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40 | Chapter 3 presence of carotid plaque between the young untreated FH patients and controls have diminished later in life, owing to statin treatment of the FH patients. It is possible that the small, not significant difference found in this study is mainly caused by those FH patients who did not start earlywith aggressive statin treatment. Therefore, we cannot be sure that our results are applicable to all treated FH patients. It is possible that the control subjects with carotid plaque also have increased coronary artery calcification, but these data were not available. Further research is needed to determine whether carotid plaque presence predicts future cardiovascular events in statin-treated FH-patients. We observed no statistical differences in C-IMT between long-treated FH patients and healthy controls. These results are in line with a previous report using 40 FH patients treated for more than 5 years with statins (9). With 0.58 mm, the mean C-IMT values we measured are similar to several other studies on healthy subjects with approximately the same age, indicating that our control group does not have increased C-IMT values (9,22,24,25). Moreover the mean C-IMT value of our long-term statin treated FH patients are much lower than in the ASAP study population (10), and even lower than in the ENHANCE study population (26), or than in FH patients that have been treated for at least 5 years with statins (12). Characteristics of the ENHANCE population were similar to our cohort of FH patients, except that the treated LDL-C cholesterol in our patients (3.3±1.0mmol/L) is lower than in statin+ ezetimibe treated armof the ENHANCE (3.7±1.4 mmol/L; p<0.01). C-IMT values of the ENHANCE study (0.67±0.16 mm) were higher than in our study (0.58±0.13 mm; p<0.01) which might be explained by the combination of higher on-treatment LDL-C values, different measuring systems, or possibly, a longer period of statin treatment. We previously reported that subclinical coronary artery disease, as determined by coronary CT angiography, was increased in asymptomatic FH patients compared with statin-treated (3±4 years), non-anginal chest pain patients (27). In another study in the same patients, no differences in C-IMT were found (28), which is in line with our findings. In the current study we could not compare coronary CT angiography results between the FH patients and controls as calcium scoring was not performed because of the undesirable radiation exposure in the healthy controls. In the present study, a subgroup of these FH patients (n=30) was included and 19 FH patients were added, who only received non-enhanced cardiac CT scans. In these patients coronary artery calcification was strongly correlated with carotid plaque presence, but not with C-IMT. The lack of association of C-IMT and coronary artery calcification was also previously shown in non-statin treated FH patients (29,30).