Acute impact of apheresis on oxidized phospholipids in patients with familial hypercholesterolemia

Arai, Kiyohito; Orsoni, Alexina; Mallat, Ziad; Tedgui, Alain; Witztum, Joseph L.; Bruckert, Éric; Tselepis, Alexandros D.; Chapman, M. John; Tsimikas, Sotirios

doi:10.1194/jlr.p027235

Cited by 57 publications

(35 citation statements)

References 39 publications

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“…Lp(a) is a carrier of proinflammatory oxidized phospholipids. Their substantial reduction by different apheresis techniques may constitute an additional beneficial mechanism of apheresis beyond lowering apoBcontaining lipoproteins [11]. The two lipoprotein apheresis techniques LF and DSA are safe and efficient therapeutic options for lipoprotein elimination and prevention of cardiovascular disease [12].…”

Section: Discussionmentioning

confidence: 99%

Long-term therapeutic efficacy of lipoprotein apheresis on circulating oxidative stress parameters – A comparison of two different apheresis techniques

Kopprasch

Bornstein

Bergmann

et al. 2015

Atherosclerosis Supplements

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Section: Discussionmentioning

confidence: 99%

Long-term therapeutic efficacy of lipoprotein apheresis on circulating oxidative stress parameters – A comparison of two different apheresis techniques

Kopprasch

Bornstein

Bergmann

et al. 2015

Atherosclerosis Supplements

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“…19 Association of oxidized phospholipids with small apo(a) isoforms may be a key determinant of cardiovascular risk. 20 High Lp(a) levels and small apo(a) sizes are associated with endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Lipoprotein Apheresis for Lipoprotein(a)-Associated Cardiovascular Disease

Roeseler

Julius

Heigl

et al. 2016

ATVB

174

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Objective— Lipoprotein(a)-hyperlipoproteinemia (Lp(a)-HLP) along with progressive cardiovascular disease has been approved as indication for regular lipoprotein apheresis (LA) in Germany since 2008. We aimed to study the long-term preventive effect of LA and to assess hypothetical clinical correlations of apolipoprotein(a) (apo(a)) by analyzing genotypes and phenotypes. Approach and Results— This prospective observational multicenter study included 170 patients with Lp(a)-HLP and progressive cardiovascular disease (48.9 years median age at diagnosis) despite other cardiovascular risk factors, including low-density lipoprotein cholesterol had maximally been treated (mean baseline low-density lipoprotein cholesterol: measured, 2.56 mmol/L [98.9 mg/dL] and corrected, 1.72 mmol/L [66.3 mg/dL]). Patients were prospectively investigated during a 5-year period about annual incidence rates of cardiovascular events. In addition, apo(a) isoforms and polymorphisms at the apo(a) gene ( LPA ) were characterized. One hundred fifty-four patients (90.6%) completed 5 years of follow-up. Mean Lp(a) concentration before commencing regular LA was 108.1 mg/dL. This was reduced by a single LA treatment by 68.1% on average. Significant decline of the mean annual cardiovascular event rate was observed from 0.58±0.53 2 years before regular LA to 0.11±0.15 thereafter ( P <0.0001); 95.3% of patients expressed at least 1 small apo(a) isoform. Small apo(a) isoform (35.2%) carrying phenotypes were not tagged by single-nucleotide polymorphisms rs10455872 or rs3798220. Conclusions— Results of 5 years of prospective follow-up confirm that LA has a lasting effect on prevention of cardiovascular events in patients with Lp(a)-HLP. Patients clinically selected by progressive cardiovascular disease were characterized by a highly frequent expression of small apo(a) isoforms. Only Lp(a) concentration seemed to comprehensively reflect Lp(a)-associated cardiovascular risk, however.

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“…ELISAs can then be used to measure total apo(a) and Lp(a) with apo(a)/apo(a) antibodies and apo(a)/ apoB antibodies, as described [56,57,70]. These assays can be complemented by western blots stained for apoB-100 and apo(a) and density gradient ultracentrifugation with fine-density cuts of aliquots in the LDL and Lp(a) range, and subsequent direct measurement chemical measurement of lipoproteins or using a variety of ELISA techniques to measure apoB, apo(a), and Lp(a) on each density fraction, as described [54,72]. The clinical significance of lipid-poor apo(a) in the setting of ultra-low LDL-C levels is not known and these techniques may allow characterization of these phenomena in clinical populations.…”

Section: Proposals For Research Studies Of Current Clinical Trials Wimentioning

confidence: 99%

‘LDL-C’ = LDL-C + Lp(a)-C

Yeang

Witztum

Tsimikas

2015

Current Opinion in Lipidology

Self Cite

127

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As the new era of ultralow LDL-C levels ensues, it is imperative to understand the contribution of Lp(a)-C to measured LDL-C and the consequences of achieving ultralow or potentially absent LDL-C in the setting of elevated Lp(a) levels and possibly free apo(a). We review this concept and suggest avenues of research, including analyses of existing datasets in current clinical trials and new research studies, to understand its pathophysiological and clinical significance.

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Acute impact of apheresis on oxidized phospholipids in patients with familial hypercholesterolemia

Cited by 57 publications

References 39 publications

Long-term therapeutic efficacy of lipoprotein apheresis on circulating oxidative stress parameters – A comparison of two different apheresis techniques

Long-term therapeutic efficacy of lipoprotein apheresis on circulating oxidative stress parameters – A comparison of two different apheresis techniques

Lipoprotein Apheresis for Lipoprotein(a)-Associated Cardiovascular Disease

‘LDL-C’ = LDL-C + Lp(a)-C

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