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Effect of the progestogen medrogestone on plasma lipoprotein levels in postmenopausal women using conjugated estrogens: an open, randomized comparative study
28
Monday 10 October 1994: Poster Abstracts Riskfactors
code and plasma cholesterol with 55 control subjects recruited from the same source. Blood pressure (mean f SE) was higher in cases than in controls (138 f 4.0/84 f 1.3 vs 130 + 3.H7’8.4f 2.0 mmHg, P < 0.03). Only two subjects in each group were current cigarette smokers. Fasting plasma lipids and apoproteins, including Lp(a), and post-prandial triglyceride responses to a standard test meal did not differ in cases and controls. Glucose and insulin postprandial responses were greater in CHD subjects (P
We investigated the association of LDL subclass and coronary risk factors with CAD in 217 subjects (170 M, 47 I!), aged 2382 years. The presence of CAD was defined angiographically as >75% stenosis of major coronary arteries. LDL subclasses were classified into small LDL and normal LDL, based on LDL particle size by non-denaturing 2.5-168 polyacrylamide gradient gel electrophoresis. Gels were stained with Oil Red 0 and LDL migration distances were measured by densitometry. Plasma lipid levels were measured and diabetes mellitus, obesity, hypertension and smoking were also examined. Small LDL were associated with higher plasma levels of triglyceride, LDL-C and apo B than normal LDL (172f67 vs 124f50, 124+44 vs 112+35, 113rt27 vs 96+24mg/dl) and with high body mass index and hypertension. They were found together with lower plasma levels of HDL-C and apo A-I than normal LDL (36fll vs 49f12, 104f26 vs 119f27mg/dl), but plasma levels of total cholesterol were not different between the two groups. The prevalence of CAD in small LDL was significantly higher than in normal LDL (85.9% vs 62.9%). Patients with small LDL were more likely to have 2- and 3-vessel disease compared with l-vessel disease (50% vs 42.9%). These results suggest that small LDL are significantly associated with high plasma triglyceride and low HDL-C and might be a discriminator for CAD in normocholesterolemia. 1101 m,
Insulin resistance in smokers is a function of smoking habits Attvall S, Taskinen M-R*, Smith U, Dept. oflntemal
Medicine, Sahlgrenska Univ. Hospital, S-413 45 Giiteborg, Sweden; *3rd Dept. of Internal Medicine, Univ. of Helsinki, Helsinki, Finland
Smokers exhibit several metabolic risk factors for cardiovascular disease (CVD) which may be related to smoking-induced insulin resistance. The objective of this study was to investigate the relationships between smoking habits, degree of insulin resistance and the various manifestations of the insulin resistance syndrome (IRS) in middle-aged men. The participants were 57 healthy normal-weight (BMI mean 23.7 f SD 2.0) chronic smokers (mean nicotine consumption per day 23.3 zb 10.9 mg). 40-60 years of age (mean 48.9 f 6.3 years).
A 2-h euglycemic hyperinsulinemic (1.0 mU/kg/min) clamp was performed to determine degree of insulin sensitivity, measured as amount of glucose infused per kg lean body mass and minute (glucose infusion rate, GIR). Smoking habits were related to GIR and the various biochemical manifestations of IRS. Daily nicotine consumption correlated with GIR as well as various markers of IRS such as fasting insulin values, HDL-C, triglycerides and plasminogen activator inhibitor 1 (PAI-1) activity. Smoking habits, independent of GIR, were also related to total and LDL cholesterol. In a multiple linear regression analysis, considering the effects of antbropometric data, age and alcohol consumption, only smoking habits and % body fat were independently related to GIR. Smokers are insulin resistant and exhibit several characteristics of IRS which may explain the increased CVD in smokers. Degree of insulin resistance as well as IRS are functions of smoking habits. However, the increased cholesterol levels seen in smokers are not related to degree of insulin resistance. Hydrogen- and lipo-peroxides in acute smokinginduced platelet hyperactivity Blache D, INSERM, Lab. de Biochimie des Lipoproteines, Univ.
