Intensive Plasmapheresis as a Risk Factor for Arteriosclerotic Cardiovascular Disease?

Abstract

Recent studies suggest that the analogy between intensive plasmapheresis and the nephrotic syndrome with respect to plasma protein loss includes events which are generally recognized as risk factors for the development of arteriosclerotic cardiovascular disease. Experimental nephrosis and plasmapheresis alike increase the synthesis of very low density and low density lipoproteins in response to the hypoproteinemic stimulation of plasma protein synthesis. During electrophoresis, these lipoproteins move with the alpha2- and beta-globulins, and the serum levels of these fractions are often elevated in humans subjected to intensive plasmapheresis. Hyperlipoproteinemias of the alpha2- and beta-types are recognized risk factors in the genesis of arteriosclerosis. Another such factor appears to be an increased synthesis of fibrinogen. This protein enhances plasma viscosity and red cell aggregation and may play a role in myocardial infarction. Intensive plasmapheresis thus not only creates an unphysiological and partly depletional state; it is also, like the nephrotic syndrome, capable of producing surplus abnormalities of plasma constituents with a potential for delayed, insidious injury.