Abstract

BackgroundLow-density lipoprotein (LDL) cholesterol lowering is a primary goal in clinical management of patients with cardiovascular disease, but traditional cholesterol levels may not accurately reflect the true atherogenicity of plasma lipid profiles. The size and concentration of lipoprotein particles, which transport cholesterol and triglycerides, may provide additional information for accurately assessing cardiovascular risk. This study evaluated changes in plasma lipoprotein profiles determined by nuclear magnetic resonance (NMR) spectroscopy in patients participating in a prospective, nonrandomized lifestyle modification program designed to reverse or stabilize progression of coronary artery disease (CAD) to improve our understanding of lipoprotein management in cardiac patients.ResultsThe lifestyle intervention was effective in producing significant changes in lipoprotein subclasses that contribute to CAD risk. There was a clear beneficial effect on the total number of LDL particles (-8.3%, p < 0.05 compared to matched controls), small dense LDL particles (-9.5%, p < 0.05), and LDL particle size (+0.8%; p < 0.05). Likewise, participants showed significant improvement in traditional CAD risk factors such as body mass index (-9.9%, p < 0.01 compared to controls), total cholesterol (-5.5%, p < 0.05), physical fitness (+37.2%, p < 0.01), and future risk for CAD (-7.9%, p < 0.01). Men and women responded differently to the program for all clinically-relevant variables, with men deriving greater benefit in terms of lipoprotein atherogenicity. Plasma lipid and lipoprotein responses to the lifestyle change program were not confounded by lipid-lowering medications.ConclusionIn at risk patients motivated to participate, an intensive lifestyle change program can effectively alter traditional CAD risk factors and plasma lipoprotein subclasses and may reduce risk for cardiovascular events. Improvements in lipoprotein subclasses are more evident in men compared to women.

Highlights

  • Low-density lipoprotein (LDL) cholesterol lowering is a primary goal in clinical management of patients with cardiovascular disease, but traditional cholesterol levels may not accurately reflect the true atherogenicity of plasma lipid profiles

  • Participants excluded from the analysis due to non-matching were older (64.6 ± 10.8 compared to 60.3 ± 8.0; p < 0.05) and had larger high-density lipoprotein (HDL) particles (8.8 ± 0.4 versus 8.6 ± 0.3; p < 0.05) and higher HDL-cholesterol (49.6 ± 11.1 versus 43.7 ± 13.1; p < 0.01) than participants included in the study

  • Effects of lifestyle changes on lipoproteins The lifestyle intervention led to significant changes in nuclear magnetic resonance (NMR)-defined lipoprotein subclasses, in particular, clinically important LDL variables that contribute to coronary artery disease (CAD) risk (Figure 1)

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Summary

Introduction

Low-density lipoprotein (LDL) cholesterol lowering is a primary goal in clinical management of patients with cardiovascular disease, but traditional cholesterol levels may not accurately reflect the true atherogenicity of plasma lipid profiles. Traditional cholesterol levels, may not accurately reflect the true atherogenicity of plasma lipid profiles because patients with similar cholesterol levels may have differences in the number and size of lipoprotein particles that transport cholesterol and triglycerides and may differ in terms of CAD risk. More recent studies using nuclear magnetic resonance (NMR) spectroscopy, which exploits spectral differences between lipoprotein subspecies to directly quantify particle size and concentration, have shown that small LDL particles and a greater number of LDL particles are associated with CAD development and progression in the general population and in patients with coronary disease [7,8,9,10]. Because lipoprotein characteristics may be important for assessing cardiovascular risk [11], it is important to understand how lipoproteins respond during cardiovascular treatment and prevention programs to identify interventions that favorably modify atherogenic lipid profiles

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