莎，黄洁，江建军，等．基质金属蛋白酶诱导因子和白三烯B4在急性冠状动脉综合征中表达[J]．临床心血管病杂志，2011，27（3）：220-222．［13］ 吴超能，唐礼江，江建军，等．急性冠状动脉综合征患者血浆白三烯B4和基质金属蛋白酶-9的水平变化及意义[J]．临床心血管病杂志,2007，23（3）：167-169．
2012, Vol. 22 
