[Plaque stabilization by LDL apheresis?].
Vulnerable lipid-rich plaques are often the cause of atherothrombotic events leading to unstable angina and/or to acute myocardial infarction. Consequent long-term LDL-lowering by drugs as shown by the most important intervention studies lead to plaque stabilization as shown by the significant reduction of myocardial reinfarction. First studies in patients undergoing regular extracorporeal LDL-elimination indicate, that clinical events might be reduced much earlier as by drug therapy alone: A more than 60% reduction of LDL at weekly intervals is obviously associated with an early regression of lipid-rich vascular lesions. LDL-apheresis, mainly by HELP and by double filtration reduces the shear-stress of the flowing blood on vulnerable plaques either by its effect on plasmaviscosity and/or on the vasomotoric reserve thus leading to a lower peripheral arterial resistance. Furthermore oxidized LDL, which might counteract plaque stabilisation by its inflammatory effects are effectively eliminated by LDL-apheresis. The affinity of different LDL-apheresis procedures to coagulation factors normalizes hypercoagulatory states thus avoiding atherothrombotic events at the site of vulnerable or erosive plaques.
Schuff-Werner
P
P
Institut für Klinische Chemie und Pathobiochemie, Medizinische Fakultät, Universität Rostock. pschuffw@med.uni-rostock.de
Schettler
V
V
D001779:Blood Coagulation Factors / Q000378:metabolism; D008078:Cholesterol, LDL / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood / Q000628:therapy*; D003328:Coronary Thrombosis / Q000097:blood / Q000517:prevention & control; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000517:prevention & control; D010956:Plasmapheresis; D011379:Prognosis
D001779:Blood Coagulation Factors; D008078:Cholesterol, LDL