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From the King Gustaf V Research Institute, Karolinska Institute, and Departments of Cardiology (P.T.) and Internal Medicine, (F.K., A.H.), Karolinska Hospital, Stockholm, and the Department of Medical Biochemistry and Biophysics (G.O., T.O.), University of Umeå, Umeå, Sweden.
Correspondence to Dr Per Tornvall, King Gustaf V Research Institute, Karolinska Hospital, Karolinska Institute, S-171 76 Stockholm, Sweden.
Abstract Lipoprotein lipase (LPL) activity and mass in plasma and their increase after heparin administration were measured in 61 men who had suffered myocardial infarction before the age of 45 years and in 69 population-based age- and sex-matched control subjects without coronary heart disease to study the relations between these parameters in plasma and their correlations with plasma lipoproteins in subjects with a wide range of lipoprotein and LPL levels. There was a relatively large amount of LPL protein compared with LPL activity in preheparin plasma, indicating that the majority of circulating LPL is catalytically inactive. LPL mass and activity in postheparin plasma (postheparin minus preheparin values) were highly correlated, and the calculated mean specific activity (0.35 mU/ng) was in the range expected for catalytically active LPL. Hence, heparin releases mainly active LPL. The four LPL parameters (mass and activity in plasma and their increase after heparin administration) were not related to each other, except for postheparin plasma LPL mass and activity, and they showed different correlations with plasma lipoprotein lipid concentrations. There was a strong positive correlation between LPL mass in preheparin plasma and the HDL cholesterol level as well as weak negative relations to VLDL triglyceride and cholesterol concentrations in the patients. In contrast, preheparin LPL activity showed no correlation with the HDL cholesterol level but weak positive relations to VLDL triglyceride and cholesterol concentrations in the control subjects. Postheparin plasma LPL activity related positively to the HDL cholesterol level and negatively to the VLDL triglyceride concentration in the control subjects. Case subjects differed from control subjects in that they had higher preheparin plasma LPL activity and a tendency toward lower specific activity of postheparin plasma LPL. The different relations of the measured LPL parameters to plasma lipoproteins and the difference in preheparin plasma LPL activity between patients and control subjects might reflect a disturbance of the LPL system in the patients.
Key Words: lipoprotein lipase plasma lipoproteins coronary heart disease
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