Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease

Abstract

The prevalence of abnormalities of lipoprotein cholesterol and apolipoproteins A-I and B and lipoprotein (a) [Lp(a)] was determined in 321 men (mean age 50 +/- 7 years) with angiographically documented coronary artery disease and compared with that in 901 control subjects from the Framingham Offspring Study (mean age 49 +/- 6 years) who were clinically free of coronary artery disease. After correction for sampling in hospital, beta-adrenergic medication use and effects of diet, patients had significantly higher cholesterol levels (224 +/- 53 vs. 214 +/- 36 mg/dl), triglycerides (189 +/- 95 vs. 141 +/- 104 mg/dl), low density lipoprotein (LDL) cholesterol (156 +/- 51 vs. 138 +/- 33 mg/dl), apolipoprotein B (131 +/- 37 vs. 108 +/- 33 mg/dl) and Lp(a) levels (19.9 +/- 19 vs. 14.9 +/- 17.5 mg/dl). They also had significantly lower high density lipoprotein (HDL) cholesterol (36 +/- 11 vs. 45 +/- 12 mg/dl) and apolipoprotein A-I levels (114 +/- 26 vs. 136 +/- 32 mg/dl) (all p less than 0.005). On the basis of Lipid Research Clinic 90th percentile values for triglycerides and LDL cholesterol and 10th percentile values for HDL cholesterol, the most frequent dyslipidemias were low HDL cholesterol alone (19.3% vs. 4.4%), elevated LDL cholesterol (12.1% vs. 9%), hypertriglyceridemia with low HDL cholesterol (9.7% vs. 4.2%), hypertriglyceridemia and elevated LDL cholesterol with low HDL cholesterol (3.4% vs. 0.2%) and Lp(a) excess (15.8% vs. 10%) in patients versus control subjects, respectively (p less than 0.05). Stepwise discriminant analysis indicates that smoking, hypertension, decreased apolipoprotein A-I, increased apolipoprotein B, increased Lp(a) and diabetes are all significant (p less than 0.05) factors in descending order of importance in distinguishing patients with coronary artery disease from normal control subjects. Not applying a correction for beta-adrenergic blocking agents, sampling bias and diet effects leads to a serious underestimation of the prevalence of LDL abnormalities and an overestimation of HDL abnormalities in patients with coronary artery disease. However, 35% of patients had a total cholesterol level less than 200 mg/dl after correction; of those patients, 73% had an HDL cholesterol level less than 35 mg/dl.

Hydrogenation impairs the hypolipidemic effect of corn oil in humans. Hydrogenation, trans fatty acids, and plasma lipids.

“…15 The PROC MEANS procedure was used for paired / test analysis to assess the statistical significance of dietary effects on biochemical variations. Since responses in men and women were similar and since paired t test analysis was used, both groups were pooled.…”

“…Lipoprotein(a) [Lp(a)] was quantified using an enzyme-linked assay with a polyclonal antibody as the first antibody and a monoclonal antibody that does not cross-react with plasminogen as the second antibody (Terumo Medical Corp., Elkton, Md.). 15 …”

Apolipoprotein B, ratio of total cholesterol to HDL-C, and blood pressure in abdominally obese white and black American women

“…12 Thus, the ability to adequately identify individuals at high risk of CVD solely on the basis of TC/HDL is at variance with evidence showing that up to 50% of subjects with CVD may have clinically acceptable values for these lipids. [13][14][15][16][17] Data also indicates that patients undergoing cholesterol-lowering treatments who achieve a significant decrease in low-density liproprotein-cholesterol (LDL-C) levels nonetheless carry risk for CVD. 18 Using polyacrylamide gel electrophoresis, data further suggest that patients with visceral adiposity often possess greater proportion of small, dense, cholesterol depleted LDL-C particles than total cholesterol and LDL-C. 19 Indeed, it has been estimated that patients with visceral obesity have 15-20% higher than normal plasma ApoB levels despite having normal total cholesterol and LDL-C. 13 Thus, ApoB concentration in abdominally obese subjects could be a more potent atherogenic marker for predicting CVD than conventional lipids.…”

Inflammation and cardiovascular disease: is abdominal obesity the missing link?

“…1,2 Although several lipid-lowering trials have clearly established the importance of targeting LDLcholesterol in order to reduce the risk of a first or recurrent coronary heart disease (CHD) event, [3][4][5][6][7][8][9] it has become evident that the relative risk reduction achieved by lipid-lowering therapy only reached about 30%, a finding that clearly indicates that high-risk individuals treated with lipid-lowering drugs do remain at high absolute risk for a first or recurrent CHD event. Furthermore, a substantial proportion of CHD patients do not have LDL-cholesterol levels that are different from the healthy asymptomatic population, 10,11 suggesting that there is a need to go beyond the lipid hypothesis and classical risk factors in order to properly assess and manage a significant proportion of high-risk individuals if we aim at achieving optimal clinical benefits.…”