Low and high density lipoprotein metabolism in atherothrombotic brain infarction.

Alam, Rita; Yatsu, Frank M.; Kasturi, R; Bui, G.

doi:10.1161/01.str.23.9.1265

Cited by 13 publications

(4 citation statements)

References 42 publications

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“…Observational studies found an association between hypercholesterolaemia and carotid stenosis[2,3,4]. However, elevated plasma cholesterol has been inconsistently associated with brain infarction (BI)[5,6,7,8,9].…”

Section: Introductionmentioning

confidence: 99%

Blood Lipids in Brain Infarction Subtypes

Amarenco

Labreuche²,

Elbaz³

et al. 2006

Cerebrovasc Dis

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Background: Little is known about the relationship between hypercholesterolaemia and specific aetiological subtypes of brain infarction (BI). Methods: In a cross-sectional study of 492 pairs of patients with a BI proven by MRI and matched hospital controls, we determined the blood levels of triglycerides, total, HDL and LDL cholesterol, and apolipoprotein A₁ and B, in the same centralized laboratory. We performed aetiological BI subtype classification. Results: Except for triglycerides, the risk of BI increased continuously with the lipid levels, without any heterogeneity between the main BI subtypes or the group on lipid-lowering therapy. The adjusted odds ratio per standard deviation in LDL cholesterol (0.93 mmol/l) was 1.74 (95% confidence interval, 1.02–2.98) in atherothrombotic strokes (n = 109) and 2.71 (95% confidence interval, 1.60–4.55) in lacunar strokes (n = 105). Eighty percent of patients were above the ATP-III guideline threshold LDL cholesterol of 2.59 mmol/l (100 mg/dl), with a major contribution of both atherothrombotic and lacunar stroke subtypes to this group. Conclusions: These findings suggest that blood lipids, particularly total and LDL cholesterol levels, are associated with all subtypes of BI, and that LDL above 2.59 mmol/l is highly prevalent.

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Section: Introductionmentioning

confidence: 99%

Blood Lipids in Brain Infarction Subtypes

Amarenco

Labreuche²,

Elbaz³

et al. 2006

Cerebrovasc Dis

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“…[24] show that the majority of the studies reviewed, namely, 23 of 26 assess ing lipid abnormalities in ABls, demonstrate a correlation between cholesterol and ABls, although techniques, crite ria and study design differed substantially. Whether the dynamic process of plaque formation at the carotid bifur cation is due to lipid or coagulation/plalelet aggregation defects, Grolta et al [25] reported a significant increase in carotid stenosis of 2:23% over 30 m on th s was associated with a significant increase in LD L. In addition, evaluation of the dynamic aspects of L D L and IID L metabolism by assessing in vivo metabolism o f autologously labelled lipoproteins demonstrated a slower catabolism of LD L and a faster one for I IDL, suggesting that increased resi dent lime in serum combined with enhanced catabolism of H D L is associated with ABls [26], In addition to metabolic parameters supporting the role o f impaired or abnormal cholesterol transport in ABls, altered gene function for proteins involved in cho lesterol metabolism may likely play an important role in determining ABI susceptibility. For example, in a study of gene polymorphism o f the major apoprotein of I IDL, Kasturi et al [27] reported on the occurrence of restric tion fragment length polymorphism (RFLP) of the tandemly arranged apoproteins of A l, ( 'III, and AIV on the long arm o f chromosome 11.…”

Section: Investigations On Abi: Multiple Factorsmentioning

confidence: 97%

Pathogenesis of Atherothrombotic Brain Infarction: Role of Lipids

Yatsu¹,

Kataoka²

1993

Cerebrovasc Dis

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Atherothrombotic brain infarction (ABI) is the most common cause of strokes in the industrialized world and the primary pathology is atherosclerosis. As with coronary heart and peripheral vascular diseases, ABI appears to be provoked by abnormal cholesterol metabolism and characterized by increased proliferation of smooth muscle cells of arteries and an inflammatory response in atheromas with increased inflammatory cells including macrophages. Abnormal genes regulating cholesterol, such as those for LDL, HDL and VLDL plus those affecting vasomotor activity such as angiotensin-converting enzyme and endothelin appear to play a role. Efforts to reduce serum cholesterol, as for the prevention of coronary disease, are a reasonable approach to minimize ABIs.

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“…A role of lipoprotein(a) (lp(a)) as an ischemic stroke biomarker and as a predictor of recurrence has also been suggested [122]. Studies have shown an inverse relationship between high-density lipoprotein cholesterol (HDLc) and ischemic stroke, particularly in atherothrombotic subtype [123,124], wherein low HDLc concentrations are associated with increased stroke severity and poor clinical outcome [42]. It is of interest to consider the values of HDLc, along with those of LDLc, in order to better predict the risk of stroke.…”

Section: Lipids and Lipoproteinsmentioning

confidence: 99%

Search for Reliable Circulating Biomarkers to Predict Carotid Plaque Vulnerability

Puig

Jiménez‐Xarrié

Camps‐Renom

et al. 2020

IJMS

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Atherosclerosis is responsible for 20% of ischemic strokes, and the plaques from the internal carotid artery the most frequently involved. Lipoproteins play a key role in carotid atherosclerosis since lipid accumulation contributes to plaque progression and chronic inflammation, both factors leading to plaque vulnerability. Carotid revascularization to prevent future vascular events is reasonable in some patients with high-grade carotid stenosis. However, the degree of stenosis alone is not sufficient to decide upon the best clinical management in some situations. In this context, it is essential to further characterize plaque vulnerability, according to specific characteristics (lipid-rich core, fibrous cap thinning, intraplaque hemorrhage). Although these features can be partly detected by imaging techniques, identifying carotid plaque vulnerability is still challenging. Therefore, the study of circulating biomarkers could provide adjunctive criteria to predict the risk of atherothrombotic stroke. In this regard, several molecules have been found altered, but reliable biomarkers have not been clearly established yet. The current review discusses the concept of vulnerable carotid plaque, and collects existing information about putative circulating biomarkers, being particularly focused on lipid-related and inflammatory molecules.

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Low and high density lipoprotein metabolism in atherothrombotic brain infarction.

Cited by 13 publications

References 42 publications

Blood Lipids in Brain Infarction Subtypes

Blood Lipids in Brain Infarction Subtypes

Pathogenesis of Atherothrombotic Brain Infarction: Role of Lipids

Search for Reliable Circulating Biomarkers to Predict Carotid Plaque Vulnerability

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