Author + information
- S0735109716348410-6f1a1202396fb116aa433179c0ed6f80Levent Cerit, MD∗ ()
- ↵∗Department of Cardiology, Near East University, Near East Hospital University Hospital, Near East Boulevard, Nicosia, Cyprus 07100
I read the article by Driver et al. (1), which was recently published in the Journal, with great interest. The investigators reported that to assess the initial risk of atherosclerotic cardiovascular disease in an untreated patient, fasting or nonfasting total cholesterol and high-density lipoprotein cholesterol (HDL-C) levels provide all that is required. Among those with a nonfasting non–HDL-C level ≥220 mg/dl, a familial cause of hyperlipidemia should be suspected and evaluated further (1).
Plasma levels of triglycerides were organized by synthesis and degradation of triglyceride-rich lipoproteins. Triglyceride-rich lipoproteins are degraded by lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL). Previous studies have shown that estrogen decreases LPL and H-TGL activities (2). Nii et al. (3) have reported that although 17-beta-estradiol does not affect plasma concentrations of triglycerides, oral conjugated equine estrogen increased plasma concentrations of triglycerides.
The stronger association is between triglycerides and the risk of ischemic heart disease (4). In addition, there is a stronger association between triglycerides and the risk of ischemic cardiovascular disease in women than there is in men (4).
With this knowledge, not only the use of estrogen but also the type of estrogen being used is important when evaluating the fasting or nonfasting lipid profile. The effect of estrogen on triglycerides should be considered especially in women when evaluating lipid profiles, and classification of patients should depend on their age, and pre- and post-menopausal states.
Please note: Dr. Cerit has reported that he has no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation