Abstract
Background: It has been suggested that an oxidative mechanism is involved with the impaired endothelium‐dependent vasodilatation that occurs after a high‐fat meal.
Hypothesis: The study was undertaken to evaluate the effect of a single oral dose of vitamin C (2 g) on postprandially impaired endothelium‐dependent vasodilatation in patients with coronary heart disease (CHD).
Methods: This study included 74 patients with CHD and 50 subjects without CHD with risk factors. The two groups were divided into two subgroups that did or did not receive 2 g of vitamin C (CHD/VitC and CHD/control, n = 37; non‐CHD/VitC and non‐CHD/control, n = 25) after a high‐fat meal (800 calories, 50 g fat). Serum levels of triglyceride, total cholesterol, low‐density lipoprotein cholesterol, and high‐density lipoprotein cholesterol in the fasting state and at 2, 4, 5, and 7 h after the high‐fat meal were measured. Endothelial function was assessed in the brachial artery by high‐resolution ultrasound at baseline and at 4 h postprandially.
Results: The postprandial serum triglyceride concentration increased significantly at 2‐5 h after the high‐fat meal in all groups. The fasting flow‐mediated dilatation (FMD) (p < 0.02) and nitroglycerin‐induced dilatation (NID) (p < 0.05) of patients with CHD were impaired compared with those of non‐CHD subjects. Postprandial FMD was significantly aggravated in the non‐CHD/control group (p<0.01) and the CHD/ control group (p < 0.001), but the postprandial FMD in patients and subjects taking vitamin C showed no significant change, although the CHD/VitC group had a mild tendency toward improvement (p = 0.064) and non‐CHD/VitC group had a mild tendency toward aggravation (p = 0.852). The change of NID after a high‐fat meal did not reach statistical significance in the four groups. The decrement of postprandial FMD correlated positively with the increment of 2‐h serum triglyceride concentration in the patients without vitamin C (n = 62, r = 0.545, p < 0.001).
Conclusions: The postprandial state after a high‐fat meal is critical in atherogenesis, as it induces endothelial dysfunction through an oxidative stress mechanism. Vitamin C treatment has a promising benefit for patients with CHD.
Keywords: coronary heart disease, high‐fat meal, endothelial dysfunction, oxidative stress
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References
- 1. Zhang YL, You K, Fang Q, Chen BS, Liu CY, Chen W: Postprandial abnormal metabolism of serum triglyceride as an independent risk factor of coronary heart disease. Chin J Cardiol 1998; 26:89–93 [Google Scholar]
- 2. Vogel RA, Corretti MC, Plotnick GD: Effect of a single high‐fat meal on endothelial function in healthy subjects. Am J Cardiol 1997; 79:350–354 [DOI] [PubMed] [Google Scholar]
- 3. Kugiyama K, Motoyama T, Doi H, Kawano H, Hirai N, Soejima H, Miyao Y, Takazoe K, Moriyama Y, Mizuno Y, Tsunoda R, Ogawa H, Sakamoto T, Sugiyama S, Yasue H: Improvement of endothelial vasomotor dysfunction by treatment with alpha‐tocopherol in patients with high remnant lipoproteins levels. J Am Coll Cardiol 1999; 33:1512–1518 [DOI] [PubMed] [Google Scholar]
- 4. Vita JA, Keaney JF Jr, Raby KE, Morrow JD, Freedman JE, Lynch S, Koulouris SN, Hamkin BR, Frei B: Low plasma ascorbic acid independently predicts the presence of an unstable coronary syndrome. J Am Coll Cardiol 1998; 31:980–986 [DOI] [PubMed] [Google Scholar]
- 5. Chambers JC, McGregor A, Jean‐Marie J, Obeid OA, Kooner JS: Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia: An effect reversible with vitamin C therapy. Circulation 1999; 99:1156–1160 [DOI] [PubMed] [Google Scholar]
- 6. Gokce N, Keaney JF Jr, Frei B, Holbrook M, Olesiak M, Zachariah BJ, Leeuwenbargh C, Heineche JW, Vita JA: Long‐term ascorbic acid administration reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation 1999; 99:3234–3240 [DOI] [PubMed] [Google Scholar]
