May Heidi T, Horne Benjamin D, Anderson Jeffrey L, Wolfert Robert L, Muhlestein Joseph B, Renlund Dale G, Clarke Jessica L, Kolek Matthew J, Bair Tami L, Pearson Robert R, Sudhir Krishnankutty, Carlquist John F
Cardiovascular Department, LDS Hospital, Salt Lake City, UT 84143, USA.
Am Heart J. 2006 Nov;152(5):997-1003. doi: 10.1016/j.ahj.2006.01.011.
Whereas C-reactive protein (CRP) is a nonspecific marker of coronary artery disease (CAD) and cardiovascular (CV) events, Lp-PLA2 may be a nonvariable inflammatory biomarker. We evaluated the independent association of lipoprotein-associated phospholipase A2 (Lp-PLA2) to angiographic CAD and CV events adjusting for standard factors, lipids, and CRP.
Lipoprotein-associated phospholipase A2 (PLAC test, diaDexus, Inc, San Francisco, CA) and CRP were measured from samples donated by consecutive consenting patients (N = 1493) enrolled in the registry of the Intermountain Heart Collaborative Study. All patients underwent coronary angiography (1996-1998) for CAD determination and were followed for 6.7 +/- 0.5 years (range 5.7-7.9 years) for CV events (death [including all-cause, CAD, and non-CAD CV death], myocardial infarction, and cerebrovascular accident).
Lipoprotein-associated phospholipase A2 weakly correlated with lipids (low-density lipoprotein: r = 0.22, P < .001; high-density lipoprotein: r = -0.13, P < .001), but not CRP (r = 0.03, P = .26). Increasing quartile (Q) of Lp-PLA2 predicted greater the presence of CAD (vs Q1) for Q2 (adjusted odds ratio [OR] 1.15, 95% CI 0.78-1.71, P = .48), for Q3 (OR 1.53, 95% CI 1.02-2.31, P = .042), and for Q4 (OR 2.44, 95% CI 1.58-3.79, P < .001), although CRP was also predictive (vs Q1, Q2: OR 1.47, P = .057; Q3: OR 1.93, P = .002; Q4: OR 3.43, P < .001). In Cox regression, Lp-PLA2 predicted CAD death (vs Q1; Q2: adjusted hazard ratio [HR] 1.27, 95% CI 0.58-2.78, P = .55; Q3: HR 2.18, 95% CI 1.04-4.57, P = .04; Q4: HR 1.73, 95% CI 0.84-3.61, P = .14).
Lipoprotein-associated phospholipase A2 was confirmed to predict the presence of CAD, even among patients undergoing coronary angiography. Uniquely, Lp-PLA2 predicted the risk of CAD death, but not all-cause death, myocardial infarction, or cerebrovascular accident.
C反应蛋白（CRP）是冠状动脉疾病（CAD）和心血管（CV）事件的非特异性标志物，而脂蛋白相关磷脂酶A2（Lp-PLA2）可能是一种不变的炎症生物标志物。我们评估了脂蛋白相关磷脂酶A2（Lp-PLA2）与血管造影CAD及CV事件的独立关联，并对标准因素、血脂和CRP进行了校正。
从山间心脏协作研究登记处连续同意参与的患者（N = 1493）捐赠的样本中测量脂蛋白相关磷脂酶A2（PLAC检测，diaDexus公司，加利福尼亚州旧金山）和CRP。所有患者均接受冠状动脉造影（1996 - 1998年）以确定CAD，并随访6.7±0.5年（范围5.7 - 7.9年）以观察CV事件（死亡[包括全因、CAD和非CAD CV死亡]、心肌梗死和脑血管意外）。
脂蛋白相关磷脂酶A2与血脂轻度相关（低密度脂蛋白：r = 0.22，P <.001；高密度脂蛋白：r = -0.13，P <.001），但与CRP无关（r = 0.03，P =.26）。Lp-PLA2四分位数（Q）增加预示CAD存在的可能性增大（与Q1相比），Q2时（校正优势比[OR] 1.15，95% CI 0.78 - 1.71，P =.48），Q3时（OR 1.53，95% CI 1.02 - 2.31，P =.042），Q4时（OR 2.44，95% CI 1.58 - 3.79，P <.001），尽管CRP也具有预测性（与Q1、Q2相比：OR 1.47，P =.057；Q3：OR 1.93，P =.002；Q4：OR 3.43，P <.001）。在Cox回归分析中，Lp-PLA2可预测CAD死亡（与Q1相比；Q2：校正风险比[HR] 1.27，95% CI 0.58 - 2.78，P =.55；Q3：HR 2.18，95% CI 1.04 - 4.57，P =.04；Q4：HR 1.73，95% CI 0.84 - 3.61，P =.14）。
脂蛋白相关磷脂酶A2被证实可预测CAD的存在，即使在接受冠状动脉造影的患者中也是如此。独特的是，Lp-PLA2可预测CAD死亡风险，但不能预测全因死亡、心肌梗死或脑血管意外。
