Document Detail

Angiotensin receptor blockade and angiotensin-converting-enzyme inhibition limit adverse remodeling of infarct zone collagens and global diastolic dysfunction during healing after reperfused ST-elevation myocardial infarction.
MedLine Citation:
PMID:  17426929     Owner:  NLM     Status:  MEDLINE    
To determine whether therapy with the angiotensin II type 1 receptor blocker (ARB) candesartan and the comparator angiotensin-converting-enzyme inhibitor (ACEI) enalapril during healing after reperfused ST-elevation myocardial infarction (RSTEMI) limit adverse remodeling of infarct zone (IZ) collagens and left ventricular (LV) diastolic dysfunction, we randomized 24 dogs surviving anterior RSTEMI (90-min coronary occlusion) to placebo, candesartan, and enalapril therapy between day 2 and 42. Six other dogs were sham. We measured regional IZ and non-infarct zone (NIZ) collagens (hydroxyproline; types I/III; cross-linking), transforming growth factor-beta (TGF-beta) and topography at 6 weeks, and hemodynamics, LV diastolic and systolic function, and remodeling over 6 weeks. Compared to sham, placebo-RSTEMI differentially altered regional collagens, with more pronounced increase in TGF-beta, hydroxyproline, and type I, insoluble, and cross-linked collagens in the IZ than NIZ, and increased IZ soluble and type III collagens at 6 weeks, and induced persistent LV filling pressure elevation, diastolic and systolic dysfunction, and LV remodeling over 6 weeks. Compared to placebo-RSTEMI, candesartan and enalapril limited adverse regional collagen remodeling, with normalization of type III, soluble and insoluble collagens and decrease in pyridinoline cross-linking in the IZ at 6 weeks, and attenuation of LV filling pressure, diastolic dysfunction, and remodeling over 6 weeks. The results suggest that candesartan and enalapril during healing after RSTEMI prevent rather than worsen adverse remodeling of IZ collagens and LV diastolic dysfunction, supporting the clinical use of ARBs and ACEIs during subacute RSTEMI.
Bodh I Jugdutt; Halliday Idikio; Richard R E Uwiera
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-04-11
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  303     ISSN:  0300-8177     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-09     Completed Date:  2007-10-18     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  27-38     Citation Subset:  IM    
2C2 Walter Mackenzie Health Sciences Centre, Division of Cardiology, Department of Medicine, University of Alberta and Hospitals, Edmonton, Alberta, Canada.
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MeSH Terms
Angiotensin II Type 1 Receptor Blockers / therapeutic use
Angiotensin Receptor Antagonists*
Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
Benzimidazoles / therapeutic use
Collagen / drug effects,  metabolism*
Enalapril / therapeutic use
Hydroxyproline / metabolism
Myocardial Infarction / drug therapy*,  pathology
Myocardial Reperfusion
Peptidyl-Dipeptidase A / chemistry*,  metabolism
Tetrazoles / therapeutic use
Transforming Growth Factor beta1 / metabolism
Ventricular Dysfunction, Left / drug therapy*,  etiology,  pathology
Ventricular Remodeling / drug effects*
Wound Healing
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Angiotensin Receptor Antagonists; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Benzimidazoles; 0/Tetrazoles; 0/Transforming Growth Factor beta1; 51-35-4/Hydroxyproline; 75847-73-3/Enalapril; 9007-34-5/Collagen; EC A; S8Q36MD2XX/candesartan

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

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