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Aldosterone: Cardiovascular assault
Background Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo...
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Published in: | The American heart journal 2002-11, Vol.144 (5), p.S2-S7 |
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description | Background Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo studies were evaluated to determine the mechanisms by which aldosterone contributes to morbidity and mortality. Results Aldosterone has several deleterious properties. It causes a vasculopathy with both endothelial dysfunction and a reduction in fibrinolysis, leading to heart, brain, and kidney damage. Aldosterone causes myocardial hypertrophy and fibrosis, autonomic imbalance, and electrolyte abnormalities, contributing to myocardial dysfunction, arrhythmias, and sudden cardiac death. Studies have shown that all of these deleterious effects can, at least in part, be reversed by aldosterone receptor blockade. This may explain why adding an aldosterone blocker to standard heart failure therapy, including angiotensin-converting enzyme inhibitors, reduces morbidity and mortality rates by an additional 30% compared with standard therapy alone. Conclusions Eplerenone is a selective aldosterone blocker whose role in reducing morbidity and mortality rates in patients with cardiovascular disease is being investigated. (Am Heart J 2002;144:S2-7.) |
doi_str_mv | 10.1067/mhj.2002.129969 |
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However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo studies were evaluated to determine the mechanisms by which aldosterone contributes to morbidity and mortality. Results Aldosterone has several deleterious properties. It causes a vasculopathy with both endothelial dysfunction and a reduction in fibrinolysis, leading to heart, brain, and kidney damage. Aldosterone causes myocardial hypertrophy and fibrosis, autonomic imbalance, and electrolyte abnormalities, contributing to myocardial dysfunction, arrhythmias, and sudden cardiac death. Studies have shown that all of these deleterious effects can, at least in part, be reversed by aldosterone receptor blockade. This may explain why adding an aldosterone blocker to standard heart failure therapy, including angiotensin-converting enzyme inhibitors, reduces morbidity and mortality rates by an additional 30% compared with standard therapy alone. Conclusions Eplerenone is a selective aldosterone blocker whose role in reducing morbidity and mortality rates in patients with cardiovascular disease is being investigated. (Am Heart J 2002;144:S2-7.)</description><identifier>ISSN: 0002-8703</identifier><identifier>EISSN: 1097-6744</identifier><identifier>DOI: 10.1067/mhj.2002.129969</identifier><identifier>PMID: 12422134</identifier><identifier>CODEN: AHJOA2</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>ACE inhibitors ; Aldosterone - physiology ; Autonomic Nervous System Diseases - etiology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiomegaly - etiology ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Drug therapy ; Endothelium, Vascular - physiopathology ; Fibrinolysis ; Fibrosis - etiology ; Heart attacks ; Heart Failure - complications ; Heart Failure - drug therapy ; Humans ; Magnesium - metabolism ; Medical sciences ; Mineralocorticoid Receptor Antagonists - therapeutic use ; Mortality ; Myocardium - pathology ; Necrosis ; Potassium - metabolism ; Rodents ; Sodium - metabolism</subject><ispartof>The American heart journal, 2002-11, Vol.144 (5), p.S2-S7</ispartof><rights>2002</rights><rights>2003 INIST-CNRS</rights><rights>Copyright Elsevier Limited Nov 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-9b610254be16d2cf3a8b5cb4fbcb2c2a0629aef1c9adbab49f9fd32ffe496b003</citedby><cites>FETCH-LOGICAL-c401t-9b610254be16d2cf3a8b5cb4fbcb2c2a0629aef1c9adbab49f9fd32ffe496b003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14369334$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12422134$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Struthers, Allan D.</creatorcontrib><title>Aldosterone: Cardiovascular assault</title><title>The American heart journal</title><addtitle>Am Heart J</addtitle><description>Background Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo studies were evaluated to determine the mechanisms by which aldosterone contributes to morbidity and mortality. Results Aldosterone has several deleterious properties. It causes a vasculopathy with both endothelial dysfunction and a reduction in fibrinolysis, leading to heart, brain, and kidney damage. Aldosterone causes myocardial hypertrophy and fibrosis, autonomic imbalance, and electrolyte abnormalities, contributing to myocardial dysfunction, arrhythmias, and sudden cardiac death. Studies have shown that all of these deleterious effects can, at least in part, be reversed by aldosterone receptor blockade. This may explain why adding an aldosterone blocker to standard heart failure therapy, including angiotensin-converting enzyme inhibitors, reduces morbidity and mortality rates by an additional 30% compared with standard therapy alone. Conclusions Eplerenone is a selective aldosterone blocker whose role in reducing morbidity and mortality rates in patients with cardiovascular disease is being investigated. (Am Heart J 2002;144:S2-7.)