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In the modern world in which we exist, atherosclerotic cardiovascular disease has become the major cause of death in patients with diabetes mellitus.1 Increasingly evident in patients with and without diabetes is the fact that the development and progression of the atherosclerotic plaque represents an interaction between systemic and local factors.2,3 Multiple cell types and mediators have been implicated, and therapeutic strategies have and will continue to be targeted at modification of factors involved in this complex interaction.
Over the last several decades, clinical trials have demonstrated the importance of the reduction in low density lipoprotein (LDL) in favorably modifying the natural history of atherosclerotic cardiovascular disease (ASCVD), specifically coronary artery disease. Yet, despite the benefit of reduction in LDL cholesterol on primary4–6 or recurrent7–9 events, or on the rate of progression of disease as assessed by quantitative coronary angiography,10–12 this favorable modification alone has only resulted in modest to moderate modifications in measured outcomes. In the Familial Atherosclerosis Treatment Study (FATS),13 favorable changes in LDL cholesterol and the antiatherogenic HDL cholesterol accounted for 24% of the change in coronary stenosis. The large majority of the outcome effect was influenced by factors other than these classic predictors of ASCVD.
More recent investigation into lipid and lipoprotein risk factors for ASCVD involves small dense LDL.14,15 Small dense LDLs are believed to be relatively more atherogenic than other risk factors, because they have greater access to the subendothelial space where they are more likely to be oxidized and taken …
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