Effect of specific lipoprotein(a) apheresis on coronary atherosclerosis regression assessed by quantitative coronary angiography

Safarova, Maya; Ezhov, M.; Афанасьева, О. И.; Matchin, Yu. G.; Atanesyan, R V; Adamova, I. Yu.; Utkina, E.; Konovalov, G A; Pokrovsky, S.

doi:10.1016/j.atherosclerosissup.2012.10.015

Cited by 111 publications

(55 citation statements)

References 21 publications

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“…17,18 A recent small study investigated the effect of a specific Lp(a) apheresis in patients with CVD verified by angiography, an Lp(a) level above 50 mg/dL and LDL-cholesterol ≤2.5 mmol/L. 19 They used immunabsorption columns with sheep polyclonal monospecific antibodies directed against human apo(a), resulting in a 73% decrease of Lp(a) without other major changes in lipid profile. A quantitative coronary angiography revealed a significant improvement in the median percent diameter stenosis and the minimal lumen diameter of the coronary arteries during a 18 months treatment period in the Lp(a) apheresis group when compared with a parallel atorvastatin control group.…”

Section: February 11 2014mentioning

confidence: 99%

Lipoprotein(a)

Kronenberg

2014

Circulation

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When the first prospective studies on lipoprotein(a) [Lp(a)] were published in the early 1990s, the career of Lp(a) as a risk factor for cardiovascular disease (CVD) was almost stopped right at its beginning. A few of these prospective studies were negative 1 and resulted in a major discussion whether Lp(a) had its best times already behind it. However, numerous later studies and meta-analysis of the data strengthened the association between high Lp(a) concentrations and CVD.2 Finally, genetic research on Lp(a) became the basis for what revolutionized epidemiological research during the last decade in general. This is based on the observation that Lp(a) concentrations are largely determined by a copy number variation in the LPA gene, which results in an interindividually highly variable and large number of so-called kringle-IV repeats of the apolipoprotein(a) [apo(a)] protein. This polymorphism explains between 30% and 70% of the Lp(a) concentrations, which makes Lp(a) to the lipoprotein with the strongest genetic determination.3 Individuals with a low number of kringle-IV repeats (small isoform carriers) have on average markedly higher Lp(a) concentrations. 4 Because the number of kringle-IV repeats are subject of inheritance, it is already determined at the time of conception whether one inherits apo(a) isoforms associated with high or low Lp(a) concentrations. Consequently, those who inherit small isoforms are exposed life-long to high Lp(a) concentrations and are expected to have a high CVD risk. This was indeed the case when the first studies using this concept were published in the early 1990s. They demonstrated that individuals carrying small isoforms have indeed a high CVD risk.5 Studies using SNPs that tag a subfraction of the small apo(a) isoforms took the same line. 6 This concept using genetic variants that determine an important fraction of the risk factor under suspicion to demonstrate an association with the outcome of interest was later called Mendelian Randomization.7 It was a major step not only for Lp(a) research but for epidemiology in general because usually epidemiological studies can hardly prove causality. However, the Mendelian randomization concept can provide a very strong support of causality. With the help of this concept several risk factors have been reevaluated and some of them changed their status from a risk factor to a risk marker that is not necessarily involved in the causal chain of the disease. For Lp(a) it was even a starting point because all of a sudden it became an interesting object for intervention. Article see p 635In the past it was discussed controversially whether high Lp(a) concentrations are only a risk factor when also other well-known CVD risk factors are present in an individual. In this issue of Circulation, Khera et al 8 investigated whether Lp(a) is a significant determinant of residual CVD risk in the JUPITER trial that recruited individuals without a history of CVD at baseline, with low-density lipoprotein (LDL)-cholesterol <130 mg/dL and a high-sensitiv...

