Reddy Cardiac Wellness, Cardiology, 3519 Town Center BLVD, Suite A, Sugar Land, TX, USA.
J Clin Lipidol. 2009 Aug;3(4):275-80. doi: 10.1016/j.jacl.2009.06.004. Epub 2009 Jul 4.
Lipoprotein-associated phospholipase A2 (Lp-PLA(2)) is a novel inflammatory biomarker that is associated with increased cardiovascular disease risk independent of and additive to traditional risk factors. Lp-PLA(2) activity is correlated with the degree of inflammation in the atherosclerotic plaque. In human blood, approximately 80% of Lp-PLA(2) is associated with low-density lipoproteins (LDL). Thus, it is hypothesized that changes in Lp-PLA(2) should imitate the changes in the LDL cholesterol.
In this present study, we examined the efficacy of lifestyle intervention and combination lipid-lowering therapy on reducing the Lp-PLA(2) levels and determined the relationship between changes in LDL-C and Lp-PLA(2).
This retrospective chart review study includes two hundred forty eight patients (58% men and 42% women) who completed the life style intervention in combination with pharmacologic therapy for an average period of 10.5 months. Life style modification included diet and exercise counseling. Combination therapy included omega 3 fish oil (2000mg/d), extended-release niacin (500-1000mg/d), ezetimibe (10mg/d), fenofibrate 160mg/d and colesevelam HCI (1850mg/d), as well as statins. The statins used were either simvastatin (20-40mg/d) or rosuvastatin (5-20mg/d). Sixty five percent (n=161) received low to medium doses of simvastatin, whereas 35% (n=87) received low to medium doses of rosuvastatin.
The study revealed a 32.5% reduction in mean Lp-PLA(2) values (baseline 181.1±41.5 vs 122.1±28.1 ng/mL after treatment; P<.001). The change observed in LDL-C was 41%, (baseline 126.2±43 vs 73.9±37.7mg/dL after treatment), which also was significant (P < .001). However, a Pearson correlation test analysis revealed only a weak positive association between changes in Lp-PLA(2) and LDL-C (r(2)=0.052, P < .001).
Lp-PLA(2) is reduced with the use of life style counseling and combination lipid lowering therapy. Results also revealed that changes in Lp-PLA(2) may be partially explained by the changes in LDL-C.
脂蛋白相关磷脂酶 A2（Lp-PLA2）是一种新型炎症生物标志物，它与心血管疾病风险的增加相关，并且独立于传统危险因素，还具有附加作用。Lp-PLA2 活性与动脉粥样硬化斑块中的炎症程度相关。在人体血液中，约 80%的 Lp-PLA2 与低密度脂蛋白（LDL）结合。因此，人们假设 Lp-PLA2 的变化应该模仿 LDL 胆固醇的变化。
本研究旨在检验生活方式干预和联合降脂治疗对降低 Lp-PLA2 水平的疗效，并确定 LDL-C 和 Lp-PLA2 变化之间的关系。
这是一项回顾性图表审查研究，共纳入 248 例患者（58%为男性，42%为女性），他们接受了生活方式干预联合药物治疗，平均治疗时间为 10.5 个月。生活方式改变包括饮食和运动咨询。联合治疗包括欧米伽 3 鱼油（2000mg/d）、缓释烟酸（500-1000mg/d）、依折麦布（10mg/d）、非诺贝特 160mg/d 和考来烯胺 HCI（1850mg/d），以及他汀类药物。使用的他汀类药物为辛伐他汀（20-40mg/d）或瑞舒伐他汀（5-20mg/d）。65%（n=161）接受低至中剂量辛伐他汀治疗，35%（n=87）接受低至中剂量瑞舒伐他汀治疗。
研究显示，Lp-PLA2 平均值降低了 32.5%（基线 181.1±41.5 与治疗后 122.1±28.1ng/mL；P<.001）。LDL-C 的变化为 41%（基线 126.2±43 与治疗后 73.9±37.7mg/dL；P<.001），也具有统计学意义。然而，Pearson 相关分析显示，Lp-PLA2 和 LDL-C 的变化之间仅存在微弱的正相关（r2=0.052，P<.001）。
生活方式咨询和联合降脂治疗可降低 Lp-PLA2。结果还表明，Lp-PLA2 的变化可能部分解释了 LDL-C 的变化。