1
de Bourgogne, Dijon, France
Previous studies established that blood platelets develop a hyperaggregability after acute cigarette smoking. We investigated whether changes in plasma oxidative properties could occur after smoking and whether such changes could be responsible for this enhanced platelet activity. In the present work, we report that platelets from non-smokers become hyperactive by incubating them with plasma prepared from blood of smokers obtained 10 min after smoking. This effect was not observed with presmoking plasma and could be inhibited in vitro by adding either catalase or reduced glutathione plus peroxidase to plasma or the antioxidant BHT to platelets before incubation. Nicotine added to presmoking plasma in the concentration range found in smokers did not reproduce the platelet activation effect and d-tubocurarine, a nicotinic receptor antagonist, did not inhibit the enhanced response of platelets to aggregation induced by post-smoking plasma. By chemical analysis in post-smoking plasma, we found a decrease in vitamin E (188, P < 0.01) and an increase in conjugated dienes (35510,P < O.OOl), thiobarbituric acid reactive substances (TBARS, 23%, P< 0.02) and free fatty acids (FFA, 40%, P < 0.005). By means of its specific reaction with N,N-dimethylp-phenylenediamine, the FFA fraction was shown to be peroxidized to a higher extent in post-smoking than in pre-smoking plasma. This peroxidized FPA fraction enhanced the thrombininduced aggregation of platelets from non-smokers. The increased response was inhibited either when the peroxidized FFA fractions were isolated from plasma treated with reduced glutathione and peroxidase or by pretreatment of the platelets with BHT. The results indicate that acute smoking exerts an oxidative stress on plasma lipids which enhances platelet aggregability. In addition to the lipoprotein modification, these changes could explain the reported accelerated atherothrombogenesis in smokers which might benefit from antioxidant supplementation. Effect of the progestogen medrogestone on plasma lipoprotein levels in postmenopausal women using conjugated estrogens: an open, randomized comparative study f&vets I.&&& van der Mooren MJ*, Buytenhek M, Gaubius
1
Laboratom PC-TN0 Zernikedreef 9, 2333 CK Leiden, The Netherlands; **Univ.Hospital Ntjmegen Sint Radboud, Nijmegen, The Netherlands
The objective of this study was to assess the effect of the pro-
Atherosclerosis X, Montreal, October 1994
Monday 10 October 1994: Poster Abstracts Risk factors gestogen medrogestone on conjugated estrogen (CE)- induced changes in plasma lipoprotein levels. Plasma lipid and lipoprotein levels were determined in 114 postmenopausal hysterectomized women aged 49-64 years before and during 13 cycles of continuous oral treatment with 0.625 mg of CEs. The women were randomly assigned to two groups receiving either CEs (group I; n = 55) or CEs plus 5 mg of medrogestone orally during the last 12 days of each 28-day cycle (group 2; n = 59). Gradient ultracentrifugation was used in all assessments At cycles 3, 6, and 13, HDb-C levels were increased from baseline by 40%, 44% and 458, respectively, in group 1 and by 27%, 34% and 30%, respectively, in group 2 (P < 0.001 at all assessments; difference between groups not significant). HDL3-C was increased by 6%, 6% and 7% in the respective cycles in group 1 (P < 0.001 at all assessments), but no change in HDL3 was found in group 2 (difference between groups P = 0.011 only at cycle 3). Medrogestone had no effect on the estrogen-induced increases in triglycerides or apo A-I, or on the decreases in LDLC and apo B; neither hormone significantly affected VLDL-C or Lp(a) levels. Conclusion: medrogestone did not adversely affect changes in lipoprotein levels evoked by conjugated estrogens in postmenopausal women. 1
Changes in coronary heart disease risk factors associated with menopause, and influence of substitutive hormone therapy
vtlle J, Marecaux N, Isorez D, Zylberberg G, Fruchart JC, Amouyel P, Inst. Pasteur de Lille, I rue du Pr Calmette, 59019 Lille, France The relationships between menopause and cardiovascular risk factors, and the effect of progestin alone or in combination with estrogen on these risk factors, were analyzed in a sample of French women. We studied 5555 consecutive women, aged between 40 and 65 years, attending a systematic health check-up. All biological measurements were performed at a central laboratory. The effects of menopause on cardiovascular risk factors were determined in 3332 women between 40 and 65 years of age (premenopausal n = 1945, postmenopausal n = 1387) none of whom was receiving hormone replacement therapy. The effect of hormone replacement