title: The expression of angiotensin-I converting enzyme in human atherosclerotic plaques is not related to the deletion/insertion polymorphism but to the risk of restenosis after coronary interventions.
abstract: Plasma and tissue concentrations of the angiotensin-I converting enzyme (ACE) have been shown to be associated with the ACE insertion/deletion (I/D) polymorphism. The purpose of this study was to examine the relation of ACE levels in atherosclerotic plaques to the ACE I/D polymorphism and to restenosis after balloon angioplasty and directional atherectomy (DCA). The study included 104 patients who underwent DCA and received angiographic follow-up at 12 to 18 months. The amount of ACE protein in various morphologically defined plaque components (fibrous, atheromatous, and complicated lesions) of the atherectomy specimens was determined by qualitative and semiquantitative immunohistochemistry. ACE levels were related to the ACE genotype, to plaque morphology and to the risk of restenosis. Sequential staining revealed that pathologic ACE overexpression of the atherosclerotic lesions occurred in intimal smooth muscle cells, fibrocytes/fibroblasts and macrophage/foam cells. The ACE content of the whole plaques and of the single plaque components was not associated with the I/D polymorphism, but with restenosis after coronary interventions. In addition, ACE levels in the atherosclerotic lesions correlated with the severity of vessel wall damage. The ACE phenotype might serve as an indicator for the risk of restenosis after coronary interventions.
authors.affiliation: Department of Internal Medicine, Justus Liebig University of Giessen, Germany. wernerg.haberbosch@innere.med.uni-giessen.de
authors.forename: W
authors.initials: W
authors.lastname: Haberbosch
authors.forename: R M
authors.initials: RM
authors.lastname: Bohle
authors.forename: F E
authors.initials: FE
authors.lastname: Franke
authors.forename: S
authors.initials: S
authors.lastname: Danilov
authors.forename: F
authors.initials: F
authors.lastname: Alhenc-Gelas
authors.forename: R
authors.initials: R
authors.lastname: Braun-Dullaeus
authors.forename: H
authors.initials: H
authors.lastname: Hölschermann
authors.forename: W
authors.initials: W
authors.lastname: Waas
authors.forename: H
authors.initials: H
authors.lastname: Tillmanns
authors.forename: A
authors.initials: A
authors.lastname: Gardemann
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D017225:Atherectomy, Coronary; D003324:Coronary Artery Disease / Q000201:enzymology* / Q000235:genetics / Q000473:pathology / Q000628:therapy; D003331:Coronary Vessels / Q000201:enzymology* / Q000473:pathology; D004251:DNA Transposable Elements; D005260:Female; D005838:Genotype; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism*; D011110:Polymorphism, Genetic; D012008:Recurrence; D012307:Risk Factors; D017384:Sequence Deletion
chemical_list: D004251:DNA Transposable Elements; D007703:Peptidyl-Dipeptidase A