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Open AccessJournal ArticleDOI

Association of coronary atherosclerosis with hyperapobetalipoproteinemia [increased protein but normal cholesterol levels in human plasma low density (beta) lipoproteins].

TLDR
Results indicate that not only does LDL B better separate coronary and noncoronary groups than other lipid parameters studied, but also, among those with coronary artery disease, there exists a group with normal LDL cholesterol but with levels of LDL B protein similar to those observed in type II hyperlipoproteinemia.
Abstract
Most patients with coronary artery disease do not have elevated plasma or low density lipoprotein (LDL) cholesterol. To test whether the protein moiety of LDL, LDL B, might be a parameter to identify ischemic heart disease, the plasma cholesterol, triglyceride, LDL cholesterol, and LDL B were measured in 100 consecutive patients undergoing cardiac catheterization. On the basis of coronary angiography, these patients were divided into two groups: group I, 31 patients without, and group II, 59 patients with significant coronary artery disease. Although cholesterol, triglyceride, and LDL cholesterol levels were all significantly higher in group II, discriminant analysis indicated that LDL B concentrations most clearly separated the two groups. In group I (noncoronary), LDL B was 82 +/- 22 mg/100 ml, whereas in group II, LDL B was 118 +/- 22 mg/100 ml. The B protein level in group I was similar to other normal groups studied (35 asymptomatic male physicians, 83 +/- 11 mg/100 ml; 90 normolipidemic medical students, 72 +/- 17 mg/100 ml). The results therefore indicate that not only does LDL B better separate coronary and noncoronary groups than other lipid parameters studied, but also, among those with coronary artery disease, there exists a group with normal LDL cholesterol but with levels of LDL B protein similar to those observed in type II hyperlipoproteinemia. The explanation for the altered LDL composition observed in this group remains to be elucidated.

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Journal ArticleDOI

Regression of Coronary Artery Disease as a Result of Intensive Lipid-Lowering Therapy in Men with High Levels of Apolipoprotein B

TL;DR: In men with coronary artery disease who were at high risk for cardiovascular events, intensive lipid-lowering therapy reduced the frequency of progression of coronary lesions, increased the frequencyof regression, and reduced the incidence of cardiovascular events.
Journal ArticleDOI

Low-Density Lipoprotein Subclass Patterns and Risk of Myocardial Infarction

TL;DR: The association of low-density lipoprotein (LDL) subclass patterns with coronary heart disease was investigated in a case-control study of nonfatal myocardial infarction and multivariate logistic regression analyses showed that both high-density cholesterol and triglyceride levels contributed to the risk associated with the small, dense LDL subclass pattern.
Journal ArticleDOI

Prevention of coronary heart disease in clinical practice: recommendations of the Second Joint Task Force of European and other Societies on Coronary Prevention.

TL;DR: The Task Force has summarized the most important clinical issues on coronary heart disease prevention on which there is good agreement in order to give cardiologists and physicians, and other health care professionals, the best possible advice to facilitate their work on coronaryHeart disease prevention.
Journal ArticleDOI

Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease risk.

TL;DR: The proposed genetic locus responsible for LDL subclass phenotypes also results in an atherogenic lipoprotein phenotype, found to be closely associated with variations in plasma levels of other lipid, lipop protein, and apolipoprotein measurements.
Journal ArticleDOI

Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease.

TL;DR: Although body fat distribution is now considered as a more significant risk factor for CVD and related death rate than obesity per se, further research is clearly needed to identify the determinants of bodyfat distribution and the causal mechanisms involved in the metabolic alterations.
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