therapy was assessed in an additional group of 472 peri- and postmenopausal women. Menopause was associated with higher levels of serum TC (6.4 vs 5.7 mmolil; P < O.OOOl), triglycerides (1.2 vs 1 .O mmol/l; P < O.OOl), apo B (1.3 vs 1.1 g/l; P < 0.0001). apo A-l (1.9 vs and diastolic blood pressure (79.7 vs 1.8 g/l; P < 0.0001) 75.3 mmHg; P < 0.05). These effects were independent of the classical confounding variables, Perimenopausal women treated with progestin alone (n = 96) were compared to p&menopausal women not using hormonal replacement therapy (n = 3 12). There were no statistically significant differences in the levels of biological parameters between the two groups. In contrast, postmenopausal women using a combination of estrogen and progestin (n = 376) had significantly lower levels of serum cholesterol (6.1 vs 6.4 mmol/l; P< O.OOOl), triglycerides (1.0 vs 1.2 mmohl; P < O.OOOl), apo B (1.2 vs 1.3 g/l; P < 0.0001). systolic (131.7 vs 137.9 mmHg; P
pig
29
Rationale and design of a large mu&enter study of CVD in familial hyperchobzsterolemic (FH) patients: HALF (homocysteine, atherosclerosis, llpiis and FH)
WittekQ&M&, Knipscheer HC, Btiller HR. Kastelein JJP, Centre for Vascular Medicine, Academic Medical Centre, Amsterdam, The Netherlands There is substantial variation in the onset and severity of CVD symptoms among FH patients, even with identical LDL-receptor gene defects, Hypercholesterolemia per se cannot explain the appearance of CVD in a proportion of FH patients: additional atherogenic risk factors must contribute to the clinical manifestations In view of recent interest in novel risk factors, we initiated a multicenter investigation to study their impact on atherosclerosis. HALF is both a cross-sectional and prospective cohort study with a followup period of 3 years. 150 FH patients with clinically manifest CVD will be selected and an equal number of FH patients free of CVD, matched for age and sex, will be included. Baseline data such as homocysteine metabolism, lipoprotein subfractionation and oxidative resistance, Lp(a), endothelin, heat shock proteins, carbohydrate metabolism and insulin resistance, coagulation, tibrinolysis, blood pressure regulation and intimamedia wall thickness will be obtained from all patients. After analysis at baseline, patients will be followed up to study the relationship between these risk factors and the development of CVD. In a pilot study, profound differences with respect to fibrinolysis (D-dimer; P < 0.02, PA1 + @‘A; P < 0.04), homocysteine (P < 0.05) and Lp(a) (P < 0.01) were discovered between 12 FH patients with and without CVD. These preliminary results suggest that HALF can contribute to a better understanding of the interaction between additional risk factors and LDL-C in FH-patients and might lead to the identification of new factors that either damage or protect the vessel wall during atherogenesis.
11061
Small dense LDL are a major determinant for the severity of angiographically assessed CAD, even in groups,with simv triglyceride levels Berg A , Halle M’, Rensing UFE2, Roskamm
Med. Universitiitsklinik, D-79106 Freiburg; ‘Benedikt Kreutz Rehabilitationszentrum ,fiir Herz- und Kreisla@ranke, D-79189 Bad Krozingen, Germany
m1
In 314 patients who underwent coronary angiography, the concentration and composition of six LDL-subfractions were determined by preparative ultracentrifugation. The patients were grouped into four categories (O-3) according to the number of vessels with stenosis >50% (diameter). Interestingly, there were no differences in serum triglyceride (TG) levels between these groups, possibly because patients with TG > 300 were excluded from the study. Despite similar serum TGs, levels of small-dense LDL (d > 1.040 g/ml) were significantly higher in patients with severe coronary artery disease (CAD). This finding was confirmed using two other angiographic scores (Kaltenbach, Friesinger) of severity of atherosclerosis and stenosis. Both correlated positively and significantly with the concentration of small-dense LDL. In addition, a weak association of IDL (d = 1.006-I ,019 g/ml) and light LDL (d < 1.031 g/ml) with the severity of CAD could also be demonstrated. The discrepancy between these findings and previous studies, where differences in LDL-particle size between cases and healthy controls were no longer significant after adjustment for triglycerides, is easily explained by two factors: (1) There was no need to adjust for triglycerides, as TG were similar in all groups. (2) We used concentrations of ultracentrifugally prepared LDL subfractions, which can be precisely measured, rather than LDL sizes from gradient gels to assess the atherogenicity of LDL subclasses.
