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6 93 | Lp(a) is not associated with carotid plaques and C-IMT in FH and we did not find significant differences in the baseline characteristics between these groups (Table 1). Plaque prevalence was similar in both groups: 33 (36%) vs 31 (31%) (p=0.4). There were no differences in C-IMT between the high Lp(a) group and the low Lp(a) group; 0.59±0.13 mm and 0.59±0.13mm (p=0.8). Qualitatively similar results were obtained when restricting the analyses to the mutation confirmed FH patients, or when other cut-off values of Lp(a) (0.5g/L and 1.0g/L, data not shown) were used. In the regression analyses, there were no statistically significant associations between Lp(a) levels and plaque presence (p=0.5) and C-IMT (p=0.4). These results did not change in the sub-analysis in those with a treated LDL-C above 4mmol/L. In addition, no other variable except age was associated with carotid plaques (p= <0.001), and C-IMT (p= <0.001). Finally, Lp(a) levels did not differ between patients with and without plaques present in the carotids: (0.349 (0.571) and 0.243 (0.641)) g/L, p = 0.4). Discussion In our study, Lp(a) levels are not associated with presence of carotid plaque and C-IMT in statin-treated FH patients. This is unexpected since Lp(a) is a residual risk factor in treated FH patients[10, 11], and Lp(a) levels are associated with C-IMT [17, 18]. As our FH patients received aggressive long-term statin therapy, theymay have effectively delayed carotid atherosclerosis and vessel wall thickening, such that the association with Lp(a) levels is no longer evident. In a previous study in a subgroup of our FH patients, Lp(a) is also not associated with subclinical coronary atherosclerosis, depicted by coronary calcium scoring [23]. An explanation for the lack of association between Lp(a) and carotid plaques is the relative young age of our FH patients. The prevalence of carotid plaques in our patients with mean age 48 years is 33.5%. Recent studies has shown a 43% prevalence in a Swedish population with a mean age 57 years [1], and a 42% prevalence in 61±10 year old healthy Americanmulti-ethnic population [16]. In adverse plaques were increased in a group of young, newly diagnosed and mostly untreated, FH patients [24]. This suggest that our study group has a low prevalence of carotid plaques which might be due to the aggressive statin treatment. The very low C-IMT did not associate with Lp(a). In healthy young men with mean age 29 years, a C-IMT of 0.54 mm is observed [25]. Additionally, the healthy controls of the ARIC study with a mean age of 56 years have a C-IMT of 0.60 mm [17]. Therefore, the