进行性冠状动脉疾病,脂蛋白(a)升高,需要脂质分离术

IF 4.3 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Susan Alideeb MD
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引用次数: 0

摘要

治疗领域心血管疾病/降低心血管疾病风险病例介绍这是一名 55 岁的女性患者,病史包括家族性高胆固醇血症、脂蛋白 (a) (Lp (a)) 升高、糖尿病、2020 年心肌梗死、多次经皮冠状动脉介入治疗冠状动脉疾病和 2022 年冠状动脉搭桥术后状况、2022 年冠状动脉近距离治疗再狭窄后状况、2023 年再狭窄。患者正在服用瑞舒伐他汀 40 毫克、依折麦布 10 毫克和埃沃洛单抗 140 毫克。尽管接受了良好的药物治疗,但患者的冠状动脉疾病仍在进展,因此患者被转诊接受脂质清除术(LA)治疗。尽管患者的低密度脂蛋白(LDL)只有 85 mg/dl,但却出现了进行性冠状动脉疾病(CAD)。脂蛋白(a)会增加患 CAD、中风、血栓形成和主动脉狭窄的风险,尤其是当脂蛋白(a)大于 125 nmol/L 时。脂蛋白(a)具有促炎症作用、促血栓形成作用和促动脉粥样硬化作用。其结构类似于组织纤溶酶原激活剂,会干扰溶栓的自然途径。目前,LA 是唯一适用于 CAD 和胆固醇升高情况下 Lp(a) 升高的治疗方法。2018 年胆固醇指南》指出 Lp(a) 是一种心血管增强风险特征。Evolocumab 和 Inclisiran 可使 Lp(a) 降低 30%,但不作为治疗手段。欧洲指南建议,Lp(a)水平升高达 60 mg/dl,且尽管风险因素已得到良好控制,但仍有进行性动脉粥样硬化性心血管疾病的患者使用 LA。LA可降低60%的脂蛋白(a)和70%的低密度脂蛋白。结论LA应被视为在最大限度降脂治疗后仍有进展性CAD的患者中脂蛋白(a)升高达125nnmol/l时的主要治疗选择,目的是使低密度脂蛋白(a)达到70 mg/dl,脂蛋白(a)降低60%,以减轻其他心血管风险结果。据德国血脂净化注册机构报告,治疗第一年的主要不良心血管事件风险降低了 70%。Lp(a) 治疗药物 Pelacarsen 和 Olpasiran 短期内不会上市。这些药物可能会改变进行 LA 治疗的必要性。这位患者患有进行性冠状动脉粥样硬化,接受过多种干预,脂蛋白(a)水平很高,但他从 LA 治疗中获益匪浅,脂蛋白(a)水平降低了 80% 以上。Lp(a) 每两周上升一次,因此需要每周治疗一次。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PROGRESSIVE CORONARY ARTERY DISEASE, ELEVATED LP (A) REQUIRING LIPID APHERESIS

Therapeutic Area

ASCVD /CVD Risk Reduction

Case Presentation

This is a 55-year-old female with a medical history of familial hypercholesterolemia, elevated lipoprotein (a) (Lp (a)), diabetes mellitus, myocardial infarction 2020, coronary artery disease with multiple percutaneous coronary intervention and status post coronary artery bypass surgery 2022, status post coronary brachytherapy for re-stenosis 2022, re-stenosis in 2023. The patient is on Rosuvastatin 40 mg, Ezetimibe 10mg, and Evolocumab 140 mg. Due to progressive coronary disease despite good medical therapy, the patient was referred for lipid apheresis (LA).

Background

This case demonstrates the accelerated effect of atherosclerosis mitigated by Lp(a). This patient developed progressive coronary artery disease (CAD), despite a low-density lipoprotein (LDL) of 85 mg/dl. Lp(a) is associated with increased risks of CAD, stroke, thrombosis, and aortic stenosis, particularly when greater than 125 nmol/L. Lp(a) has a pro-inflammatory effect, prothrombotic effect, and pro-atherosclerotic. Structurally similar to tissue plasminogen activator, which interferes with the natural pathways of thrombolysis. Currently, LA is the only treatment indicated for elevated Lp(a) in the setting of CAD and elevated cholesterol. The 2018 Cholesterol Guidelines state Lp(a) is a cardiovascular-enhancing risk feature. Evolocumab and Inclisiran can reduce Lp(a) up to 30 % but are not indicated as treatments. The European guidelines recommend LA for patients with elevated Lp(a) levels > 60 mg/dl, and progressive atherosclerotic cardiovascular disease despite risk factors well controlled. LA can lower Lp(a) by 60 % and LDL up to 70 %.

Conclusions

LA should be regarded as a principal therapeutic option with elevated Lp(a) >125nnmol/l in patients with progressive CAD despite maximal lipid-lowering therapy, aiming to achieve an LDL < 70 mg/dl and reduce Lp(a) > 60 % to mitigate other cardiovascular risk outcomes. A 70 % risk reduction in major adverse cardiovascular events in the first year of treatment was reported by the German Lipid Apheresis Registry. Lp(a) treatment options Pelacarsen and Olpasiran will not be available in the near future. These agents may change the need to do LA. This patient with progressive CAD, multiple interventions with very high Lp(a) benefitted from LA with greater than 80 % reduction in Lp(a) levels. Rise in Lp(a) bi-weekly, will require weekly treatments.
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来源期刊
American journal of preventive cardiology
American journal of preventive cardiology Cardiology and Cardiovascular Medicine
CiteScore
6.60
自引率
0.00%
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审稿时长
76 days
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