Atherosclerosis X, Montreal, October I994
Monday 10 October 1994: Poster Abstracts Riskfactors
code and plasma cholesterol with 55 control subjects recruited from the same source. Blood pressure (mean f SE) was higher in cases than in controls (138 f 4.0/84 f 1.3 vs 130 + 3.H7’8.4f 2.0 mmHg, P < 0.03). Only two subjects in each group were current cigarette smokers. Fasting plasma lipids and apoproteins, including Lp(a), and post-prandial triglyceride responses to a standard test meal did not differ in cases and controls. Glucose and insulin postprandial responses were greater in CHD subjects (P
We investigated the association of LDL subclass and coronary risk factors with CAD in 217 subjects (170 M, 47 I!), aged 2382 years. The presence of CAD was defined angiographically as >75% stenosis of major coronary arteries. LDL subclasses were classified into small LDL and normal LDL, based on LDL particle size by non-denaturing 2.5-168 polyacrylamide gradient gel electrophoresis. Gels were stained with Oil Red 0 and LDL migration distances were measured by densitometry. Plasma lipid levels were measured and diabetes mellitus, obesity, hypertension and smoking were also examined. Small LDL were associated with higher plasma levels of triglyceride, LDL-C and apo B than normal LDL (172f67 vs 124f50, 124+44 vs 112+35, 113rt27 vs 96+24mg/dl) and with high body mass index and hypertension. They were found together with lower plasma levels of HDL-C and apo A-I than normal LDL (36fll vs 49f12, 104f26 vs 119f27mg/dl), but plasma levels of total cholesterol were not different between the two groups. The prevalence of CAD in small LDL was significantly higher than in normal LDL (85.9% vs 62.9%). Patients with small LDL were more likely to have 2- and 3-vessel disease compared with l-vessel disease (50% vs 42.9%). These results suggest that small LDL are significantly associated with high plasma triglyceride and low HDL-C and might be a discriminator for CAD in normocholesterolemia. 1101 m,
Insulin resistance in smokers is a function of smoking habits Attvall S, Taskinen M-R*, Smith U, Dept. oflntemal
Medicine, Sahlgrenska Univ. Hospital, S-413 45 Giiteborg, Sweden; *3rd Dept. of Internal Medicine, Univ. of Helsinki, Helsinki, Finland
Smokers exhibit several metabolic risk factors for cardiovascular disease (CVD) which may be related to smoking-induced insulin resistance. The objective of this study was to investigate the relationships between smoking habits, degree of insulin resistance and the various manifestations of the insulin resistance syndrome (IRS) in middle-aged men. The participants were 57 healthy normal-weight (BMI mean 23.7 f SD 2.0) chronic smokers (mean nicotine consumption per day 23.3 zb 10.9 mg). 40-60 years of age (mean 48.9 f 6.3 years).
A 2-h euglycemic hyperinsulinemic (1.0 mU/kg/min) clamp was performed to determine degree of insulin sensitivity, measured as amount of glucose infused per kg lean body mass and minute (glucose infusion rate, GIR). Smoking habits were related to GIR and the various biochemical manifestations of IRS. Daily nicotine consumption correlated with GIR as well as various markers of IRS such as fasting insulin values, HDL-C, triglycerides and plasminogen activator inhibitor 1 (PAI-1) activity. Smoking habits, independent of GIR, were also related to total and LDL cholesterol. In a multiple linear regression analysis, considering the effects of antbropometric data, age and alcohol consumption, only smoking habits and % body fat were independently related to GIR. Smokers are insulin resistant and exhibit several characteristics of IRS which may explain the increased CVD in smokers. Degree of insulin resistance as well as IRS are functions of smoking habits. However, the increased cholesterol levels seen in smokers are not related to degree of insulin resistance. Hydrogen- and lipo-peroxides in acute smokinginduced platelet hyperactivity Blache D, INSERM, Lab. de Biochimie des Lipoproteines, Univ.
