File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction

TitleEffects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction
Authors
Issue Date2001
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jac
Citation
Journal Of The American College Of Cardiology, 2001, v. 38 n. 4, p. 1207-1215 How to Cite?
AbstractOBJECTIVES: The goal of this study was to compare the relative efficacy of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) in suppressing the histopathologic changes that lead to ventricular remodeling after an acute myocardial infarction (AMI). BACKGROUND: Myocardial interstitial fibrosis in the noninfarcted region is a major histologic landmark resulting in cardiac dysfunction after AMI. However, the relative potency of an ACE inhibitor and ARB on suppressing the histopathologic changes was unclear. METHODS: Rats with AMI were randomized to fosinopril, valsartan or a combination of the two drugs for two or four weeks. The total, type I and type III collagen and activated fibroblasts and macrophages were quantified by histomorphometry. The expression of transforming growth factor-beta 1 (TGF-beta 1) messenger ribonucleic acid (mRNA) was determined by reverse transcription polymerase chain reaction. RESULTS: Acute myocardial infarction resulted in significant elevation of total (p < 0.001) and type I (p < 0.001) collagen and a twofold increase in TGF-beta 1 mRNA expression (p < 0.001) in the septum at two and four weeks. Macrophages and activated myofibroblasts infiltrated extensively in the infarct zone. Treatment with valsartan or combination therapy normalized the total and type I collagen (p < 0.001) as well as TGF-beta 1 mRNA level (p < 0.01) in the septum and was associated with the suppression of macrophages and myofibroblasts in the infarct zone (p < 0.01). Fosinopril was less effective than valsartan or combination therapy. CONCLUSIONS: The use of valsartan, especially combined with fosinopril, was more effective than fosinopril in the suppression of histopathologic changes resulting in cardiac remodeling after AMI. This study has important therapeutic implications in pharmacotherapy of clinical practice. (J Am Coll Cardiol 2001;38:1207-1215) © 2001 by the American College of Cardiology.
Persistent Identifierhttp://hdl.handle.net/10722/149599
ISSN
2015 Impact Factor: 17.759
2015 SCImago Journal Rankings: 10.097
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, CMen_US
dc.contributor.authorTipoe, GLen_US
dc.contributor.authorWingHon Lai, Ken_US
dc.contributor.authorLau, CPen_US
dc.date.accessioned2012-06-26T05:55:46Z-
dc.date.available2012-06-26T05:55:46Z-
dc.date.issued2001en_US
dc.identifier.citationJournal Of The American College Of Cardiology, 2001, v. 38 n. 4, p. 1207-1215en_US
dc.identifier.issn0735-1097en_US
dc.identifier.urihttp://hdl.handle.net/10722/149599-
dc.description.abstractOBJECTIVES: The goal of this study was to compare the relative efficacy of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) in suppressing the histopathologic changes that lead to ventricular remodeling after an acute myocardial infarction (AMI). BACKGROUND: Myocardial interstitial fibrosis in the noninfarcted region is a major histologic landmark resulting in cardiac dysfunction after AMI. However, the relative potency of an ACE inhibitor and ARB on suppressing the histopathologic changes was unclear. METHODS: Rats with AMI were randomized to fosinopril, valsartan or a combination of the two drugs for two or four weeks. The total, type I and type III collagen and activated fibroblasts and macrophages were quantified by histomorphometry. The expression of transforming growth factor-beta 1 (TGF-beta 1) messenger ribonucleic acid (mRNA) was determined by reverse transcription polymerase chain reaction. RESULTS: Acute myocardial infarction resulted in significant elevation of total (p < 0.001) and type I (p < 0.001) collagen and a twofold increase in TGF-beta 1 mRNA expression (p < 0.001) in the septum at two and four weeks. Macrophages and activated myofibroblasts infiltrated extensively in the infarct zone. Treatment with valsartan or combination therapy normalized the total and type I collagen (p < 0.001) as well as TGF-beta 1 mRNA level (p < 0.01) in the septum and was associated with the suppression of macrophages and myofibroblasts in the infarct zone (p < 0.01). Fosinopril was less effective than valsartan or combination therapy. CONCLUSIONS: The use of valsartan, especially combined with fosinopril, was more effective than fosinopril in the suppression of histopathologic changes resulting in cardiac remodeling after AMI. This study has important therapeutic implications in pharmacotherapy of clinical practice. (J Am Coll Cardiol 2001;38:1207-1215) © 2001 by the American College of Cardiology.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jacen_US
dc.relation.ispartofJournal of the American College of Cardiologyen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntihypertensive Agents - Pharmacologyen_US
dc.subject.meshCollagen - Metabolismen_US
dc.subject.meshDrug Combinationsen_US
dc.subject.meshFibrosisen_US
dc.subject.meshFosinopril - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Infarction - Pathologyen_US
dc.subject.meshMyocardium - Pathologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTetrazoles - Pharmacologyen_US
dc.subject.meshTransforming Growth Factor Beta - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta1en_US
dc.subject.meshValine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshVentricular Remodeling - Drug Effectsen_US
dc.titleEffects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarctionen_US
dc.typeArticleen_US
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_US
dc.identifier.authorityTipoe, GL=rp00371en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0735-1097(01)01518-2en_US
dc.identifier.pmid11583905-
dc.identifier.scopuseid_2-s2.0-0034806667en_US
dc.identifier.hkuros63870-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034806667&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume38en_US
dc.identifier.issue4en_US
dc.identifier.spage1207en_US
dc.identifier.epage1215en_US
dc.identifier.isiWOS:000171244500046-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYu, CM=7404976646en_US
dc.identifier.scopusauthoridTipoe, GL=7003550610en_US
dc.identifier.scopusauthoridWingHon Lai, K=6503860178en_US
dc.identifier.scopusauthoridLau, CP=35275317200en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats