Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty

Samani, Nilesh J.; Brack, M. J.; Cullen, James H.; Bono, David P. de; Gershlick, AH; Martin, Daniel; Lodwick, David; Swales, J. D.; Chauhan, Anoop; Harley, A

doi:10.1016/s0140-6736(95)90756-4

Cited by 72 publications

(36 citation statements)

References 16 publications

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“…Many studies have shown that the ACE I/D polymorphism in humans is not associated with restenosis after balloon angioplasty. 20,21,61 Moreover, two randomized trials (MERCATOR 62 and MARCATOR 63 ) have failed to demonstrate any beneficial effect of ACE inhibition on the occurrence of angiographic restenosis after balloon angioplasty. Nevertheless, experimental 64,65 and clinical 66 studies have suggested that the contribution of neointimal hyperplasia to restenosis after balloon angioplasty is relatively limited and that lumen renarrowing is in fact related primarily to vessel remodeling.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, cell and tissue ACE levels have also been shown to be modulated by ACE gene polymorphism in humans. 11,12 Since Cambien et al 13 first described a significant association between the I/D polymorphism and myocardial infarction, many studies have tried to examine the association of the ACE genotype, not only with ischemic heart disease 14 -17 but with a variety of conditions ranging from hypertension 18,19 to coronary artery restenosis, 14,20,21 cardiac hypertrophy, 16,22,23 pulmonary hypertension, 24 diabetes, 25 and nephropathy. 26 -28 The results of these studies are contradictory and stress the importance of experimental models for testing the impact of the ACE gene polymorphism and its associated modulation of ACE expression on the cardiovascular and renal responses to these pathological processes.…”

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confidence: 99%

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Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Challah

Villard

Philippe

et al. 1998

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Abstract-Two normotensive strains of rat, the Lou and Brown Norway (BN) strains, have contrasting levels of plasma angiotensin-converting enzyme (ACE). To investigate the degree of genetic determination of ACE expression, a polymorphic marker of the ACE gene was analyzed in inbred rats of the two strains. The two inbred strains were shown to bear different alleles for a polymorphic marker at the ACE gene. The segregation of the alleles of this marker and the plasma ACE levels were studied in a group of F2 rats issued from a cross between Lou and BN rats. The degree of genetic determination of plasma ACE activity was estimated to be 94% in the F2 cohort. The ACE locus accounts for 74% of total plasma ACE variance. ACE activity and mRNA expression in lungs were also genetically determined. The difference observed in ACE mRNA accumulation in the lungs between the two strains was due to a difference in the transcriptional rate of the ACE gene, as shown in nuclear run-on experiments. No differences were observed in arterial blood pressure of homozygous F2 progeny. In these animals, ACE genotype did not interfere with the pressor or the depressor responses to ACE-dependent vasoactive peptides. There was a significant effect of strain on constitutive or inducible membrane or soluble ACE activity in primary cultures of vascular cells. Neointima formation in the carotid artery 14 days after balloon injury was also influenced by the genotype in F2 homozygous progeny, whereas the medial area was not. These results demonstrate that there is a close relationship between the genetically determined ACE expression and the inducibility of the ACE gene. The degree of genetic determination of ACE expression in inbred rat strains offers a unique opportunity to study the interaction between genetic and environmental determinants of ACE expression and its involvement in response to experimental cardiovascular and renal injury. (Arterioscler Thromb Vasc Biol. 1998;18:235-243.)

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Challah

Villard

Philippe

et al. 1998

ATVB

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“…36,37 On the other hand, restenosis following coronary angioplasty without stent, which appears to be primarily due to vessel remodelling, 38 was not associated with ACE genotype. [39][40][41] Percutaneous transluminal renal angioplasty (PTRA) has become the treatment of first choice for renal artery FMD. Therefore, current diagnosis and classification of FMD is based on the angiographic rather than histologic appearance.…”

Section: 21mentioning

confidence: 99%

Polymorphisms of the renin-angiotensin system in patients with multifocal renal arterial fibromuscular dysplasia

et al. 2001

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“…In the absence of any known strong predictors for post-PTCA restenosis, we selected this disease entity as a test case for a more comprehensive approach, with regard to both breadth of genotyping and analytical algorithms. In a cohort of post-PTCA patients three times larger than the largest sample studied so far, 4 a panel of 94 polymorphic markers was tested from 62 'candidate' genes (representing, broadly, genes related to lipid and homocysteine metabolism, vascular tone regulation, cellmatrix adhesion and interaction, matrix integrity, inflammatory and immune responses, thrombosis/coagulation, cellular homeostasis/cytoprotection mechanisms, and cell cycle/apoptotic pathways; see Table 1). …”

Section: Introductionmentioning

confidence: 99%

Multi-locus interactions predict risk for post-PTCA restenosis: an approach to the genetic analysis of common complex disease

et al. 2002

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The complexity of recognizing the potential contribution of a number of possible predictors of complex disorders is increasingly challenging with the application of large-scale single nucleotide polymorphism (SNP) typing. In the search for putative genetic factors predisposing to coronary artery restenosis following balloon angioplasty, we determined genotypes for 94 SNPs representing 62 candidate genes, in a prospectively assembled cohort of 342 cases and 437 controls. Using a customized coupled-logistic regression procedure accounting for both additive and interactive effects, we identified seven SNPs in seven genes that, together, showed a statistically significant association with restenosis incidence (P Ͻ0.0001), accounting for 11.6% of overall variance observed. Among them are candidate genes for cardiovascular pathophysiology (apolipoprotein-species and NOS), inflammatory response (TNF receptor and CD14), and cell-cycle control (p53 and p53-associated protein). Our results emphasize the need to account for complex multi-gene influences and interactions when assessing the molecular pathology of multifactorial medical entities.

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Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty

Cited by 72 publications

References 16 publications

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Polymorphisms of the renin-angiotensin system in patients with multifocal renal arterial fibromuscular dysplasia

Multi-locus interactions predict risk for post-PTCA restenosis: an approach to the genetic analysis of common complex disease

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