1
de Bourgogne, Dijon, France
Previous studies established that blood platelets develop a hyperaggregability after acute cigarette smoking. We investigated whether changes in plasma oxidative properties could occur after smoking and whether such changes could be responsible for this enhanced platelet activity. In the present work, we report that platelets from non-smokers become hyperactive by incubating them with plasma prepared from blood of smokers obtained 10 min after smoking. This effect was not observed with presmoking plasma and could be inhibited in vitro by adding either catalase or reduced glutathione plus peroxidase to plasma or the antioxidant BHT to platelets before incubation. Nicotine added to presmoking plasma in the concentration range found in smokers did not reproduce the platelet activation effect and d-tubocurarine, a nicotinic receptor antagonist, did not inhibit the enhanced response of platelets to aggregation induced by post-smoking plasma. By chemical analysis in post-smoking plasma, we found a decrease in vitamin E (188, P < 0.01) and an increase in conjugated dienes (35510,P < O.OOl), thiobarbituric acid reactive substances (TBARS, 23%, P< 0.02) and free fatty acids (FFA, 40%, P < 0.005). By means of its specific reaction with N,N-dimethylp-phenylenediamine, the FFA fraction was shown to be peroxidized to a higher extent in post-smoking than in pre-smoking plasma. This peroxidized FPA fraction enhanced the thrombininduced aggregation of platelets from non-smokers. The increased response was inhibited either when the peroxidized FFA fractions were isolated from plasma treated with reduced glutathione and peroxidase or by pretreatment of the platelets with BHT. The results indicate that acute smoking exerts an oxidative stress on plasma lipids which enhances platelet aggregability. In addition to the lipoprotein modification, these changes could explain the reported accelerated atherothrombogenesis in smokers which might benefit from antioxidant supplementation. Effect of the progestogen medrogestone on plasma lipoprotein levels in postmenopausal women using conjugated estrogens: an open, randomized comparative study f&vets I.&&& van der Mooren MJ*, Buytenhek M, Gaubius
1
Laboratom PC-TN0 Zernikedreef 9, 2333 CK Leiden, The Netherlands; **Univ.Hospital Ntjmegen Sint Radboud, Nijmegen, The Netherlands
The objective of this study was to assess the effect of the pro-
Atherosclerosis X, Montreal, October 1994
Monday 10 October 1994: Poster Abstracts Risk factors gestogen medrogestone on conjugated estrogen (CE)- induced changes in plasma lipoprotein levels. Plasma lipid and lipoprotein levels were determined in 114 postmenopausal hysterectomized women aged 49-64 years before and during 13 cycles of continuous oral treatment with 0.625 mg of CEs. The women were randomly assigned to two groups receiving either CEs (group I; n = 55) or CEs plus 5 mg of medrogestone orally during the last 12 days of each 28-day cycle (group 2; n = 59). Gradient ultracentrifugation was used in all assessments At cycles 3, 6, and 13, HDb-C levels were increased from baseline by 40%, 44% and 458, respectively, in group 1 and by 27%, 34% and 30%, respectively, in group 2 (P < 0.001 at all assessments; difference between groups not significant). HDL3-C was increased by 6%, 6% and 7% in the respective cycles in group 1 (P < 0.001 at all assessments), but no change in HDL3 was found in group 2 (difference between groups P = 0.011 only at cycle 3). Medrogestone had no effect on the estrogen-induced increases in triglycerides or apo A-I, or on the decreases in LDLC and apo B; neither hormone significantly affected VLDL-C or Lp(a) levels. Conclusion: medrogestone did not adversely affect changes in lipoprotein levels evoked by conjugated estrogens in postmenopausal women. 1
Changes in coronary heart disease risk factors associated with menopause, and influence of substitutive hormone therapy
vtlle J, Marecaux N, Isorez D, Zylberberg G, Fruchart JC, Amouyel P, Inst. Pasteur de Lille, I rue du Pr Calmette, 59019 Lille, France The relationships between menopause and cardiovascular risk factors, and the effect of progestin alone or in combination with estrogen on these risk factors, were analyzed in a sample of French women. We studied 5555 consecutive women, aged between 40 and 65 years, attending a systematic health check-up. All biological measurements were performed at a central laboratory. The effects of menopause on cardiovascular risk factors were determined in 3332 women between 40 and 65 years of age (premenopausal n = 1945, postmenopausal n = 1387) none of whom was receiving hormone replacement therapy. The effect of hormone replacement therapy was assessed in