Abstract
IntroductionSeveral studies have suggested that Lp(a) could be a risk factor mainly in hypercholesterolemic patients. MethodsA total of 909 individuals were selected for this study. 307 were diagnosed of familiar hypercholesterolemia with a pathogenic mutation in LDLR or APOB genes (FH+), 291 of familiar combined hyperlipidemia (FCH) and 311 of familial hypercholesterolemia without a pathogenic mutation in LDLR nor APOB genes (FH-). Main risk factor were studied, included statin treatment. Plasma lipids, Lp(a), HbA1c and C-reactive protein. Intima-media thickness (IMT) of common and bulb carotid in both sides were measured in all subjects. ResultsLp(a) values (median, interquartile range) were 21.9mg/dL (9.24-50.5) in FH+, 22.4mg/dL (6.56-51.6) in FCH and 32.7 (14.6-71.5) in FH- (P<.001). Regression analysis including age, gender, HDL cholesterol, LDL cholesterol corrected for Lp(a), Lp(a), C-reactive protein, packs of cigarettes/day per year, systolic blood pressure and glucose as independent variables, demonstrate that Lp(a) was associated with carotid IMT in FH- subjects. Cardiovascular disease was more frequent in subjects with Lp(a) >50mg/dL (17.9%) than in subjects with Lp(a) <15mg/dL (9.6%), and between 15-50mg/dL (10.1%), and it was concentrated mostly in FH-group (6.7, 11.3, and 23.4% for the groups of Lp(a) <15mg/dL 15-50mg/dL, and >50mg/dL, respectively). ConclusionsOur results indicate that Lp(a) is associated with atherosclerosis burden especially in subjects with FH- and concentrations of Lp(a)>50mg/dL.
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