Lipoprotein apheresis for lipoprotein(a)-associated cardiovascular disease

• Verfasst von: Röseler, Eberhard [VerfasserIn]
• Verfasst von: März, Winfried [VerfasserIn]
• Titel: Lipoprotein apheresis for lipoprotein(a)-associated cardiovascular disease
• Titelzusatz: prospective 5 years of follow-up and apolipoprotein(a) characterization
• Verf.angabe: Roeseler Eberhard, Julius Ulrich, Heigl Franz, Spitthoever Ralf, Heutling Dennis, Breitenberger Paul, Leebmann Josef, Lehmacher Walter, Kamstrup Pia R., Nordestgaard Børge G., Maerz Winfried, Noureen Asma, Schmidt Konrad, Kronenberg Florian, Heibges Andreas, Klingel Reinhard, and for the Pro(a)LiFe-Study Group, Volker Schettler, Thomas Benzing, Hildegard Christ, Sabine Wehner, Ines Schulz-Merkel, Ralf Kuehn, Albrecht Wagner, Wilfried Dschietzig, Claudia Ernst, Michael Koziolek, Johannes Bunia, Peter Kulzer, Klaus-Dieter Kraenzle, Markus Toelle, Gerhard Riechers, Christine Kuehnel, Tobias Marsen, Christina Saehn, Jens Ringel, Harald Messner, Andreas Oehring, Carsten Schuerfeld, Michael Wintergalen, Volker Schettler, Falko Neumann, Harald Kaul, Martin Haesner, Juergen Passfall, Andrea Benschneider, Stefan Heidenreich, Winfried März, Ruediger Klaes, Priska Binner, Hans Dieplinger, Gertraud Erhart, Cordula Fassbender, and Hildegard Christ
• E-Jahr: 2016
• Jahr: September 2016
• Umfang: 9 S.
• Fussnoten: Gesehen am 12.12.2019 ; Originally published14 Jul 2016
• Titel Quelle: Enthalten in: Arteriosclerosis, thrombosis, and vascular biology
• Ort Quelle: Philadelphia, Pa. : Lippincott, Williams & Wilkins, 1981
• Jahr Quelle: 2016
• Band/Heft Quelle: 36(2016), 9, Seite 2019-2027
• ISSN Quelle: 1524-4636
• ISSN Quelle: 2330-9180
• ISSN Quelle: 2330-9199
• DOI: doi:10.1161/ATVBAHA.116.307983
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1685419445

Abstract

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.