High lipoprotein(a) level promotes both coronary atherosclerosis and myocardial infarction: a path analysis using a large number of autopsy cases

High lipoprotein(a) level promotes both coronary atherosclerosis and myocardial infarction: a path analysis using a large number of autopsy cases
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DOI:
10.1136/hrt.2008.160879
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发表时间:
2009-12-15
期刊:
影响因子:
5.7
通讯作者:
Matsushita, S.
Matsushita, S.
中科院分区:
医学1区
文献类型:
--
作者:
Sawabe, M.;Tanaka, N.;Matsushita, S.

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目的:探讨高脂蛋白血症(Lp(a))是否促进冠状动脉粥样硬化、急性血栓形成导致心肌梗死(MI),或两者兼而有之。设计:回顾性图表回顾。环境:以社区为基础的老年综合医院。患者:1062例连续尸检病例(男性609例,女性453例)。死亡时的平均年龄为80岁。主要观察指标:半定量评价冠状动脉狭窄切片和心肌梗死病理定义。生前新鲜血清Lp(A)水平,通过乳胶增强浊度免疫分析法测定。结果:严重冠状动脉狭窄和病理性心肌梗死的发生率随Lp(a)水平的升高呈线性增加,无明显阈值。严重冠状动脉狭窄患者的优势比(95% CI) (200-299 mg/l为2.99 (1.70 ~ 5.28),bb0 ~ 300 mg/l为3.25(1.90 ~ 5.54))大于高血压(2.61(1.88 ~ 3.63))、糖尿病(2.09(1.41 ~ 3.11))和高胆固醇血症(2.05(1.31 ~ 3.21))。严重冠状动脉硬化发生心肌梗死的风险(6.28(4.33 ~ 9.11))明显高于高脂蛋白(a)、高血压和糖尿病。通径分析显示,Lp(A)水平对冠状动脉硬化和心肌梗死均有影响,通径系数分别为0.15和0.07(直接影响)。在严重冠状动脉硬化的病例中,Lp(a)仅影响心肌梗死(0.15)。结论:Lp(a)水平对冠状动脉硬化和心肌梗死有明显的影响,其中约一半的心肌梗死是通过冠状动脉硬化发生的。这一结果支持了Lp(a)在冠状动脉事件中的促血栓和可能的促炎症作用。
Objective: To investigate whether hyper-lipoproteinaemia(a) (Lp(a)) promotes coronary atherosclerosis, acute thrombosis resulting in myocardial infarction (MI), or both.Design: Retrospective chart review.Setting: A community-based general geriatric hospital.Patients: 1062 consecutive autopsy cases (609 men, 453 women). The mean age at the time of death was 80 years.Main outcome measures: A semiquantitative evaluation of the coronary stenosis on cut sections and pathological definition of MI. Lp(a) levels of fresh serum taken antemortem, measured by a latex-enhanced turbidimetric immunoassay.Results: The prevalence of severe coronary stenosis and pathological MI increased linearly with increasing Lp(a) levels with no apparent threshold. The odds ratios (95% CI) of hyper-Lp(a) (2.99 (1.70 to 5.28) for 200-299 mg/l and 3.25 (1.90 to 5.54) for >300 mg/l) for severe coronary stenosis were larger than those of hypertension (2.61 (1.88 to 3.63)), diabetes mellitus (2.09 (1.41 to 3.11)) and hypercholesterolaemia (2.05 (1.31 to 3.21)). The severe coronary sclerosis was much stronger risk of MI (6.28 (4.33 to 9.11)) than hyper-Lp(a), hypertension and diabetes mellitus. A path analysis showed that the Lp(a) levels affected both coronary sclerosis and MI, with path coefficients of 0.15 and 0.07 (direct effect), respectively. In cases with severe coronary sclerosis Lp(a) affected only MI (0.15).Conclusions: Lp(a) levels have distinct effects on coronary sclerosis and MI, with about half of the overall effect on MI being via coronary sclerosis. This result supports the prothrombotic and a probable proinflammatory role of Lp(a) in coronary events.