Apolipoprotein E polymorphism does not predict risk of restenosis after coronary angioplasty

Samani, Niraj N

doi:10.1016/s0021-9150(96)05879-0

Cited by 5 publications

(6 citation statements)

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“…The apo ~4 allele homozygosity was more frequent among 59 patients with restenosis after PTCA (8.5%) than among 91 patients without restenosis (1.1%), p < 0.04 [113]. These findings could, however, not be corroborated by a more recent report [89].…”

Section: Other Genetic Factorsmentioning

confidence: 90%

Genetic risk factors and restenosis after percutaneous coronary interventions

Kastrati

Dirschinger

Schömig

2000

Herz

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Restenosis is the major limitation of percutaneous coronary interventions. Depending on the form of intervention and patients' characteristics, 20 to 50% of the treated patients incur significant restenosis. Restenosis is caused by a complex and only partially understood cascade of events. Thrombus formation at the injury site, formation of the neointima as a result of the migration and proliferation of smooth muscle cells (SMC) and extracellular matrix production, as well as constrictive remodeling of the vessel wall contribute by a variable degree to restenosis. Restenosis is not a random event but it affects selectively a certain subset of patients. These patients have some peculiar characteristics that help to identify the presence of a higher risk for restenosis. Conventional patient-related factors account only for a relatively small portion of the predictive power, much more contribution comes from lesion and procedural characteristics. There is increasing evidence that inherited factors may explain at least part of the excessive risk for restenosis observed in certain patients. Evidence exists that gene polymorphisms may lead to quantitative or functional alterations of the respective gene products. Recent studies have also found significant associations between several polymorphic alleles encoding for proteins with a relevant role in the process of lumen renarrowing and restenosis after percutaneous coronary interventions. The best studied polymorphisms in this regard are those of the genes encoding for angiotensin-converting enzyme and platelet glycoprotein-IIIa. Completed or ongoing studies have focused on polymorphisms of genes encoding for proteins interfering with lipid metabolism, hemostasis, nitric oxide production, inflammatory mechanisms, SMC proliferation and matrix production. The results of this research will have considerable pathophysiological and therapeutical implications for the battle against restenosis.

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Section: Other Genetic Factorsmentioning

confidence: 90%

Genetic risk factors and restenosis after percutaneous coronary interventions

Kastrati

Dirschinger

Schömig

2000

Herz

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“…The association of the 2/3/4 polymorphism with restenosis after balloon angioplasty of coronary arteries has been observed (17, 18), but not in all studies that addressed this subject (19,20). In the first of the positive reports (17), the 4 allele and 44 genotype were significantly more prevalent among 59 patients with restenosis than among 91 patients who did not develop restenosis (P Ͻ 0.01 and P Ͻ 0.04, respectively).…”

Section: Discussionmentioning

confidence: 99%

“…APOE polymorphisms may also be associated with angiographic and clinical outcomes after subcutaneous interventions in coronary arteries. Inconsistent results were obtained regarding the relationship between the 2/ 3/ 4 polymorphism and restenosis after balloon angioplasty in coronary arteries (17)(18)(19)(20). It has not been examined whether the APOE -219G/T, 113G/C, 334T/C, and 472C/T SNPs, or APOE haplotypes based on the 2/ 3/ 4 polymorphism, or combinations of all four SNPs are related to thrombotic and restenotic complications after coronary stenting.…”

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confidence: 99%

Apolipoprotein E gene polymorphisms and thrombosis and restenosis after coronary artery stenting

Koch

Mehilli

Pfeufer

et al. 2004

Journal of Lipid Research

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Experimental data support a protective function of apolipoprotein E (apoE) against restenosis, the main factor limiting the long-term benefit of percutaneous coronary interventions. We investigated the possibility that the single nucleotide polymorphisms (SNPs) -219G/T, 113G/C, 334T/C, and 472C/T of the gene encoding apoE (APOE) are associated with the incidence of death and myocardial infarction or restenosis after stenting in coronary arteries. In addition, we asked whether the apoE isotype-related 2/ 3/ 4 polymorphism, defined by specific allele combinations (haplotypes) of the 334T/C and 472C/T polymorphism, and other APOE haplotypes, derived from all four SNPs investigated, are associated with adverse clinical and angiographic outcomes after stenting. Our study included 1,850 consecutive patients with symptomatic coronary artery disease (CAD) who underwent stent implantation. Follow-up angiography was performed in 1,556 patients (84.1%) at 6 months after the intervention. We found that none of the APOE SNPs is associated with death and myocardial infarction or restenosis after stenting. In addition, we observed no relationship between APOE haplotypes and adverse outcomes. In conclusion, the APOE -219G/T, 113G/C, 334T/C, and 472C/T polymorphisms, either alone or in combination, do not represent genetic markers of the risk of thrombotic and restenotic complications in patients with CAD treated with coronary stenting. -

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“…The methods have been described previously. 16 Subjects completed a standard questionnaire about their personal history, which included data on age, sex, smoking status, history of hypertension and history of diabetes. All cases satisfied the World Health Organisation criteria for myocardial infarction.…”

Section: Methodsmentioning

confidence: 99%

Molecular genetics of myocardial infarction: many genes, more questions than answers

Vassalli¹

2004

European Heart Journal

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Aim To identify polymorphisms and haplotypes in candidate genes that predispose to myocardial infarction (MI) using a multilocus approach. Methods and results 1052 subjects, comprising 547 acute MI cases and 505 controls were studied. The association between MI and 58 SNPs in 35 candidate genes (generating 61 016 individual genotypes), and between MI and estimated haplotypes at 14 loci encompassing 16 genes was investigated. Two individual gene variants and haplotypes at two loci showed statistical association with MI. The a-adducin 460trp variant (OR 0.73, 95% CI 0.59-0.91, P ¼ 0:006) and the cholesteryl ester transfer protein -629A variant (OR 0.82, 95% CI 0.68-0.97, P ¼ 0:025) were both associated with a significant protective effect on MI, as was the paraoxonase 1/paraoxonase 2 haplotype comprising met55 and gln192 in paraoxonase 1 and cys311 in paraoxonase 2 (OR 0.52, 95% CI 0.39-0.77, P ¼ 0:001). The apolipoprotein C III haplotypes CCTTCG and ATCCCG at positions -641*-482*-455*1100*3175*3206 were associated with an increased risk of MI, odds ratios 1.41 (95% CI 1.06-1.76, P ¼ 0:023) and 1.71 (95% CI 1.28-2.14, P ¼ 0:038), respectively. Conclusions We report associations of two polymorphisms and haplotypes at two loci with risk of MI that warrants testing in future studies. Furthermore, we demonstrate the application of a multilocus assay in the setting of a large association study and the additional benefit gained from the study of haplotypes to identify variants influencing risk of coronary heart disease.

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Apolipoprotein E polymorphism does not predict risk of restenosis after coronary angioplasty

Cited by 5 publications

References 0 publications

Genetic risk factors and restenosis after percutaneous coronary interventions

Genetic risk factors and restenosis after percutaneous coronary interventions

Apolipoprotein E gene polymorphisms and thrombosis and restenosis after coronary artery stenting

Molecular genetics of myocardial infarction: many genes, more questions than answers

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