an additional group of 472 peri- and postmenopausal women. Menopause was associated with higher levels of serum TC (6.4 vs 5.7 mmolil; P < O.OOOl), triglycerides (1.2 vs 1 .O mmol/l; P < O.OOl), apo B (1.3 vs 1.1 g/l; P < 0.0001). apo A-l (1.9 vs and diastolic blood pressure (79.7 vs 1.8 g/l; P < 0.0001) 75.3 mmHg; P < 0.05). These effects were independent of the classical confounding variables, Perimenopausal women treated with progestin alone (n = 96) were compared to p&menopausal women not using hormonal replacement therapy (n = 3 12). There were no statistically significant differences in the levels of biological parameters between the two groups. In contrast, postmenopausal women using a combination of estrogen and progestin (n = 376) had significantly lower levels of serum cholesterol (6.1 vs 6.4 mmol/l; P< O.OOOl), triglycerides (1.0 vs 1.2 mmohl; P < O.OOOl), apo B (1.2 vs 1.3 g/l; P < 0.0001). systolic (131.7 vs 137.9 mmHg; P
pig
29
Rationale and design of a large mu&enter study of CVD in familial hyperchobzsterolemic (FH) patients: HALF (homocysteine, atherosclerosis, llpiis and FH)
WittekQ&M&, Knipscheer HC, Btiller HR. Kastelein JJP, Centre for Vascular Medicine, Academic Medical Centre, Amsterdam, The Netherlands There is substantial variation in the onset and severity of CVD symptoms among FH patients, even with identical LDL-receptor gene defects, Hypercholesterolemia per se cannot explain the appearance of CVD in a proportion of FH patients: additional atherogenic risk factors must contribute to the clinical manifestations In view of recent interest in novel risk factors, we initiated a multicenter investigation to study their impact on atherosclerosis. HALF is both a cross-sectional and prospective cohort study with a followup period of 3 years. 150 FH patients with clinically manifest CVD will be selected and an equal number of FH patients free of CVD, matched for age and sex, will be included. Baseline data such as homocysteine metabolism, lipoprotein subfractionation and oxidative resistance, Lp(a), endothelin, heat shock proteins, carbohydrate metabolism and insulin resistance, coagulation, tibrinolysis, blood pressure regulation and intimamedia wall thickness will be obtained from all patients. After analysis at baseline, patients will be followed up to study the relationship between these risk factors and the development of CVD. In a pilot study, profound differences with respect to fibrinolysis (D-dimer; P < 0.02, PA1 + @‘A; P < 0.04), homocysteine (P < 0.05) and Lp(a) (P < 0.01) were discovered between 12 FH patients with and without CVD. These preliminary results suggest that HALF can contribute to a better understanding of the interaction between additional risk factors and LDL-C in FH-patients and might lead to the identification of new factors that either damage or protect the vessel wall during atherogenesis.
11061
Small dense LDL are a major determinant for the severity of angiographically assessed CAD, even in groups,with simv triglyceride levels Berg A , Halle M’, Rensing UFE2, Roskamm
Med. Universitiitsklinik, D-79106 Freiburg; ‘Benedikt Kreutz Rehabilitationszentrum ,fiir Herz- und Kreisla@ranke, D-79189 Bad Krozingen, Germany
m1
In 314 patients who underwent coronary angiography, the concentration and composition of six LDL-subfractions were determined by preparative ultracentrifugation. The patients were grouped into four categories (O-3) according to the number of vessels with stenosis >50% (diameter). Interestingly, there were no differences in serum triglyceride (TG) levels between these groups, possibly because patients with TG > 300 were excluded from the study. Despite similar serum TGs, levels of small-dense LDL (d > 1.040 g/ml) were significantly higher in patients with severe coronary artery disease (CAD). This finding was confirmed using two other angiographic scores (Kaltenbach, Friesinger) of severity of atherosclerosis and stenosis. Both correlated positively and significantly with the concentration of small-dense LDL. In addition, a weak association of IDL (d = 1.006-I ,019 g/ml) and light LDL (d < 1.031 g/ml) with the severity of CAD could also be demonstrated. The discrepancy between these findings and previous studies, where differences in LDL-particle size between cases and healthy controls were no longer significant after adjustment for triglycerides, is easily explained by two factors: (1) There was no need to adjust for triglycerides, as TG were similar in all groups. (2) We used concentrations of ultracentrifugally prepared LDL subfractions, which can be precisely measured, rather than LDL sizes from gradient gels to assess the atherogenicity of LDL subclasses.
Atherosclerosis X, Montreal, October I994