Abstract

BackgroundAtherogenic dyslipidemia (AD) is a common feature in persons with premature coronary heart disease. While several linkage studies have been carried out to dissect the genetic etiology of lipid levels, few have investigated the AD lipid triad comprising elevated serum triglyceride, small low density lipoprotein (LDL) particles, and reduced high density lipoprotein (HDL) cholesterol levels. Here we report the results of a whole-genome screen for AD using the Framingham Heart Study population.ResultsOur analyses provide some evidence for linkage to AD on chromosomes 1q31, 3q29, 10q26, 14p12, 14q13, 16q24, 18p11, and 19q13.ConclusionAD susceptibility is modulated by multiple genes in different chromosomes. Our study confirms results from other populations and suggests new areas of potential importance.

Highlights

  • Atherogenic dyslipidemia (AD) is a common feature in persons with premature coronary heart disease

  • 11 markers showed some evidence for linkage in parametric analysis, but no marker showed two-point LOD scores ≥ 2.0 or p < 0.001

  • From an original set of 90 families with at least one affected individual, 21 were informative. Due to this limited sample size, we carried out statistical analyses using four alternative approaches that take advantage of the different family structures that were available: affected/unaffected parametric LOD score analysis, affected relative pair nonparametric linkage analysis (NPL) analysis, affected sib-pair MLS analysis, and the sib-pair Haseman-Elston regression analysis

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Summary

Introduction

Atherogenic dyslipidemia (AD) is a common feature in persons with premature coronary heart disease. While several linkage studies have been carried out to dissect the genetic etiology of lipid levels, few have investigated the AD lipid triad comprising elevated serum triglyceride, small low density lipoprotein (LDL) particles, and reduced high density lipoprotein (HDL) cholesterol levels. Atherogenic dyslipidemia (AD) is characterized by three lipid abnormalities: elevated serum triglyceride, small low density lipoprotein (LDL) particles, and reduced high density lipoprotein (HDL) cholesterol levels [1]. This lipid triad occurs commonly in persons with premature coronary heart disease [2]. We carried out a whole-genome screen with the aim of identifying susceptibility genes for AD using the Framingham Heart Study population

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