Relation of plasma lipid and apoprotein levels to progressive intimal hyperplasia after arterial endarterectomy.

Colyvas, Nicholas; Rapp, Joseph H.; Phillips, Nancy; Stoney, Ronald J.; Perez, S; Kane, John P.; Havel, Richard J.

doi:10.1161/01.cir.85.4.1286

Cited by 29 publications

(11 citation statements)

References 24 publications

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“…[25][26][27][28][29][30] An inverse relationship between restenosis after percutaneous coronary transluminal angioplasty and restenosis after carotid endarterectomy has also been demonstrated in some, but not all, studies. [31][32][33][34] There are, however, several exceptions to this general rule that should be mentioned. For example, some genetically determined low HDL states due to mutations in apolipoprotein A-I are not associated with an increased risk of atherosclerosis.…”

Section: Relationship Of Hdl/apolipoprotein A-i To Atherosclerosis Anmentioning

confidence: 99%

Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins

Shah¹,

Kaul²,

Nilsson³

et al. 2001

Circulation

217

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Section: Relationship Of Hdl/apolipoprotein A-i To Atherosclerosis Anmentioning

confidence: 99%

Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins

Shah¹,

Kaul²,

Nilsson³

et al. 2001

Circulation

217

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“…The genetic polymorphism of ApoE results from the existence of three alleles (ε2, ε3 and ε4) encoding three proteins (E2, E3 and E4) and combining in six different genotypes (ε2/ε2, ε2/ε3, ε2/ε4, ε3/ε3, ε3/ε4, ε4/ε4) [1]. Studies have suggested that ApoE-ε4 genotype predisposes to the early development of atherosclerosis [2,3,4,5,6] and coronary artery disease [7,8,9]. Associations between ApoE-ε4 and Alzheimer’s disease [10, 11], cerebral hemorrhage [12, 13] and poststroke dementia have also been reported [14].…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein E Polymorphism and Stroke Subtypes in an Italian Cohort

et al. 2005

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Background: Studies have indicated that apolipoprotein E (ApoE)-ε4 is a risk factor for ischemic cerebrovascular diseases (ICVD), but the existence of this association is still controversial. The aims of this study were: (1) to compare ApoE genotype and allele frequencies in Italian cases with ICVD and in healthy control subjects and (2) to compare ApoE allele frequencies among ischemic stroke subtypes. Methods: A hospital-based cohort of 302 Italian subjects with ICVD and 228 healthy subjects have been recruited to investigate the role of ApoE polymorphisms as risk factors for ICVD. TOAST criteria were employed to stratify ICVD cases by subtypes. Results: No significant differences in ApoE genotype and allele frequencies were found between cases and control subjects. The frequency of ApoE-ε4 was lower in cases than in control subjects (6% vs. 10.1%), although not significantly. No differences in ApoE genotype and allele frequencies were evident among ICVD subtypes. However, out of 36 ApoE-ε4 alleles 23 (3.7%) were found in subjects with ICVD related to primary degenerative arterial disease related to large vessel disease and small vessel disease, and 13 (2.1%) in remaining subjects. Using logistic regression analysis we assessed whether ApoE-ε4 allele was independently associated with risk of ICVD related to a primary degenerative arterial disease compared to other ICVD subtypes. While classical risk factors were significantly associated with higher risk for ICVD due to large vessel disease and small vessel disease than other ICVD subtypes, the role of ApoE-ε4 allele was not significant (OR 1.25, 95% CI 0.57–2.74). Conclusion: Our study shows similar ApoE-ε4 genotype and allele frequencies in patients with ICVD and in control subjects. No differences were found among different ICVD subtypes either.

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“…Indeed, nearly half of all patients with coronary artery disease have low HDL-C (2, 3). Low HDL-C appears to be associated with, among other factors, an enhanced risk of angioplasty restenosis (4) and with a number of clinical syndromes such as the "metabolic syndrome", which combines low HDL with hypertriglyceridemia and abdominal obesity (5). Raising HDL-C concentrations may have therapeutic value in reducing risk of reinfarction and stroke in coronary patients (6,7).…”

mentioning

confidence: 99%

Targeted Replacement of Mouse Apolipoprotein A-I with Human ApoA-I or the Mutant ApoA-IMilano

Parolini

Chiesa

Zhu

et al. 2003

Journal of Biological Chemistry

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Relation of plasma lipid and apoprotein levels to progressive intimal hyperplasia after arterial endarterectomy.

Abstract: Elevated lipid levels usually associated with an increased risk of atherosclerosis may predispose patients to an increased incidence of intimal hyperplasia after endarterectomy.

Cited by 29 publications

References 24 publications

Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins

Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins

Apolipoprotein E Polymorphism and Stroke Subtypes in an Italian Cohort

Targeted Replacement of Mouse Apolipoprotein A-I with Human ApoA-I or the Mutant ApoA-IMilano

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