Lipoprotein(a)-apheresis in the secondary prevention of coronary heart disease

Abstract

Lipoprotein(a) [Lp(a)] is one important cause of atherosclerosis. It consists of one molecule of low density lipoprotein and an additional molecule of apo(a) linked to apoB-100 by a disulfide bridge. Apo(a)s are partially homologous to plasminogen, with one kringle 5 and 10–40 repeats of kringle 4. As there is no drug therapy available, we treated three patients who had suffered from at least one myocardial infarction and had Lp(a) as the only risk factor for atherosclerosis. Since October 1992, 186 immunoadsorption treatments have been carried out weekly with Sepharose-coupled antiLp(a)-columns. To achieve a reduction in Lp(a) from 78–250 mg/dL before apheresis to below 25 mg/dL immediately after apheresis, patient plasma volume had to be treated two to three times. Treatments lasted 3–5 h. Immediately reversible side-effects such as flushing and tachycardia during the first treatment were seen in 9% of immunoadsorptions. Non-specific protein loss remained tolerable, if one takes into. account that the patients received approximately 1 L of ACDB with heparin as anticoagulant and some of the column-rinsing buffer. One patient's clinical condition and exercise test improved dramatically as did coronary angiography after 2 years. Another patient had no change after 1 year; the third patient showed subjective improvement and has not yet had repeat angiography after 1 year of treatment. We conclude that Lp(a)apheresis may retard progression of atherosclerosis in patients with selective Lp(a) elevation. Further studies to support this hypothesis are needed.