BACKGROUND AND AIM: Impaired elimination of triglycerides (TG) after postprandial lipemia is often observed in patients with ischemic heart disease (IHD). Longer retention of TG-rich lipoproteins in the circulation may in turn be the cause of hemostatic disturbances in the form of hypercoagulation. The aim of this study was to evaluate the influence of postprandial lipemia on the hemostatic system in normolipemic patients with angiographically documented atherosclerotic changes of coronary arteries. METHODS AND RESULTS: 20 males under 60 years of age with IHD and 10 healthy males matched for age were studied. Hemostatic and lipid parameters were determined in blood collected before (fasting) and after (2, 4, 6 and 8 hours) an oral fat load (200 ml of 30% cream). A statistically significant increase in factor VII (FVIIc-%) was found during postprandial lipemia in comparison with fasting. Although in patients with IHD the area under the curve for FVIIc was not significantly different than in the control group, it was observed that FVIIc in the IHD group exceeded the fasting level earlier (4, 6 and 8 h) than in controls (8 h). Levels of FVIIc reached for the IHD group: fasting value = 96.3 +/- 16.3; postprandial 4 h = 103.2 +/- 21.3, 6 h = 105.2 +/- 21.8, 8 h = 106.0 +/- 21.4; for the controls: fasting value = 96.8 +/- 17.2; postprandial 8 h = 107.7 +/- 22.0. In the IHD group, unlike in controls, postprandial lipemia was accompanied by a statistically significant rise in fibrinogen levels (Fb-g/l) as compared with fasting (fasting value = 3.69 +/- 0.59; postprandial 2 h = 3.89 +/- 0.65, 4 h = 3.93 +/- 0.63). Mean values for PAI-1 were lower in the IHD than in the control group, but PAI-1 activity during postprandial lipemia rose earlier in the IHD group (4 and 6 h) than in the controls (6 h). PAI-1 levels were in the IHD: fasting values = 1.4 +/- 1.2; postprandial 4 h = 2.3 +/- 1.6, 6 h = 2.5 +/- 1.7; in the control: fasting value 2.9 +/- 1.7; postprandial 6 h = 3.9 +/- 2.0. The level of fragment 1 + 2 (F1 + 2) during postprandial lipemia decreased in both groups. CONCLUSIONS: The lipemic stimulus in fasting normolipemics induces a hypercoagulant effect with greater changes in patients with ischemic heart disease than in healthy subjects. Longer periods of postprandial lipemia might constitute an additional factor promoting thrombus formation in patients with dysfunction of the vascular endothelium.
BACKGROUND AND AIM: Impaired elimination of triglycerides (TG) after postprandial lipemia is often observed in patients with ischemic heart disease (IHD). Longer retention of TG-rich lipoproteins in the circulation may in turn be the cause of hemostatic disturbances in the form of hypercoagulation. The aim of this study was to evaluate the influence of postprandial lipemia on the hemostatic system in normolipemic patients with angiographically documented atherosclerotic changes of coronary arteries. METHODS AND RESULTS: 20 males under 60 years of age with IHD and 10 healthy males matched for age were studied. Hemostatic and lipid parameters were determined in blood collected before (fasting) and after (2, 4, 6 and 8 hours) an oral fat load (200 ml of 30% cream). A statistically significant increase in factor VII (FVIIc-%) was found during postprandial lipemia in comparison with fasting. Although in patients with IHD the area under the curve for FVIIc was not significantly different than in the control group, it was observed that FVIIc in the IHD group exceeded the fasting level earlier (4, 6 and 8 h) than in controls (8 h). Levels of FVIIc reached for the IHD group: fasting value = 96.3 +/- 16.3; postprandial 4 h = 103.2 +/- 21.3, 6 h = 105.2 +/- 21.8, 8 h = 106.0 +/- 21.4; for the controls: fasting value = 96.8 +/- 17.2; postprandial 8 h = 107.7 +/- 22.0. In the IHD group, unlike in controls, postprandial lipemia was accompanied by a statistically significant rise in fibrinogen levels (Fb-g/l) as compared with fasting (fasting value = 3.69 +/- 0.59; postprandial 2 h = 3.89 +/- 0.65, 4 h = 3.93 +/- 0.63). Mean values for PAI-1 were lower in the IHD than in the control group, but PAI-1 activity during postprandial lipemia rose earlier in the IHD group (4 and 6 h) than in the controls (6 h). PAI-1 levels were in the IHD: fasting values = 1.4 +/- 1.2; postprandial 4 h = 2.3 +/- 1.6, 6 h = 2.5 +/- 1.7; in the control: fasting value 2.9 +/- 1.7; postprandial 6 h = 3.9 +/- 2.0. The level of fragment 1 + 2 (F1 + 2) during postprandial lipemia decreased in both groups. CONCLUSIONS: The lipemic stimulus in fasting normolipemics induces a hypercoagulant effect with greater changes in patients with ischemic heart disease than in healthy subjects. Longer periods of postprandial lipemia might constitute an additional factor promoting thrombus formation in patients with dysfunction of the vascular endothelium.
Authors: Julie A Bastarache; Lorraine B Ware; Timothy D Girard; Arthur P Wheeler; Todd W Rice Journal: JPEN J Parenter Enteral Nutr Date: 2012-02-07 Impact factor: 4.016
Authors: G Kolovou; D Daskalova; K Anagnostopoulou; I Hoursalas; V Voudris; D P Mikhailidis; D V Cokkinos Journal: J Clin Pathol Date: 2003-12 Impact factor: 3.411