[Pathologic decrease in lipoprotein lipase activity in relation to the development of hyperlipemias and their significance for coronary heart disease].

There is much evidence that altered lipid metabolism contributes to the development of coronary artery disease (CAD). It is generally accepted that there is a direct association between the extent of CAD and total plasma cholesterol, as well as an inverse association between the extent of CAD and plasma HDL-cholesterol. No general agreement exists about the atherogenetic potential of plasma triglycerides and of triglyceride-rich lipoproteins. Since lipoprotein lipase (LPL) is the key-enzyme in the catabolism of triglyceride-rich lipoproteins (chylomicrons and very low-density lipoproteins), we examine the relationship between triglyceride-rich lipoproteins and LPL in vitro and in vivo. The concentrations of the main lipoprotein density classes, namely very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3, are measured by rate zonal ultracentrifugation. The preparation of VLDL, IDL, LDL, HDL2, and HDL3 is performed by sequential ultracentrifugation. The activity of LPL is measured radioenzymatically in a glycerol-based triolein emulsion. It can be demonstrated in vitro that VLDL, IDL, and HDL2 from normal plasma are able to increase LPL-activity in contrast to VLDL, IDL, and HDL2 from hyperlipemic plasma. This difference seems to be caused by an altered composition of apolipoproteins in hyperlipemic lipoproteins. An artificial acidosis in three healthy subjects shows in contrast to alkalotic and neutral blood-pH a significant decrease of LPL-activity. This result seems to be of some interest, since diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show secondary hyperlipemias caused by a deficit of LPL-activity. It can be shown in 15 male patients who produce a secondary type-V hyperlipemia during severe abuse of alcohol, that LPL-activity is decreased significantly as compared to 15 healthy controls. During sober phases, this alcohol-induced hyperlipemia and the impairment of LPL-activity disappears completely. In an other group of 8 male patients, who are not producing severe secondary hyperlipemia during approximately the identical alcohol intake, LPL-activity is also significantly decreased, but the activity of hepatic lipase is significantly increased. This increase of the activity of hepatic lipase seems to protect these patients from the development of secondary type-V hyperlipemia. In 89 male patients with angiographically assessed CAD a very strong inverse association between the activity of LPL and the extent of CAD is found.(ABSTRACT TRUNCATED AT 400 WORDS)