TY - JOUR
T1 - Lipoprotein (a) levels are not associated with carotid plaques and carotid intima media thickness in statin-treated patients with familial hypercholesterolemia
AU - Bos, S.
AU - Duvekot, M.H.C.
AU - Touw-Blommesteijn, A.C.
AU - Verhoeven, A.J.M.
AU - Mulder, M.T.
AU - Watts, Gerald
AU - Sijbrands, E.J.G.
AU - Roeters Van Lennep, J.E.
PY - 2015
Y1 - 2015
N2 - © 2015 Elsevier Ireland Ltd. Background: Lipoprotein (a), also called Lp(a), is a cardiovascular disease (CVD) risk factor. Statins do not lower Lp(a), this may at least partly explain residual CVD risk in statin-treated patients with familial hypercholesterolemia (FH). We investigated the association of Lp(a) levels with atherosclerosis in these patients. Methods and results: We performed ultrasonography in 191 statin-treated FH patients (50% men; 48±15 years) to detect carotid plaques and determine carotid intima-media thickness (C-IMT).Patients with high versus low Lp(a) levels (≤0.3g/L) had similar plaque prevalence (36 and 31%, p=0.4) and C-IMT (0.59±0.12 and 0.59±0.13mm, p=0.8). Patients with and without plaques had similar Lp(a) levels (median 0.35 (IQR: 0.57) and 0.24 (0.64) g/L, respectively, p=0.4). Conclusions: The Lp(a) levels were not associated with atherosclerosis in the carotid arteries of statin-treated FH patients. This suggests that adequate statin treatment delays carotid atherosclerosis in FH independently of Lp(a) levels.
AB - © 2015 Elsevier Ireland Ltd. Background: Lipoprotein (a), also called Lp(a), is a cardiovascular disease (CVD) risk factor. Statins do not lower Lp(a), this may at least partly explain residual CVD risk in statin-treated patients with familial hypercholesterolemia (FH). We investigated the association of Lp(a) levels with atherosclerosis in these patients. Methods and results: We performed ultrasonography in 191 statin-treated FH patients (50% men; 48±15 years) to detect carotid plaques and determine carotid intima-media thickness (C-IMT).Patients with high versus low Lp(a) levels (≤0.3g/L) had similar plaque prevalence (36 and 31%, p=0.4) and C-IMT (0.59±0.12 and 0.59±0.13mm, p=0.8). Patients with and without plaques had similar Lp(a) levels (median 0.35 (IQR: 0.57) and 0.24 (0.64) g/L, respectively, p=0.4). Conclusions: The Lp(a) levels were not associated with atherosclerosis in the carotid arteries of statin-treated FH patients. This suggests that adequate statin treatment delays carotid atherosclerosis in FH independently of Lp(a) levels.
U2 - 10.1016/j.atherosclerosis.2015.07.024
DO - 10.1016/j.atherosclerosis.2015.07.024
M3 - Article
C2 - 26222903
SN - 0021-9150
VL - 242
SP - 226
EP - 229
JO - Atherosclerosis
JF - Atherosclerosis
IS - 1
ER -
