Martin Ericsson

Quantitative and qualitative serum lipoprotein analysis

Preparative ultracentrifugal and electrophoretic analysis of serum lipoproteins was performed in 30-70-year-old healthy, fasting males (N = 80) and females (N = 77), randomly selected from the Uppsala region, Sweden. The concentrations of cholesterol and triglycerides in total serum and in VLDL,LDL and HDL lipoprotein classes are reported. Total serum, VLDL and LDL triglycerides and cholesterol concentrations increased with age, while HDL cholesterol and triglyceride concentrations did not vary with age. Overweight persons had higher total serum triglyceride, higher VLDL cholesterol and triglyceride and lower HDL cholesterol levels. The upper 90% population limit values for non-overweight males/females were: total triglycerides (mmol/l) 2.5/2.0, total cholesterol (mg/100 ml) 298/300, VLDL triglyceride 1.80/1.05, VLDL-cholesterol 32/33, LDL triglyceride 0.69/0.69, LDL cholesterol 210/218, HDL triglyceride 0.32/0.34 and HDL-cholesterol 69/93. The 2 major differences between males and females were that females had lower VLDL but higher HDL concentrations. For VLDL there was a very strong and for LDL a moderately strong positive correlation between cholesterol and triglyceride contents. In HDL however, the mearsured amounts of cholesterol and triglycerides did not correlate at all. Sinking pre-beta lipoproteins was found in about 25% of cases and a second pre-beta band floating at d 1.006, late pre-beta, was found in 35% of male and 25% of female subjects. Subjects with sinking pre-beta lipoprotein did not differ from other subjects with regard to the concentration of cholesterol and triglycerides in the 3 lipoprotein classes. Males, but not females, with the late pre-beta (LPB), had an increased amount of cholesterol in VLDL and a raised cholesterol-triglyceride ratio in this lipoprotein class. Also the LDL triglyceride level was increased in males with the late pre-beta lipoprotein.

Quantitative and qualitative serum lipoprotein analysis: Part 2. Studies in male survivors of myocardial infarction☆

The fasting concentration of cholesterol and triglycerides in serum and in very low (VLDL), low (LDL) and high (HDL) density lipoproteins (LP) was determined 3 months after a myocardial infarction (MI) in 54 men, and the values obtained were compared to those in 61 healthy male control subjects. The mean triglyceride concentration in MI patients was significantly increased in serum, VLDL, LDL and HDL by 74%, 110%, 30% and 12% respectively, compared to controls. The mean cholesterol concentration was significantly raised by 16%, 120% and 14% in serum, VLDL and LDL but decreased by 22% in HDL. Hypertriglyceridaemia occurred in 58% of MI patients. Of these patients, two-fifths had hypertriglyceridaemia only and three-fifths had combined hyperlipidaemia. The hypertriglyceridaemia was caused by elevation of only VLDL triglycerides in 26%, only LDL triglycerides in 19%, VLDL and LDL triglycerides in 23% and by various other combinations of raised LP triglyceride levels in 25% of cases. Hypercholesterolaemia was found in 41% of MI subjects. Of these, one-sixth had elevation of cholesterol levels, while five-sixths had combined hyperlipidaemia. The LP abnormalities underlying hypercholesterolaemia were increased of only VLDL cholesterol levels in 36%, only LDL cholesterol in 14% and both VLDL and LDL cholesterol in 50% of cases. The low HDL cholesterol values in comparison to controls were related to higher VLDL triglyceride values in MI patients, since HDL cholesterol fell significantly with increasing VLDL triglyceride levels. When HDL cholesterol was related to similar VLDL triglyceride levels, there were no major differences between controls and MI.

Correlations between intravenous fat tolerance and serum lipoproteins in normal and atherosclerotic subjects.

Triglyceride (TG) and cholesterol concentrations in the major lipoprotein fractions and the intravenous fat tolerance test (IVFTT) k2 value were determined in healthy controls (n = 35), in survivors of myocardial infarction (MI, n = 43) and in patients with peripheral vascular disease (PVD, n = 33). MI patients had the highest lipid concentrations in the lipoproteins except for HDL-cholesterol which was 26% lower in both MI and PVD patients compared to controls. For the other lipid concentrations, PVD patients had values between MI patients and control values. The mean k2 values were, for MI patients 2.8%/min, for PVD patients 3.3%/min, and for controls 4.4%/min. Data were pooled from all 111 individuals and correlations between lipids in the lipoprotein fractions and the k2 value were calculated. The highest r value was found for log k2 versus log VLDL-TG (r = −0.65, P < 0.001), but significant negative correlations between k2 and LDL- as well as HDL-TG were also demonstrated. A strong positive correlation was found between k2 and HDL-cholesterol. When partial regression analysis was carried out, this relationship prevailed also when the effects of both VLDL-TG and total TG were eliminated (r = 0.32, P < 0.001). These results support the concept that the IVFTT k2 value independently gives an estimate of TG removal processes from plasma and reflects HDL activity on TG catabolism.