METHODS: We evaluated the postprandial lipid metabolism in patients with normolipemic peripheral arterial disease (PAD) after the administration of an oral fat load. Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), HDL2 and HDL3 subfractions, triglycerides (TGs), lipoprotein(a), and LDL size were determined at baseline and for 8 hours after the meal. RESULTS: In patients with PAD, TGs increased significantly at the 4th, 6th, and 8th hours postprandially; in control subjects, TGs increased at the 4th and 6th hours. HDL decreased significantly at the 4th, 6th, and 8th hours in patients with PAD and at the 6th hour in control subjects. The magnitude of postprandial lipemia, expressed as "the area under the incremental curve for TGs," was higher in patients with PAD than in control subjects (770 +/- 476 vs 391 +/- 195 mg/dL at 8 hours, P <.05). Multiple-regression analysis showed that baseline TGs were positively related to the magnitude of postprandial lipemia (P =.01) and that LDL size was negatively related (P =.05). CONCLUSIONS: This is the first documentation of postprandial behavior in patients with normolipemic PAD, suggesting the relevance of postprandial lipoprotein metabolism in the pathogenesis of peripheral atherosclerosis.
Increased postprandial lipemia in patients with normolipemic peripheral arterial disease.
LUPATTELLI, Graziana;PASQUALINI, Leonella;SIEPI, Donatella;PIRRO, Matteo;VAUDO, Gaetano;CIUFFETTI, Giovanni;MANNARINO, Elmo
2002
Abstract
METHODS: We evaluated the postprandial lipid metabolism in patients with normolipemic peripheral arterial disease (PAD) after the administration of an oral fat load. Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), HDL2 and HDL3 subfractions, triglycerides (TGs), lipoprotein(a), and LDL size were determined at baseline and for 8 hours after the meal. RESULTS: In patients with PAD, TGs increased significantly at the 4th, 6th, and 8th hours postprandially; in control subjects, TGs increased at the 4th and 6th hours. HDL decreased significantly at the 4th, 6th, and 8th hours in patients with PAD and at the 6th hour in control subjects. The magnitude of postprandial lipemia, expressed as "the area under the incremental curve for TGs," was higher in patients with PAD than in control subjects (770 +/- 476 vs 391 +/- 195 mg/dL at 8 hours, P <.05). Multiple-regression analysis showed that baseline TGs were positively related to the magnitude of postprandial lipemia (P =.01) and that LDL size was negatively related (P =.05). CONCLUSIONS: This is the first documentation of postprandial behavior in patients with normolipemic PAD, suggesting the relevance of postprandial lipoprotein metabolism in the pathogenesis of peripheral atherosclerosis.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
