Low-density lipoprotein subclass patterns and risk of myocardial infarction

Austin, Melissa A.

doi:10.1001/jama.260.13.1917

Cited by 759 publications

(673 citation statements)

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“…But many studies have shown that factors other than total cholesterol and LDL-C must be considered when evaluating coronary artery disease (CAD) risks [12]. Recent studies have shown that the size of LDL particle is more important as compared to LDL-C concentration in atherogenesis [13,14]. In routine clinical practice estimation of LDL particle size is not applicable due to complicated methodology [15].…”

Section: Discussionmentioning

confidence: 99%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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Acute myocardial Infarction is one of the major causes of morbidity & mortality in world and atherosclerosis is the major cause of ischemic heart disease. In order to determine the better clinical marker of atherosclerosis, we estimated serum low-density lipoprotein (LDL-C) and high sensitivity C-reactive protein (hsCRP). Hundred patients of myocardial infarction and 100 controls irrespective of age and sex were studied for these parameters over a period of 2 years. The statistical analysis showed that the serum hsCRP was significantly raised in myocardial infarction cases than controls (P \ 0.01) but LDL-C was not (P [ 0.05). We conclude that the serum hsCRP has better predictive value for risk of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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“…The most common way to separate LDL subclasses has been the use of gradient gel electrophoresis (GGE). Small dense LDL is defined as a particle with a mean diameter of the major LDL-peak less than 25.5 nm and it is the major component in pattern B, whereas pattern A consists of LDL particles with a greater diameter [100]. Small dense LDL differs from large LDL with respect to chemical composition and binding affinity to proteoglycans.…”

Section: Is Postprandial Lipidemia a Hazard?mentioning

confidence: 99%

“…A several set of observations witnesses that the reduced LDL size is linked to the increased risk of CHD [116,117,118,119]. Both LDL size and the number of particles seems to increase synergistically the risk of CHD [120,121].…”

Section: Why Is Small Dense Ldl Highly Atherogenic?mentioning

confidence: 99%

Diabetic dyslipidaemia: from basic research to clinical practice*

2003

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The recognition that the increase of plasma triglyceride rich lipoproteins (TRLs) is associated with multiple alterations of other lipoproteins species that are potentially atherogenic has expanded the picture of diabetic dyslipidaemia. The discovery of heterogeneity within major lipoprotein classes VLDL, LDL and HDL opened new avenues to reveal the specific pertubations of diabetic dyslipidaemia. The increase of large VLDL 1 particles in Type 2 diabetes initiates a sequence of events that generates atherogenic remnants, small dense LDL and small dense HDL particles. Together these components comprise the atherogenic lipid triad. Notably the malignant nature of diabetic dyslipidaemia is not completely shown by the lipid measures used in clinical practice. The key question is what are the mechanisms behind the increase of VLDL 1 particles in diabetic dyslipidaemia? Despite the advances of recent years, our understanding of VLDL assembly and secretion is still surprisingly incomplete. To date it is still unclear how the liver is able to regulate the amount of triglycerides incorporated into VLDL particles to produce either VLDL 1 or VLDL 2 particles. The current evidence suggests that the machinery driving VLDL assembly in the liver includes (i) low insulin signalling via PI-3 kinase pathway that enhances lipid accumulation into "nascent" VLDL particles (ii) up-regulation of SREBP-1C that stimulates de novo lipogenesis and (iii) excess availability of "polar molecules" in hepatocytes that stabilizes apo B 100. Recent data suggest that all these steps could be fundamentally altered in Type 2 diabetes explaining the overproduction of VLDL apo B as well as the ability of insulin to suppress VLDL 1 apo B production in Type 2 diabetes.Recent discoveries have established the transcription factors including PPARs, SREBP-1 and LXRs as the key regulators of lipid assembly in the liver. These observations suggest these factors as a new target to tailor more efficient drugs to treat diabetic dyslipidaemia. [Diabetologia (2003) 46:733-749]

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“…Analyses carried out in a case-control study of men and women with myocardial infarction survivors indicated a three-fold increased risk of acute myocardial ~nf~rction associated with subrilass pattern B [Austin et al, 1988a). This relationship was recently confirmed in a study of subjects with coronary disease documented by angiography [Campos et al, 1992).…”

mentioning

confidence: 83%

Lipoprotein subclasses in genetic studies: The Berkeley data set

Krauss

Williams

Blanche

et al. 1993

Genetic Epidemiology

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In conjunction with a study examining the inheritance of LDL subclass patterns in a healthy population, measurements of lipids, lipoproteins, and lipoprotein subclasses were performed in 301 individuals in 27 kindreds. Questionnaires were used to obtain information on use of medications, hormones, cigarettes, and alcohol. Laboratory data from this study (the Berkeley data set) include measurements of LDL and HDL size subclasses by nondenaturing gradient gel electrophoresis, and measurement of apolipoprotein A‐I by radial immunodiffusion. © 1993 Wiley‐Liss, Inc.

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Low-density lipoprotein subclass patterns and risk of myocardial infarction

Cited by 759 publications

References 0 publications

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Diabetic dyslipidaemia: from basic research to clinical practice*

Lipoprotein subclasses in genetic studies: The Berkeley data set

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