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Published on: January 13, 2012
Carotid artery plaques and intima medial thickness in familial hypercholesteraemic patients on long-term statin
Sven Bos1, Martijne H C Duvekot1, Gert-Jan R Ten Kate2
1Department of Internal Medicine, Division Pharmacology, Vascular and Metabolic Diseases, Erasmus MC, Rotterdam, The Netherlands.
Insights
Long-term statin therapy in familial hypercholesterolemia (FH) patients normalized carotid atherosclerosis compared to healthy controls. Carotid ultrasound has limited value for monitoring these patients.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Familial hypercholesterolemia (FH) patients are at high risk for atherosclerotic cardiovascular disease (ASCVD).
- Statins are effective in reducing ASCVD risk, but some FH patients still develop the condition.
- Subclinical atherosclerosis assessment is crucial for risk stratification in FH.
Purpose of the Study:
- To compare subclinical atherosclerosis in long-term statin-treated FH patients and healthy controls.
- To evaluate carotid ultrasonography findings in relation to subclinical coronary atherosclerosis.
Main Methods:
- Carotid plaque presence and intima-media thickness (C-IMT) were assessed in 221 FH patients and 103 controls.
- Patients were on long-term statin treatment (10.0 ± 7.8 years).
- Coronary artery calcification was evaluated in a subgroup of FH patients.
Main Results:
- No significant difference in carotid plaque presence or C-IMT was observed between FH patients and controls.
- Coronary artery calcification correlated with carotid plaque presence (R=0.47; p=0.001) but not C-IMT (R=0.20; p=0.2).
Conclusions:
- Long-term statin treatment effectively reduces carotid atherosclerosis in FH patients to levels seen in healthy individuals.
- Carotid ultrasonography appears to have limited value in monitoring statin-treated FH patients.
- Carotid plaque presence may be a better indicator of subclinical atherosclerosis than C-IMT in this population.
Background And Aims:
Statins reduce subclinical atherosclerosis and premature atherosclerotic cardiovascular disease (ASCVD) in patients with familial hypercholesterolemia (FH). However, some FH patients still develop ASCVD despite statin therapy. We compared subclinical atherosclerosis assessed by carotid plaque presence and intima media thickness (C-IMT), in long-term statin-treated FH patients and healthy controls. Furthermore, we analysed whether carotid ultrasonography findings associated with subclinical coronary atherosclerosis.
Methods:
We assessed the presence of carotid plaques and C-IMT in 221 asymptomatic heterozygous FH patients (48% men; 46 ± 15 years) on long-term (10.0 ± 7.8 years) statin treatment and 103 controls (32% men, 47 ± 16 years).
Results:
The frequency of carotid plaques and C-IMT did not differ significantly between the FH patients and controls (69 (31%) versus 24 (23%), p = 0.1 and 0.58 ± 0.13 versus 0.58 ± 0.12 mm, p = 0.9, respectively). In a subgroup of 49 FH patients who underwent cardiac computed tomography, coronary artery calcification correlated with carotid plaque presence (R = 0.47; p = 0.001), but not with C-IMT (R = 0.20; p = 0.2).
Conclusions:
Carotid plaques and C-IMT did not differ between long-term statin-treated heterozygous FH patients and healthy controls. This shows that long-term statin treatment in these FH patients reduces carotid atherosclerosis to a degree of a healthy population. These findings strongly suggests that sonography of the carotid arteries during follow-up of statin-treated FH patients has limited value.
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