(Circulation. 1999;99:2852-2854.)
© 1999 American Heart Association, Inc.
Editorial |
From the Atherosclerosis Research Unit, Division of Cardiology, University of Southern California School of Medicine, Los Angeles, Calif.
Correspondence to Howard N. Hodis, MD, Associate Professor of Medicine and Preventive Medicine, Director, Atherosclerosis Research Unit, Division of Cardiology, University of Southern California School of Medicine, 2250 Alcazar St, CSC 132, Los Angeles, CA 90033.
Key Words: Editorials atherosclerosis lipoproteins risk factors
More than 3 decades of clinical research have suggested a relationship between triglycerides and coronary heart disease.1 However, because of the complexity of what is actually measured by a plasma triglyceride determination, establishing a firm relationship between triglycerides and coronary heart disease has been difficult. Triglycerides are carried in virtually all plasma lipoproteins and present a different risk profile in both the fasting and postprandial states, making triglyceride-rich lipoproteins highly heterogenous. This heterogeneity is a major contributing factor to the complexity of the relationship between triglycerides and coronary heart disease.
Accumulating evidence indicates that specific triglyceride-rich lipoprotein remnants of differing size and composition, such as VLDL, IDL, lipoprotein Bcontaining particles (LP-B:C, LP-B:C:E, and LP-A-II:B:C:D:E), and markers of triglyceride-rich lipoprotein metabolism such as apolipoprotein C-III (apoC-III), are more related to progression of atherosclerosis than triglycerides per se.2
In this issue of Circulation, Kugiyama et al3 present further evidence for the relationship between coronary heart disease and triglyceride-rich lipoproteins, demonstrating in patients with coronary artery disease that remnant lipoprotein levels in the fasting state predict future clinical coronary events independently of other risk factors. This is an important observation because it is consistent with a previous report that showed that calculated IDL plus estimated remnant VLDL as a measure of triglyceride-rich lipoprotein remnants was significantly correlated with the progression of coronary artery disease and clinical coronary events.4
The assertion by Kugiyama et al3 that fasting remnant
lipoproteins may reflect postprandial remnant lipoproteins is
consistent with the long circulatory residence time of
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