Vascular function as an early sign of trouble:

How can the inhibition of cholesterol absorption reduce the atherogenic load of intestinal lipoproteins? 

Postprandial hyperlipidemia is caused by the increased influx of lipids from the intestine after a meal. Very small remnant particles are left in the circulation. These very small remnant particles can interact with the vessel wall and can even penetrate the vessel wall. Nonfasting triglyceride plasma levels are associated with increased CVD risk; in the postprandial phase HDL-c plasma levels drop.

Postprandial lipids (triglyceride-rich lipoprotein or lipoprotein-remnant particles) are associated with endothelial dysfunction, elevated small LDL particles, Factor VII, plasminogen activator inhibitor-1 (PAI-1) and C-reactive protein (CRP).

Postprandial hyperlipidemia can be reduced with lipid-lowering therapy. The PostprAndial eNdothelial function After Combination of Ezetimibe and simvAstatin (PANACEA) Study was designed to evaluate the effect of simvastatin/ezetimibe or high-dose simvastatin alone on fasting and postprandial endothelial function. Statin monotherapy and ezetimibe monotherapy preserve post-fatload endothelial function and also a combination of low-dose statin with ezetimibe preserves post-fatload endothelial function. There is a protective effect of both treatments. Although an appealing pathophysiological concept, the clinical usefulness of postprandial hyperlipidemia remains to be determined.

View the expert opinion interview with Prof. Visseren