METHODS:We conducted a multicenter, observational study in Italian patients with hyperLp(a) andpremature CAD with (n518)/without (n516) LA in which blood samples were analyzed for Lp(a)parameter and CLSQ10. Genetic profiling of LPAQ11was conducted in patient receiving LA.RESULTS:Mean macrophage CLC of the pre-LA serum was significantly higher than that of nor-molipidemic controls (19.760.9mg/mg vs 16.0160.98mg/mg of protein, respectively). After LA,serum macrophage CLC was markedly lower relative to preapheresis (16.160.8mg/mg protein;P5.003) and comparable with CLC of the normolipidemic serum. LA did not significantly affectaverage apo(a) isoform size distribution. No anthropometric or lipid parameters studied were relatedto serum CLC, but there was a relationship between CLC and the Lp(a) plasma concentration(P5.035). DNA analysis revealed a range of common genetic variants. Two rare, new variantswere identified: LPA exon 21, c.3268C.G, p.Pro1090Arg, and rs41259144 p.Arg990Gln, c.2969G.ACONCLUSIONS:LA reduces serum Lp(a) and also reduces macrophage CLC. Novel genetic vari-ants of the LPA gene were identified, and geographic variations were noted. The complexity of thesepolymorphisms means that genetic assessment is not a predictor of CAD risk in hyperLp(a)
Lipoprotien(a) concentration, genetic variants, apo(a) isoform size, and cellular cholesterol efflux in patients with elevated Lp(a) and coronary heart disease submitted or not to lipoprotein apheresis: An Italian case-control multicenter study on Lp(a) / Stefanutti, C.; Pisciotta, L.; Favari, E.; Di Giacomo, S.; Vacondio, F.; Zenti, M. G.; Morozzi, C.; Berretti, D.; Mesce, D.; Vitale, M.; Pasta, A.; Ronca, A.; Garuti, A.; Manfredini, M.; Anglés-Cano, E.; Marcovina, S. M.; Watts, G. F.. - In: JOURNAL OF CLINICAL LIPIDOLOGY. - ISSN 1933-2874. - (2020). [10.1016/j.jacl.2020.05.002]
Lipoprotien(a) concentration, genetic variants, apo(a) isoform size, and cellular cholesterol efflux in patients with elevated Lp(a) and coronary heart disease submitted or not to lipoprotein apheresis: An Italian case-control multicenter study on Lp(a)
Pisciotta, L.;Favari, E.;Vacondio, F.;Pasta, A.;Ronca, A.;Manfredini, M.;
2020-01-01
Abstract
METHODS:We conducted a multicenter, observational study in Italian patients with hyperLp(a) andpremature CAD with (n518)/without (n516) LA in which blood samples were analyzed for Lp(a)parameter and CLSQ10. Genetic profiling of LPAQ11was conducted in patient receiving LA.RESULTS:Mean macrophage CLC of the pre-LA serum was significantly higher than that of nor-molipidemic controls (19.760.9mg/mg vs 16.0160.98mg/mg of protein, respectively). After LA,serum macrophage CLC was markedly lower relative to preapheresis (16.160.8mg/mg protein;P5.003) and comparable with CLC of the normolipidemic serum. LA did not significantly affectaverage apo(a) isoform size distribution. No anthropometric or lipid parameters studied were relatedto serum CLC, but there was a relationship between CLC and the Lp(a) plasma concentration(P5.035). DNA analysis revealed a range of common genetic variants. Two rare, new variantswere identified: LPA exon 21, c.3268C.G, p.Pro1090Arg, and rs41259144 p.Arg990Gln, c.2969G.ACONCLUSIONS:LA reduces serum Lp(a) and also reduces macrophage CLC. Novel genetic vari-ants of the LPA gene were identified, and geographic variations were noted. The complexity of thesepolymorphisms means that genetic assessment is not a predictor of CAD risk in hyperLp(a)| File | Dimensione | Formato | |
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