Background

Raised lipoprotein(a) [Lp(a)] is a cardiovascular risk factor common in patients with refractory angina. The apolipoprotein(a) component of Lp(a) exhibits structural homology with plasminogen and can enhance thrombosis and impair fibrinolysis.

Objectives

The objective of the study was to assess the effect of lipoprotein apheresis on markers of thrombosis and fibrinolysis in patients with high Lp(a).

Methods

In a prospective, single-blind, crossover trial, 20 patients with refractory angina and raised Lp(a) > 50 mg/dL were randomized to three months of weekly lipoprotein apheresis or sham. Blood taken before and after apheresis/sham was assessed using the Global Thrombosis Test, to assess time taken for in vitro thrombus formation (occlusion time) and endogenous fibrinolysis (lysis time), as well as von Willebrand Factor, fibrinogen, D-dimer, thrombin/anti-thrombin III complex, prothrombin fragments 1 + 2, and thrombin generation assays.

Results

Lp(a) was significantly reduced by apheresis (100.2 [interquartile range {IQR}, 69.6143.0] vs 24.8 [17.2,34.0] mg/dL, P = .0001) but not by sham (P = .0001 between treatment arms). Apheresis prolonged occlusion time (576 ± 116 s vs 723 ± 142 s, P < .0001) reflecting reduced platelet reactivity and reduced lysis time (1340 [1128, 1682] s vs 847 [685,1302] s, P = .0006) reflecting enhanced fibrinolysis, without corresponding changes with sham. Apheresis, but not sham, reduced von Willebrand Factor (149 [89.0, 164] vs 64.2 [48.5, 89.8] IU/dL, P = .0001), and fibrinogen (3.12 ± 0.68 vs 2.20 ± 0.53 g/L, P < .0001), and increased prothrombin fragments 1 + 2 (158.16 [128.77, 232.09] vs 795.12 [272.55, 1201.00] pmol/L, P = .0006). There was no change in D-dimer, thrombin/anti-thrombin III complex, or thrombin generation assay with apheresis or sham.

Conclusion

Lipoprotein apheresis reduces Lp(a) and improves some thrombotic and fibrinolytic parameters in patients with refractory angina.

中文翻译：

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脂蛋白单采对难治性心绞痛和脂蛋白升高的患者血栓形成参数的影响（a）：一项来自随机对照试验的结果。

背景

脂蛋白升高（a）[Lp（a）]是难治性心绞痛患者常见的心血管危险因素。Lp（a）的载脂蛋白（a）成分与纤溶酶原具有结构同源性，可增强血栓形成并损害纤维蛋白溶解。

目标

该研究的目的是评估脂蛋白单采对高Lp（a）患者血栓形成和纤溶指标的影响。

方法

在一项前瞻性，单盲，交叉试验中，将20例难治性心绞痛且Lp（a）升高> 50 mg / dL的患者随机分配至每周3个月一次脂蛋白单采或假手术。使用整体血栓形成测试评估单采血液/假手术前后的血液，以评估体外血栓形成所需的时间（阻塞时间）和内源性纤溶作用（裂解时间），以及血管性血友病因子，纤维蛋白原，D-二聚体，凝血酶/抗凝血酶III复合物，凝血酶原片段1 + 2和凝血酶生成测定。

结果

脂蛋白（a）是由显著单采（100.2 [四分位数间距{IQR}，69.6143.0]对24.8 [17.2,34.0]毫克/分升，减少的P  = 0.0001），但不被假（P  =治疗组之间0.0001 ）。剥脱延长了阻塞时间（576±116 s vs 723±142 s，P  <.0001），反映出血小板反应性降低和裂解时间缩短（1340 [1128，1682] s vs 847 [685,1302] s，P  = .0006）反映纤维蛋白溶解增强，假手术无相应变化。置换，但不假手术，降低了von Willebrand因子（149 [89.0，164] vs 64.2 [48.5，89.8] IU / dL，P  = .0001）和纤维蛋白原（3.12±0.68 vs 2.20±0.53 g / L，P <.0001）和增加的凝血酶原片段1 + 2（158.16 [128.77，232.09] vs 795.12 [272.55，1201.00] pmol / L，P  = .0006）。D-二聚体，凝血酶/抗凝血酶III复合物或单采或假单抗的凝血酶生成测定没有变化。

结论

脂蛋白单采降低难治性心绞痛患者的Lp（a）并改善一些血栓形成和纤溶参数。