</description><subject>ACE inhibitors</subject><subject>Aldosterone - physiology</subject><subject>Autonomic Nervous System Diseases - etiology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomegaly - etiology</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Drug therapy</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Fibrinolysis</subject><subject>Fibrosis - etiology</subject><subject>Heart attacks</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - drug therapy</subject><subject>Humans</subject><subject>Magnesium - metabolism</subject><subject>Medical sciences</subject><subject>Mineralocorticoid Receptor Antagonists - therapeutic use</subject><subject>Mortality</subject><subject>Myocardium - pathology</subject><subject>Necrosis</subject><subject>Potassium - metabolism</subject><subject>Rodents</subject><subject>Sodium - metabolism</subject><issn>0002-8703</issn><issn>1097-6744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNp1kE1LAzEQhoMotlbP3qQgets2yWazG2-l-AUFL3oO-cSU3U1Ndgv-e1N3oSB4GoZ55p3hAeAawQWCtFw2n9sFhhAvEGaMshMwRZCVGS0JOQVTmCZZVcJ8Ai5i3KaW4oqegwnCBGOUkym4XdXax84E35qH-VoE7fxeRNXXIsxFjKKvu0twZkUdzdVYZ-Dj6fF9_ZJt3p5f16tNpghEXcYkRRAXRBpENVY2F5UslCRWKokVFuk4E8YixYSWQhJmmdU5ttYQRiWE-QzcD7m74L96EzveuKhMXYvW-D7yElOal2WVwNs_4Nb3oU2_cVRAUmBG6IFaDpQKPsZgLN8F14jwzRHkB3s82eMHe3ywlzZuxtxeNkYf-VFXAu5GICkStQ2iVS4eOZKnlF-ODZxJuvbOBB6VM60y2gWjOq69-_eJH2lxigA</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>Struthers, Allan D.</creator><general>Mosby, Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20021101</creationdate><title>Aldosterone: Cardiovascular assault</title><author>Struthers, Allan D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-9b610254be16d2cf3a8b5cb4fbcb2c2a0629aef1c9adbab49f9fd32ffe496b003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>ACE inhibitors</topic><topic>Aldosterone - physiology</topic><topic>Autonomic Nervous System Diseases - etiology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomegaly - etiology</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Drug therapy</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Fibrinolysis</topic><topic>Fibrosis - etiology</topic><topic>Heart attacks</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - drug therapy</topic><topic>Humans</topic><topic>Magnesium - metabolism</topic><topic>Medical sciences</topic><topic>Mineralocorticoid Receptor Antagonists - therapeutic use</topic><topic>Mortality</topic><topic>Myocardium - pathology</topic><topic>Necrosis</topic><topic>Potassium - metabolism</topic><topic>Rodents</topic><topic>Sodium - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Struthers, Allan D.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing and Allied Health Journals</collection><collection>Physical Education Index</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Healthcare Administration Database (Alumni)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>ProQuest Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The American heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Struthers, Allan D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aldosterone: Cardiovascular assault</atitle><jtitle>The American heart journal</jtitle><addtitle>Am Heart J</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>144</volume><issue>5</issue><spage>S2</spage><epage>S7</epage><pages>S2-S7</pages><issn>0002-8703</issn><eissn>1097-6744</eissn><coden>AHJOA2</coden><abstract>Background Blocking the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors has improved cardiovascular morbidity and mortality rates. However, because of aldosterone “escape,” the effectiveness of this blockade decreases over time. Methods Various in vitro and in vivo studies were evaluated to determine the mechanisms by which aldosterone contributes to morbidity and mortality. Results Aldosterone has several deleterious properties. It causes a vasculopathy with both endothelial dysfunction and a reduction in fibrinolysis, leading to heart, brain, and kidney damage. Aldosterone causes myocardial hypertrophy and fibrosis, autonomic imbalance, and electrolyte abnormalities, contributing to myocardial dysfunction, arrhythmias, and sudden cardiac death. Studies have shown that all of these deleterious effects can, at least in part, be reversed by aldosterone receptor blockade. This may explain why adding an aldosterone blocker to standard heart failure therapy, including angiotensin-converting enzyme inhibitors, reduces morbidity and mortality rates by an additional 30% compared with standard therapy alone. Conclusions Eplerenone is a selective aldosterone blocker whose role in reducing morbidity and mortality rates in patients with cardiovascular disease is being investigated. (Am Heart J 2002;144:S2-7.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>12422134</pmid><doi>10.1067/mhj.2002.129969</doi></addata></record> |
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subjects | ACE inhibitors Aldosterone - physiology Autonomic Nervous System Diseases - etiology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiomegaly - etiology Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Drug therapy Endothelium, Vascular - physiopathology Fibrinolysis Fibrosis - etiology Heart attacks Heart Failure - complications Heart Failure - drug therapy Humans Magnesium - metabolism Medical sciences Mineralocorticoid Receptor Antagonists - therapeutic use Mortality Myocardium - pathology Necrosis Potassium - metabolism Rodents Sodium - metabolism |
title | Aldosterone: Cardiovascular assault |
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