- 7. Plotnick GD, Corretti MC, Vogel RA: Effect of antioxidant vitamins on the transient impairment of endothelium‐dependent brachial artery vasoactivity following a single high‐fat meal. J Am Med Assoc 1997; 278:1682–1686 [PubMed] [Google Scholar]
- 8. Zhao SP, Li XP, Zhou XC, Gao M, Lu SK: Non‐invasive detection of endothelial dysfunction in patients with essential hypertension. Int J Cardiol 1997; 61:165–169 [DOI] [PubMed] [Google Scholar]
- 9. Zhang XY, Zhao SP, Li XP, Gao M, Zhou XC: Endothelium‐dependent and ‐independent function are impaired in patients with coronary heart disease. Atherosclerosis 2000; 149:19–24 [DOI] [PubMed] [Google Scholar]
- 10. Lundman P, Eriksson M, Schenck‐Gustafsson K, Karpe F, Tomn‐vall P: Transient triglyceridemia decreases vascular reactivity in young, healthy men without risk factors for coronary heart disease. Circulation 1997; 96:3266–3268 [DOI] [PubMed] [Google Scholar]
- 11. Doi H, Kugiyama K, Ohgushi M, Sugiyama S, Matsumura T, Ohta Y, Nakano T, Nakajima K, Yasue H: Remnants of chylomicron and very low density lipoprotein impair endothelium‐dependent vasorelaxation. Atherosclerosis 1998; 137:341–349 [DOI] [PubMed] [Google Scholar]
- 12. Grieve DJ, Avella MA, Elliott J, Botham KM: The influence of chylomicron remnants on endothelial cell function in the isolated perfused rat aorta. Atherosclerosis 1998; 139:273–281 [DOI] [PubMed] [Google Scholar]
- 13. Hiramatsu K: Increased superoxide production by mononuclear cells of patients with hypertriglyceridaemia and diabetes. Diabetes 1988; 37:832–837 [DOI] [PubMed] [Google Scholar]
- 14. Pronai L, Hiramatsu K, Saiusa Y, Nakazawa H: Low superoxide scavenging activity associated with enhanced superoxide generation by monocytes from male hypertriglyceridaemics with and without diabetes. Atherosclerosis 1991; 90:39–47 [DOI] [PubMed] [Google Scholar]
- 15. Chin JA, Azhar S, Hoffman BB: Inactivation of endothelial derived relaxing factor by oxidised lipoprotein. J Clin Invest 1992; 89:10–12 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16. Sutherland WHF, Wlaker RJ, de Jong SA, van Rij AM, Phillipis V, Walker HL: Reduced postprandial serum paraoxonase activity after a meal rich in used cooking fat. Arterioscler Thromb Vasc Biol 1999; 19:1340–1347 [DOI] [PubMed] [Google Scholar]
- 17. Watson AD, Berliner JA, Hama SY, La Du BM, Faull KF, Fogel‐man AM, Navab M: Protective effect of high density lipoprotein associated paraoxonase: Inhibition of the biological activity of minimally oxidized low density lipoprotein. J Clin Invest 1995; 96:2882–2891 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18. Byun J, Mueller DM, Fabjan JS, Heinecke JW: Nitrogen dioxide radical generated by the myeloperoxidase‐hydrogen peroxide‐nitrite system promotes lipid peroxidation of low density lipoprotein. FEBS Lett 1999; 455:243–246 [DOI] [PubMed] [Google Scholar]
- 19. Inliano L, Pedersen JZ, Camastra C, Bello V, Ceccarelli S, Violi F: Protection of low density lipoprotein oxidation by the antioxidant agent IRFI005, a new synthetic hydrophilic vitamin E analogue. Free Radic Biol Med 1999; 26:858–868 [DOI] [PubMed] [Google Scholar]
- 20. Ramasamy S, Drummond GR, Ahn J, Storek M, Pohl J, Parthasarathy S, Harrison DG: Modulation of expression of endothelial nitric oxide synthase by nordihydroguaiaretic acid, a phenolic antioxidant in cultured endothelial cells. Mol Pharmacol 1999; 56:116–123 [DOI] [PubMed] [Google Scholar]
- 21. Heller R, Munscher‐Paulig F, Grabner R, Till U: L‐ascorbic acid potentiates nitric oxide synthesis in endothelial cells. J Biol Chem 1999; 274:8254–8260 [DOI] [PubMed] [Google Scholar]
- 22. Levine GN, Frei B, Koulouris SN, Gerhard MD, Keaney JF, Vita JA: Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation 1996; 93:1107–1113 [DOI] [PubMed] [Google Scholar]
- 23. Jackson TS, Xu A, Vita JA, Keaney JF Jr: Ascorbate prevents the interaction of superoxide and nitric oxide only at very high physiological concentrations. Circ Res 1998; 83:916–922 [DOI] [PubMed] [Google Scholar]