title: [Heparin-induced extracorporeal LDL precipitation (HELP) in therapy refractory hypercholesterolemia and coronary heart disease: effect on clinical and morphological regression of coronary sclerosis].
abstract: There are now several efficient and safe extracorporeal LDL eliminating procedures for the treatment of patients with familial hypercholesterolemia (FH) resistant to diet and combined drug therapy. In Germany, the most clinical experience is available from the heparin-induced extracorporeal LDL-precipitation (HELP) system. This procedure is additionally characterized by the effective elimination of not only LDL but also fibrinogen, a further independent risk factor of coronary heart disease CHD, which mainly influences blood flow characteristics. After 3-4 HELP treatments at weekly intervals, patients with CHD report markedly fewer episodes of angina pectoris, previously resistant to conventional therapy. This is probably related to a "functional regression" of CHD, which is due to the simultaneous lowering of LDL and fibrinogen, resulting in improved rheological properties followed by an increased oxygen supply to a previously insufficiently perfused myocardium. The restoration of endothelial function by maximal cholesterol lowering, as indirectly shown by changes in the cholesterol/phospholipid ratio in cellular membranes, obviously results in an improved vasomotoric response to endogenous vasodilatative substances, thus explaining the clinical improvement of our patients. As shown by a multicenter trial, regular long-term treatment with HELP is followed by an arrest of the atherosclerotic progression in 50% of the investigated segments. In 30% of the previously progressive segments, a significant regression was observed while only 20% of the segments progressed. The mean degree of stenosis decreased by 4.3%. Regular HELP-LDL-/Fibrinogen apheresis in patients with severe CHD and angina pectoris refractory to conventional therapy results within a relatively short period in an improved coronary perfusion and long-term treatment induces regression of atherosclerotic coronary lesions.
authors.affiliation: Abteilung Klinische Chemie, Klinikum der George-August-Universität.
authors.forename: P
authors.initials: P
authors.lastname: Schuff-Werner
mesh_terms: D001781:Blood Component Removal; D008078:Cholesterol, LDL / Q000097:blood*; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000473:pathology / Q000628:therapy*; D005340:Fibrinogen / Q000378:metabolism; D005590:Fractional Precipitation; D006493:Heparin / Q000008:administration & dosage*; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000175:diagnosis / Q000473:pathology / Q000628:therapy*; D016896:Treatment Outcome
chemical_list: D008078:Cholesterol, LDL; D005340:Fibrinogen; D006493:Heparin