Plaque stabilization by LDL-apheresis?

Vulnerable lipid-rich plaques are often the cause of atherothrombotic event s leading to unstable angina and/or to acute myocardial infarction. Consequ ent long-term LDL-lowering by drugs as shown by the most important interven tion studies lead to plaque stabilization as shown by the significant reduc tion of myocardial reinfarction. First studies in patients undergoing regular extracorporeal LDL-elimination indicate, that clinical events might be reduced much earlier as by drug th erapy alone: A more than 60% reduction of LDL at weekly intervals is obviou sly associated with an early regression of lipid-rich vascular lesions. LDL -apheresis, mainly by HELP and by double filtration reduces the shear-stres s of the flowing blood on vulnerable plaques either by its effect on plasma viscosity and/or on the vasomotoric reserve thus leading to a lower periphe ral arterial resistance. Furthermore oxidized LDL, which might counteract p laque stabilisation by its inflammatory effects are effectively eliminated by LDL-apheresis. The affinity of different LDL-apheresis procedures to coa gulation factors normalizes hypercoagulatory states thus avoiding atherothr ombotic events at the site of vulnerable or erosive plaques.