Lipoprotein (a) and coronary heart disease

Maher, Vincent; Brown, Bruce

doi:10.1097/00041433-199508000-00007

Cited by 124 publications

(49 citation statements)

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“…These can explain partially the impairment of endothelial-dependent arterial dilation in people with the e4 allele. Lp(a) is an independent risk factor for atherosclerotic vascular disease [25,26]. Many prospective studies have shown that excess Lp(a) is associated with premature coronary atherosclerosis and risk of cardiovascular disease [27,28].…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein e4 allele and endothelium-dependent arterial dilation in Type 2 diabetes mellitus without angiopathy

Guang-da

Yu-hua

2003

Diabetologia

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Aims/hypothesis. Several studies have suggested a predisposing role of the e4 allele of apolipoprotein E (ApoE) in the development of atherosclerosis and cardiovascular disease in Type 2 diabetes. Therefore, we hypothesized that the e4 allele is also a risk factor for endothelial dysfunction. We attempted to assess whether Apo e4 allele is associated with endothelial dysfunction in the early stage of Type 2 diabetes. Methods. We selected 255 Chinese Han Type 2 diabtetic men without angiopathy. PCR or allele-specific oligonucleotide probes were used to analyse ApoE genotypes, and high resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperaemia and after sublingual glyceryltrinitrate. Results. The flow-mediated arterial dilation among the subjects with e4/3 or e4/4 was 3.14±0.32%, which was lower than that in subjects with e2/2 or e3/2 (4.04±0.30%) (p=0.038). The baseline vessel size, glyceryltrinitrate-induced arterial dilation and baseline flow were not different among different ApoE genotypes. On univariate analysis, reduced flow-mediated arterial dilation was related to total cholesterol, LDL, lipoprotein(a) [Lp(a)], high blood pressure, older age, family history of premature vascular disease, larger vessel size, cigarette smoking, duration of diabetes and e4 allele (p<0.05). By multiple stepwise regression analysis, reduced flow-mediated arterial dilation was associated with cigarette smoking, LDL, Lp(a), and e4 allele (p<0.01). Conclusion/interpretation. Apo e4 allele is associated with impairment of endothelium-dependent arterial dilation in the early stage of Type 2 diabetes. [Diabetologia (2003) 46:514-519]

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Section: Discussionmentioning

confidence: 99%

Apolipoprotein e4 allele and endothelium-dependent arterial dilation in Type 2 diabetes mellitus without angiopathy

Guang-da

Yu-hua

2003

Diabetologia

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“…These hypothetical cooperative effects of Lp(a) and LDL in lesions could be related to the observed additive effect of these 2 apoB lipoproteins as risk factors for atherosclerotic disease. 41 …”

Section: Discussionmentioning

confidence: 99%

Proteoglycans Contribution to Association of Lp(a) and LDL With Smooth Muscle Cell Extracellular Matrix

Lundstam

Hurt-Camejo

Olsson

et al. 1999

ATVB

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Abstract-Lp(a) interference with fibrinolysis could contribute to atherothrombosis. Additionally, accumulation of Lp(a) and LDLs, could lead to cholesterol deposition and foam cell formation in atherogenesis. The interactions between Lp(a) and LDL could cause their entrapment in the extracellular matrix of lesions. We found that association of Lp(a) with matrix secreted by cultured human arterial smooth muscle cells increased 2 to 3 times the subsequent specific binding of radioactive LDL. Chondroitin sulfate proteoglycans seem responsible for formation of the specific matrix-Lp(a) and matrix-LDL aggregates. The proteoglycans appeared also to participate in a cooperative increase of radioactive LDL binding to matrix pretreated with Lp(a). In the matrix preincubated with LDL, Ϸ50% of the additional lipoprotein was bound by ionic interactions. In the matrix preincubated with Lp(a), 20% of the additional LDL was held by ionic bonds, and the rest was held by strong nonionic associations. Binding analysis in physiological solutions confirmed that chondroitin sulfate-rich proteoglycans from the smooth muscle cell matrix have a high affinity for Lp(a) and LDL. The results provide an explanation to the observed localization of Lp(a) and LDL in the extracellular matrix of arterial lesions and suggest a mechanism for their cooperative accumulation there.

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“…It has been reported that the plasma levels of Lp(a) as well as the size of apo(a) are independent risk factors for CAD and strokes [69][70][71][72][73][74][75][76] . Several atherogenic properties of Lp(a) have been clarified 78,79) .…”

Section: ) Lp(a)mentioning

confidence: 99%