Background: The renin-angiotensin system is involved in neointlmal hyperplasia in response to arterial injury. The insertion/deletion (l/D) polymorphism of the enzyme gene largely controls angiotensin converting enzyme (ACE) plasma level, and it has been observed that D allele is associated with restenosis after coronary stenting. However, plaque remodelling, vessel tearing at the edge of the stent and longitudinal redistributing of plaque could remain important determinants of restenosis after PTCA and stent implantation; debulking prior stenting eliminates these factors, leaving neointimal hyperplasia as the major mechanism of restenosis. Directional coronary atherectomy (DCA) followed by stent implantation therefore represent an ideal model to investigate the relationship between ACE l/D polymorphism and restenosis. Methods: We prospectively evaluated 113 consecutive patients (102 male, 90%; mean age 57+/- 9 years) who underwent successful (residual stenosis ~50%) DCA followed by stent implantation for de nova coronary lesion. Angiographic criteria for enrolment include significant stenosis (>75%, ~100%) of a tnon-tortuous native vessel with a reference diameter >2.5 mm and a lesion length <15mm. Genomic DNA was prepared from peripheral blood leukocytes and analysed by means of PCR amplification. Baseline, post-DCA, post-stent and follow-up angiograms, performed after 6-12 months, were quantitatively analysed. Subject were divided into three groups according to the genotype (DD, ID, II). Results: No significant differences were observed among the three groups in terms of acute, late loss, net gain or percent of patients developing angiographic restenosis. Conclusions: Our data indicate that ACE I/D gene polymorphism is not assiciated with the risk of developing restenosis in a model of plaque debulking plus stent deployment.

Insertion/deletion polymorphism of the Angiotensin I-Converting Enzyme gene and risk of restenosis after directional coronary atherectomy followed by stent implantation

GNECCHI, MASSIMILIANO;
2001-01-01

Abstract

Background: The renin-angiotensin system is involved in neointlmal hyperplasia in response to arterial injury. The insertion/deletion (l/D) polymorphism of the enzyme gene largely controls angiotensin converting enzyme (ACE) plasma level, and it has been observed that D allele is associated with restenosis after coronary stenting. However, plaque remodelling, vessel tearing at the edge of the stent and longitudinal redistributing of plaque could remain important determinants of restenosis after PTCA and stent implantation; debulking prior stenting eliminates these factors, leaving neointimal hyperplasia as the major mechanism of restenosis. Directional coronary atherectomy (DCA) followed by stent implantation therefore represent an ideal model to investigate the relationship between ACE l/D polymorphism and restenosis. Methods: We prospectively evaluated 113 consecutive patients (102 male, 90%; mean age 57+/- 9 years) who underwent successful (residual stenosis ~50%) DCA followed by stent implantation for de nova coronary lesion. Angiographic criteria for enrolment include significant stenosis (>75%, ~100%) of a tnon-tortuous native vessel with a reference diameter >2.5 mm and a lesion length <15mm. Genomic DNA was prepared from peripheral blood leukocytes and analysed by means of PCR amplification. Baseline, post-DCA, post-stent and follow-up angiograms, performed after 6-12 months, were quantitatively analysed. Subject were divided into three groups according to the genotype (DD, ID, II). Results: No significant differences were observed among the three groups in terms of acute, late loss, net gain or percent of patients developing angiographic restenosis. Conclusions: Our data indicate that ACE I/D gene polymorphism is not assiciated with the risk of developing restenosis in a model of plaque debulking plus stent deployment.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/456313
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