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Section: February 11 2014mentioning

confidence: 99%

Lipoprotein(a)

Kronenberg

2014

Circulation

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“…Safarova et al assessed the impact of specific Lp(a) apheresis versus statin therapy on coronary atherosclerosis regression in 30 stable CHD patients with high Lp(a) levels >500 mg/L [17]. Patients were allocated to receive weekly Lp(a) apheresis (n ¼ 15), or atorvastatin only (n ¼ 15).…”

Section: Existing Evidencementioning

confidence: 99%

The impact of lipoprotein apheresis in patients with refractory angina and raised lipoprotein(a): Objectives and methods of a randomised controlled trial

Khan

Pottle

Pennell

et al. 2015

Atherosclerosis Supplements

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“…In a study, published in 2013, with coronary angiography before the start of this specific Lp(a) apheresis and after 18 months, a positive effect of the extracorporeal therapy on coronary atherosclerosis could be shown [23].…”

Section: La Yesterdaymentioning

confidence: 99%

Lipoprotein Apheresis: Yesterday, Today, Tomorrow. Review

2018

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In a previous publication the first author described the history of research in atherosclerosis, of the introduction of lipid-lowering drugs and of lipoprotein apheresis (LA) into medical practice [1]. This current review focuses on recent tendencies and is based on the rich experience of all authors with LA at the Dresden Center for Lipoprotein Apheresis, where at present more than 130 patients are treated. We are the only center worldwide where 6 different LA methods are used. We published data showing the effectiveness of these methods and differences between them [2,3]. Lipid disorders as atherogenic risk factorsLipid disorders are often seen in a population and represent severe risk factor to develop atherosclerotic lesions [4]. The latter can lead to cardiovascular diseases (CVD) like myocardial infarction, peripheral arterial occlusive disease, occlusion of the carotids, stroke, atherosclerotic plaques at the aorta, stenosis of the aortic valve.Both genetic and life-style factors underlie these lipid disorders. When genetic factors dominate several family members are affected. Two lipoproteins play a major role: low-density lipoproteins (LDL) and Lipoprotein(a) (Lp(a)). АФЕРЕЗ ЛИПОПРОТЕИДОВ: ВЧЕРА, СЕГОДНЯ, ЗАВТРАJulius U., Tselmin S., Bornstein S. R.Первые попытки лечения семейной гомозиготной гиперхолестеринемии (ГХ) плазмаферезом предпринимались в 60-70-е годы. Впоследствии, с появле-нием более специфичного метода -афереза липопротеинов (АЛ), отпала необходимость в замещении плазмы чужеродным белком. Была продемон-стрирована решающая роль АЛ в продлении жизни этих больных, в то время как медикаментозная терапия показала в этих случаях значительно меньшую эффективность по сравнению с результатами её применения для лечения больных с другими типами ГХ. Тяжелые формы ГХ были признаны показаниями к применению АЛ у больных с сердечно-сосудистыми осложнениями. Повы-шенный уровень липопротеина(а) (Лп(а)) является международно признан-ным независимым атерогенным фактором риска. В связи с этим, экстракорпо-ральная терапия всё чаще проводится больным с повышенным Лп(а), страда-ющим такими тяжёлыми сердечно-сосудистыми осложнениями, как инфаркт миокарда или инсульт. В обзоре также обсуждается роль производимых в России колонок Лп(а) Липокак ® (ЗАО НПФ "ПОКАРД", Россия) для специфи-ческого снижения липопротеина(а) в общем спектре методов АЛ. Ещё одним методом лечения станет в будущем антисмысловой олигонуклеотид для подавления синтеза аполипопротеина(а). LIPOPROTEIN APHERESIS: YESTERDAY, TODAY, TOMORROWJulius U., Tselmin S., Bornstein S. R.First attempts to treat patients with homozygous familial hypercholesterolemia (HCH) were performed in the 60s and 70s using a total plasma exchange. Later on, more selective lipoprotein apheresis (LA) methods have been developed -the replacement with foreign proteins was no longer necessary. It could be demonstrated that LA is life-saving in these patients, lipid-lowering drugs were shown to be much less effective than in other HCH patients. A severe HCH became an accepted indi...

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Effect of specific lipoprotein(a) apheresis on coronary atherosclerosis regression assessed by quantitative coronary angiography

Cited by 111 publications

References 21 publications

Lipoprotein(a)

Lipoprotein(a)

The impact of lipoprotein apheresis in patients with refractory angina and raised lipoprotein(a): Objectives and methods of a randomised controlled trial

Lipoprotein Apheresis: Yesterday, Today, Tomorrow. Review

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