Lipoprotein(a) apheresis in severe coronary heart disease: an immunoadsorption method

Lipoprotein(a) (Lp[a]) is associated with an increased cardiovascular risk. It is similar to low-density lipoprotein with an additional molecule of apo A covalently linked to apo B-100 by one disulfide bridge. Apo A is highly homologous to plasminogen. The kringle 4 motive of plasminogen is repeated between 10 and 40 times in apo (a). Currently, there is no drug therapy available to lower Lp(a). Since October 1993, we have carried out over 160 immunoadsorption treatments on 3 patients with elevated Lp(a) as their only risk factor and a history of myocardial infarction. Lp(a) was removed from plasma by sepharose coupled anti-Lp(a) columns. Lp(a) levels were lowered from above 170 mg/dl to below 30 mg/dl immediately after Lp(a) apheresis. To achieve this, the patient's plasma volume had to be treated 2 to 3 times. Nonspecific protein loss during column changes remained negligible. There were no serious unwanted effects during or after treatment. Minor circulatory problems (tachycardia, flush) occurred in 11% of the treatments but only with plasma flow rates above 55 ml/min. In 1 patient, coronary angiography after 2 years and in another patient after 1 year showed no progression. The third patient has not yet had repeat coronary angiography. Like the others, he reported subjective improvement after 1 year of apheresis. It is concluded that Lp(a) apheresis may retard progression of atherosclerosis in patients with selective Lp(a) elevation. Further studies to support this hypothesis are needed.