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.
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.
Authors: Shane A Phillips; Jason W Jurva; Amjad Q Syed; Amina Q Syed; Jacquelyn P Kulinski; Joan Pleuss; Raymond G Hoffmann; David D Gutterman Journal: Hypertension Date: 2008-01-14 Impact factor: 10.190
Authors: Saurabh S Thosar; Sylvanna L Bielko; Chad C Wiggins; James E Klaunig; Kieren J Mather; Janet P Wallace Journal: Med Sci Monit Date: 2015-04-07
Authors: Kevin C Maki; Tia M Rains; Arianne L Schild; Mary R Dicklin; Keigan M Park; Andrea L Lawless; Kathleen M Kelley Journal: Vasc Health Risk Manag Date: 2013-07-23
Authors: Fiona E Lithander; Louise K Herlihy; Deirdre M Walsh; Emma Burke; Vivion Crowley; Azra Mahmud Journal: Nutr J Date: 2013-07-10 Impact factor: 3.271
Authors: Janelle L Davis; Hunter L Paris; Joseph W Beals; Scott E Binns; Gregory R Giordano; Rebecca L Scalzo; Melani M Schweder; Emek Blair; Christopher Bell Journal: Nutr Metab Insights Date: 2016-06-20