Predictable changes in low density lipoprotein composition after acute myocardial infarction

Sniderman, Allan D.; Teng, Babie

doi:10.1016/0021-9150(77)90046-6

Cited by 12 publications

(5 citation statements)

References 15 publications

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“…In normal plasma, small amounts of an IDL (density 1.006-1.019 g/ml) would be present in the fraction of density 1.006-1.063 g/ml. We have previously investigated the amount of apoB in IDL in a similar group of patients and found that it contributed minimally to the B protein in the 1.006-1.063 g/ml range (27 (31,32), and after myocardial infarction (33). The abnormal LDL composition observed in this study was not due to the effect of lipid-lowering medication or recent myocardial infarction.…”

supporting

confidence: 50%

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

Sniderman

Shapiro

Marpole

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

506

108

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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 atients with significant coronary artery disease. Although clolesterol, 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 i 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 i 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.Atherosclerotic coronary artery disease is a major cause of morbidity and mortality in industrialized countries. The importance of plasma levels of certain lipids and lipoproteins in the pathogenesis of atherosclerosis has been supported by a number of epidemiologic and genetic studies. Briefly, increased levels of total plasma cholesterol and the major cholesterolcarrying lipoproteins, low density (/) lipoproteins (LDL), are associated with an increased risk of developing coronary artery disease (1, 2). Whether an elevated level of plasma triglycerides is an independent risk factor for coronary artery disease is controversial; conflicting evidence has been presented in both epidemiological surveys (3, 4) and in studies in kindreds with familial hypertriglyceridemia (5, 6). A low concentration of another lipoprotein, high density (a) lipoproteins (HDL), appears to be a separate risk factor for coronary artery disease (7), whereas high levels of HDL may have a protective effect (8).Many patients who develop coronary artery disease have normal plasma lipid and lipoprotein cholesterol levels. The presence of disease in some of these patients may be related to the effect of other risk factors such as hypertension and cigarette smoking. Nevertheless, the presence of coronary artery disease in a significant number of these patients remains unexplained.A high correlation between total plasma and LDL cholesterol levels has been found, and it has been assumed that the measurement of LDL by determining its cholesterol content provided an accurate assessment of the concentrat...

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supporting

confidence: 50%

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

Sniderman

Shapiro

Marpole

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

506

108

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“…Carlson (23) has suggested that in certain hyperlipidemic states, there is an inverse relationship between LDL cholesterol and triglyceride, an observation supported by the work of Myers et al (24). As well, in a recent study of changes in LDL composition after myocardial infarction, it was shown that the cholesterol ester and triglyceride fractions of LDL varied reciprocally and changed predictably with differences in absolute concentration (25). All these observations are consistent with a pseudomicellar model of LDL in which the surface components-B protein, free cholesterol, and phospholipids-are present in fixed amounts, but the interior shell of cholesterol ester and triglyceride are present in an inverse relation.…”

Section: Discussionsupporting

confidence: 52%

Low-Density Lipoprotein

2008

Encyclopedia of Obesity

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which cholesterol returns to the splanchnic bed from peripheral tissues are not well understood. To study this phenomenon in fasting man, lipoproteins were isolated from plasma obtained from hepatic vein and aorta. Cholesterol content of each lipoprotein class was determined and arteriovenous (AV) differenices could be calculated for each patient. The results in the first 24 patients indicated splanchnic secretion of very low density lipoprotein cholesterol (mean AV difference-3 mg/100 ml, P < 0.01), but not significanit AV difference for total cholesterol, high density lipoprotein cholesterol, or low denisity lipoprotein (LDL) B protein. In contrast, for LDL (d 1.006-1.063 g/mil), there was significant uptake of cholesterol across the AN' bed +8 mg/100 ml, P < 0.0002). In a further 15 patients, similar samiples were obtained and intermediate density lipoprotein isolated at d 1.006-1.019 g/ml and LDL at 1.019-1.063 g/ml. The AV difference previously noted could now be localized to the 1.019-1.063 cholesterol ester moiety (+8 mg/100 ml, P < 0.0005). In the final 14 patients, the LDL cholesterol AV difference was again confirmed and shown to be unrelated to heparin. As well, there was secretion of triglyceride in the hepatic vein LDL. These quantitative data obtained in man raise the possibility that LDL rather than high density lipoprotein transports cholesterol ester to the splanchnic bed.

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“…Since then, a wide range of alterations in serum lipids has been reported associated with hospitalization for an ACS. For example, Sniderman and Teng (10) found that LDL-C decreased by 18% to 53% in 6 patients with myocardial infarction (MI) between Day 1 and Days 7 to 9, but LDL-C increased by 13% to 32% in 3 other patients.…”

mentioning

confidence: 98%