Am Fam Physician. 2008 Jun 1;77(11):1504-1505.
Original Article: Management of Hypertriglyceridemia
Issue: May 1, 2007
Available at: http://www.aafp.org/afp/20070501/1365.html
to the editor: The article on hypertriglyceridemia by Drs. Oh and Lanier nicely summarizes our current understanding of hypertriglyceridemia and its management. However, there is no mention of the impact of postprandial hypertriglyceridemia on cardiovascular risk, especially in patients with type 2 diabetes. Although fasting triglyceride levels are routinely measured in clinical practice, studies indicate that postprandial hypertriglyceridemia may be more closely related to atherosclerosis.1–3 Results from the Physicians' Health study suggest that nonfasting or postprandial triglyceride levels strongly predict risk of myocardial infarctions.2 Post-prandial levels of chylomicron remnants have been shown to strongly correlate with the rate of progression of coronary lesions.4 Postprandial hypertriglyceridemia also results in endothelial dysfunction through oxidative stress, and this effect is abrogated by antioxidants.5 Negative effects on coagulation activation and inflammation have also been demonstrated.6 Therefore, it is important not to lose sight of this postprandial phenomenon, because most of the day is spent in the postprandial state and studies now implicate it as a strong predictor of cardiovascular events.
1. Groot PH, van Stiphout WA, Krauss XH, et al. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arterioscler Thromb. 1991;11(3):653–662.
2. Stampfer MJ, Krauss RM, Ma J, et al. A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction. JAMA. 1996;276(11):882–888.
3. Teno S, Uto Y, Nagashima H, et al. Association of post-prandial hypertriglyceridemia and carotid intima–media thickness in patients with type 2 diabetes. Diabetes Care. 2000;23(9):1401–1406.
4. Karpe F, Steiner G, Uffelman K, Olivecrona T, Hamsten A. Postprandial lipoproteins and progression of coronary atherosclerosis. Atherosclerosis. 1994;106(1):83–97.
5. Anderson RA, Evans ML, Ellis GR, et al. The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes. Atherosclerosis. 2001;154(2):475–483.
6. Silveira A, Karpe F, Johnsson H, Bauer KA, Hamsten A. In vivo demonstration in humans that large postprandial triglyceride-rich lipoproteins activate coagulation factor VII through the intrinsic coagulation pathway. Arterioscler Thromb Vasc Biol. 1996;16(11):1333–1339.
in reply: I appreciate the letter from Dr. Kapoor and agree that the body of literature is growing showing an increased cardiac risk for hypertriglyceridemia in any form—fasting or postprandial. Nonfasting triglyceride elevations have been associated with increased risk of coronary events in a recent cohort study.1 Despite the association, we need large scale, randomized trials to determine if reducing elevated triglyceride levels decreases overall mortality and cardiovascular events. Folic acid and hormone therapy for the prevention of cardiovascular disease are just two examples of overgeneralizing from positive cohort studies before negative randomized controlled studies were performed. Until then, we recommend that clinicians continue to follow the National Cholesterol Education Program guidelines—first work on low-density lipoprotein cholesterol goal, then work on non–high-density lipoprotein cholesterol as a secondary goal in overall lipid management.2
1. Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298(3):299–308.
2. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): final report. NIH publication no.: 02–5215. Bethesda, Md.: National Heart, Lung, and Blood Institute, 2002.
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