Abstract title
Are high levels of Lp(a) associated with familial hypercholesterolemia?
Co-authors
L. Schreier , V. Zago , L. Cacciagiú , M. Bursztyn , V. Bañares , G. López , G. Berg , P. Corral .
Universidad de Buenos Aires, Departamento de Bioquímica Clínica-Laboratorio de Lípidos y
Aterosclerosis, Ciudad Autonoma de Buenos Aires, Argentina.
Universidad de Buenos Aires, Departamento de Bioquímica Clínica-Laboratorio de Lípidos y
Aterosclerosis, Ciudad Autónoma de Buenos Aires, Argentina.
Centro Nacional de Genética Médica-ANLIS- Dr. Carlos Malbrán, Departamento de Genética
Experimental, Ciudad Autónoma de Buenos Aires, Argentina.
Universidad FASTA, Facultad de Medicina-Departamento de Investigación, Mar del Plata, Argentina.
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Abstract text
Background and Aims:
Lipoprotein(a) [Lp(a)] is a pro-atherogenic lipoprotein, whose concentration is genetically
determined. Familial Hypercholesterolemia (FH)-characterized by high LDL-C levels from early ageis
associated with premature atherosclerotic cardiovascular events (CVD). Although Lp(a) contains
LDL in its structure, is controversial if patients with FH diagnosis have elevated levels of Lp(a). Aim:
To analyze Lp(a) levels in patients with clinical and/or genetic diagnosis of FH.
Methods:
140 patients from the FH Detection Program in Argentina, were classified following the Dutch Lipid
Clinic Network (DLCN) score, and Lp(a) was measured by immunoturbidimetric assay. Traditional FH
genes were assessed by NGS in 85 patients. Non-parametric tests and multiple group analysis by
Kruskal Wallis and U-Mann Whitney were applied. Patients with clinical and/or genetic diagnosis of
FH.
Results
No differences in Lp(a) were observed when patients were classified according to DLCN score:
definite>8, n=45: median (range) 32.2(2.0-465.0)nmol/L; Probable 6-8, n=56: 38.9(1.3-427.0);
Possible 4-5, n=27: 43.0(3.1-311.0), Unlikely≤3, n=12: 119.3(4.9-297.0), p=0.257. When the
population was subdivided according to Lp(a) tertiles, no differences were observed in LDL-C
concentration, corrected by hypolipidemic treatment p=0.166. There were also no differences in
Lp(a) of 31 out of 85 patients genetically studied that presented variations in FH associated genes:
32.1(3.8-229.0), compared with the rest of 54 with negative genetic results: 35.3(3.5-297.0),
p=0.277.
Conclusions:
This cohort of hypercholesterolemic patients have shown an independence between Lp(a) and LDLClevels.
Lp(a) did not show association with clinical or genetic FH diagnosis. However, the
conjunction of both elevated Lp(a) and LDL-C would aggravates the prognosis an severity of CVD

04 - ARE HIGH LEVELS OF LP(A) ASSOCIATED WITH FAMILIAL HYPERCHOLESTEROLEMIA?