Long-term effects of LDL apheresis on carotid arterial atherosclerosis in familial hypercholesterolaemic patients

Citation
N. Koga et al., Long-term effects of LDL apheresis on carotid arterial atherosclerosis in familial hypercholesterolaemic patients, J INTERN M, 246(1), 1999, pp. 35-43
Citations number
21
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
JOURNAL OF INTERNAL MEDICINE
ISSN journal
09546820 → ACNP
Volume
246
Issue
1
Year of publication
1999
Pages
35 - 43
Database
ISI
SICI code
0954-6820(199907)246:1<35:LEOLAO>2.0.ZU;2-U
Abstract
Objectives. To assess the long-term effect of LDL apheresis on carotid arte rial atherosclerosis in severe familial hypercholesterolaemic (FH) patients . Design. Changes in existing plaque, new plaque formation and annual progres sion rate of carotid early plaque were evaluated by B-mode ultrasonography, Subjects. LDL apheresis group: two homozygous FH and nine heterozygous FH p atients received a combination of LDL apheresis and cholesterol-lowering dr ug therapy for a mean of 7.8 years. Control group: 10 heterozygous FH patie nts were maintained by medication only for a mean of 5.5 years. Results. As a result of LDL apheresis treatment, LDL cholesterol levels red uced from 16.0 +/- 3.60 to 6.43 +/- 0.07 mmol L-1 in homozygous FH patients and from 11.5 +/- 2.46 to 4.32 +/- 1.2 mmol L-1 in heterozygous FH patient s. During the long-term treatment period. the existing plaque tended to pro gress and new plaque formation in carotid arteries was also observed in bot h groups, The annual progression rate of mean maximum intima-media thicknes s in the common carotid artery was a mean of -0.0023 +/- 0.0246 mm year(-1) in heterozygous FH patients in the LDL apheresis group, suggesting regress ion. This was significantly lower when compared with the control group, whi ch had a mean of 0.0251 +/- 0.0265 mm year(-1) Conclusion. The results suggest that the long-term treatment with combined LDL apheresis and drugs may delay the progression of the atherosclerotic pr ocess and prompt the stabilization of atheromatous plaque in severe FH pati ents.