| Myocardial fibrosis and the concepts of cardioprotection and cardioreparation. | |
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MedLine Citation:
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PMID: 1403238 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: To examine the inter-relationship between effector hormones of the renin-angiotensin-aldosterone system and fibrosis, a determinant of abnormal myocardial stiffness, and to determine whether pharmacological interference with these hormones can prevent or regress this pathological structural remodeling. EFFECTS OF ANGIOTENSIN II AND ALDOSTERONE: Two morphological expressions of myocardial fibrosis are evident, a perivascular and interstitial fibrosis, not related to cardiac myocyte necrosis, and microscopic scarring that replaces lost myocytes. The former, a reactive fibrosis, is related to elevations in circulating mineralocorticoids (aldosterone or deoxycorticosterone) with increased dietary sodium, and not to arterial hypertension or ventricular loading. Scarring follows the cytotoxicity associated with elevated plasma angiotensin II levels and the increased K+ excretion that accompanies chronic mineralocorticoid excess. EFFECTS OF PHARMACOLOGICAL INTERFERENCE: Given the association of these hormones with fibrosis, the concept of cardioprotection was evaluated in various prevention trials. Reactive fibrosis was prevented in unilateral renal ischaemia by angiotensin converting enzyme (ACE) inhibition with captopril and in either primary or secondary hyperaldosteronism by antagonism of the aldosterone receptor with spironolactone. Scarring (and cell loss) was prevented in renal ischemia by captopril and by K(+)-sparing diuretics (spironolactone, amiloride) in primary hyperaldosteronism. In treatment trials, where reactive fibrosis was established, lisinopril promoted regression of the fibrosis and therefore was cardioprotective. CONCLUSIONS: Myocardial fibrosis is related to chronic mineralocorticoid excess (with increased dietary sodium), angiotensin II and increased K+ excretion. Cardioprotective and cardioreparative strategies that respectively prevent or regress the development of fibrous tissue have been demonstrated in experimental models and now merit clinical evaluation. |
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Authors:
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K T Weber; C G Brilla; S E Campbell; H K Reddy |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Journal of hypertension. Supplement : official journal of the International Society of Hypertension Volume: 10 ISSN: 0952-1178 ISO Abbreviation: J Hypertens Suppl Publication Date: 1992 Jul |
Date Detail:
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Created Date: 1992-11-13 Completed Date: 1992-11-13 Revised Date: 2005-11-16 |
Medline Journal Info:
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Nlm Unique ID: 8501422 Medline TA: J Hypertens Suppl Country: ENGLAND |
Other Details:
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Languages: eng Pagination: S87-94 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Missouri-Columbia. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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physiology* Cardiovascular Diseases / epidemiology Endomyocardial Fibrosis / physiopathology* Humans Mineralocorticoids / physiology* Risk Factors |
| Chemical | |
Reg. No./Substance:
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0/Mineralocorticoids; 11128-99-7/Angiotensin II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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