[Specific Lp(a) apheresis for secondary prevention of arteriosclerosis].

Lipoprotein(a) (Lp(a)) is an independent risk factor for arteriosclerosis. It consists of the Lp(a)-specific apo(a) which is bound to the apo-B of an LDL particle by a disulfide bridge. Apo(a) is homologous to parts of the plasminogen molecule: It consists of one kringle 5 and 10-40 kringles 4 of the plasminogen molecule. Due to the lack of alternative drug treatment, 3 patients with early onset of arteriosclerosis, rapid progression, and elevated Lp(a) as their dominating risk factor were treated weekly with specific Lp(a)-aphereses. Since October 1992, we carried out 229 immunoadsorptions (IA) with specific columns containing anti-Lp(a) antibodies covalently bound to sepharose. To reduce Lp(a) from preapheresis values of 142 +/- 53 mg/dl to 25 +/- 11 mg/dl immediately after apheresis, we had to adsorb 1.4-3 patient's plasma volumes. Lp(a) rise to preapheresis values took 3-4 days. Protein reduction caused by loss of plasma during column changes remained tolerable (total protein before IA: 71 +/- 4 g/l, after IA: 56 +/- 4 g/l. Immediately after IA, these values were measured after the application of 991 +/- 207 ml of ACDB with 5,000 IU of heparin as anticoagulant. Hemoglobin remained unchanged (before IA: 13.4 +/- 1.4 g/dl, after IA: 13.6 +/- 1.5 g/dl). Side effects were mainly flush and tachycardia. They were seen especially when using new columns and plasma flow rates above 55 ml/min and were immediately reverted by interrupting the IA. Control angiography performed after 2 years in 2 patients showed no progression of disease, in the 3rd patient, the stress test showed a significant improvement as did clinical parameters. In our hands, IAs are a safe and efficient method for Lp(a) reduction and secondary prevention of myocardial infarction. Therapeutic efficiency should further be proven by a controlled trial.