Document Detail


Deletion-type allele of the angiotensin-converting enzyme gene is associated with progressive ventricular dilation after anterior myocardial infarction. Captopril and Thrombolysis Study Investigators.
MedLine Citation:
PMID:  7759715     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: This study sought to determine whether patients who are homozygous for the deletion (D)-type allele of the angiotensin-converting enzyme gene display augmented ventricular dilation after myocardial infarction. BACKGROUND: Recent evidence suggests that the deletion-type allele of the angiotensin-converting enzyme gene (DD genotype) is associated with an increased prevalence of myocardial infarction and myocardial hypertrophy. However, it is unknown whether the DD genotype is associated with adverse cardiac remodeling. To address this question we determined the genotype in patients enrolled in the Captopril and Thrombolysis Study (CATS), a prospective trial in which patients received either captopril or placebo during and after thrombolysis for a first anterior myocardial infarction. METHODS: Cardiac volume was determined by echocardiography immediately after thrombolysis and at 1-year follow-up. The genotype for the angiotensin-converting enzyme was determined in 96 patients. Norepinephrine levels were assessed during and immediately after thrombolysis. RESULTS: Immediately after thrombolysis, cardiac volume did not differ between genotype groups. However, at 1-year follow-up, both end-systolic and end-diastolic left ventricular volumes were significantly greater in the DD-genotype group. Norepinephrine increased to higher levels in the DD-genotype group that received placebo therapy. Captopril treatment effectively blunted both the norepinephrine increase and cardiac dilation in the DD-genotype group. CONCLUSIONS: This exploratory study suggests that homozygosity for the angiotensin-converting enzyme deletion-type allele is associated with augmented neurohumoral activation as well as augmented cardiac dilation after an acute anterior myocardial infarction, an effect that may be susceptible to angiotensin-converting enzyme inhibition.
Authors:
Y M Pinto; W H van Gilst; J H Kingma; H Schunkert
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  25     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  1995 Jun 
Date Detail:
Created Date:  1995-06-23     Completed Date:  1995-06-23     Revised Date:  2010-03-24    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1622-6     Citation Subset:  AIM; IM    
Affiliation:
Department of Clinical Pharmacology, University of Groningen, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Alleles
Captopril / therapeutic use
Double-Blind Method
Female
Follow-Up Studies
Gene Deletion*
Homozygote
Humans
Hypertrophy, Left Ventricular / etiology,  genetics*,  ultrasonography
Male
Middle Aged
Myocardial Infarction / complications,  drug therapy,  genetics*
Norepinephrine / blood
Peptidyl-Dipeptidase A / genetics*
Prospective Studies
Streptokinase / therapeutic use
Thrombolytic Therapy
Time Factors
Chemical
Reg. No./Substance:
51-41-2/Norepinephrine; 62571-86-2/Captopril; EC 3.4.-/Streptokinase; EC 3.4.15.1/Peptidyl-Dipeptidase A
Comments/Corrections
Comment In:
J Am Coll Cardiol. 1995 Jun;25(7):1632-3   [PMID:  7759717 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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