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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e133.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Consequences of Cholesteryl Ester Transfer Protein Inhibition in Patients With Familial Hypoalphalipoproteinemia

Radjesh J. Bisoendial; G. Kees Hovingh; Karim El Harchaoui; Johannes H.M. Levels; Sotirios Tsimikas; Kewei Pu; Aeilko E. Zwinderman; Jan Albert Kuivenhoven; John J.P. Kastelein; Erik S.G. Stroes

Department of Vascular Medicine (R.J.B., G.K.H., K.E.H., J.H.M.L., J.A.K., J.J.P.K., E.S.G.S) Academic Medical Center, Amsterdam, The Netherlands Department of Medicine (S.T.) University of California, San Diego Biometrics (K.P.), Akros Pharma Inc Princeton, New Jersey Department of Clinical Epidemiology and Biostatistics (A.E.Z.) Academic Medical Center Amsterdam, The Netherlands

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

A large proportion of clinical events cannot be prevented during statin therapy, which calls for novel drug targets to further improve cardiovascular outcome. In particular, HDL-increasing strategies hold great promise. The impact of decreased HDL-C on cardiovascular disease (CVD)-related morbidity and mortality has been sharply delineated in individuals affected by familial hypoalphalipoproteinemia (FHA).¹ HDL exerts multiple antiatherogenic actions beyond its role in reverse cholesterol transport, comprising antiinflammatory, antioxidative, and direct vascular effects.² Whereas current strategies to raise HDL-C are limited, novel CETP-inhibitors are capable of mediating significant HDL-C elevation.^3,4 Therefore, we evaluated the effects of CETP inhibition on lipid metabolism and markers of oxidation in subjects with FHA.

Subjects were recruited from a Dutch population-based study to identify genes that control HDL-C levels,¹ meeting the following criteria: (1) plasma HDL-C level below 10^th percentile for age and sex; (2) absence of secondary lipid disorders; and (3) high likelihood of inherited low HDL (defined as HDL-C below 10^th percentile in at least one first-degree family member). Nineteen FHA patients (13 men and 6 women; mean±SD age: 42.9±13.9 years), all free of overt macrovascular disease, were enrolled in the study. In 9 of these subjects the underlying defect was defined: heterozygosity for an apolipoprotein A-I (L178P) mutation,¹ whereas in the remainder this genetic defect was excluded. The study protocol was approved by the Institutional Review Board at the Academic Medical Center, University Hospital of Amsterdam. All subjects gave written informed consent. This study was designed as a single-center, randomized-sequence, . . . [Full Text of this Article]

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