Haemodynamic Effects of Captopril in Acute Left Ventricular Failure Complicating Myocardial Infarction
Activation of the renin-angiotensin system in acute myocardial infarction may have important haemodynamic consequences. The effects of captopril were assessed in nine patients with acute left ventricular failure complicating myocardial infarction. Plasma angiotensin II was elevated at 16.8 (3.6) pmo...
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Veröffentlicht in: | Journal of cardiovascular pharmacology 1987, Vol.9 Suppl 2, p.S25-S30 |
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creator | McAlpine, Howard M Morton, James J Leckie, Brenda Dargie, Henry J |
description | Activation of the renin-angiotensin system in acute myocardial infarction may have important haemodynamic consequences. The effects of captopril were assessed in nine patients with acute left ventricular failure complicating myocardial infarction. Plasma angiotensin II was elevated at 16.8 (3.6) pmol/1 (mean [SE]) including high levels in three of four patients in the absence of any previous therapy, including diuretics. Repeated low doses of captopril were administered to reduce pulmonary capillary wedge pressure |
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The effects of captopril were assessed in nine patients with acute left ventricular failure complicating myocardial infarction. Plasma angiotensin II was elevated at 16.8 (3.6) pmol/1 (mean [SE]) including high levels in three of four patients in the absence of any previous therapy, including diuretics. Repeated low doses of captopril were administered to reduce pulmonary capillary wedge pressure <14 mm Hg or to a maximum total dose of 25 mg. Right atrial pressure fell from 12.4 (0.9) to 9.4 (0.7) mm Hg p < 0.001, pulmonary arterial pressure from 32.7 (3) to 26.4 (2.2) p = 0.01. and pulmonary capillary wedge pressure from 25.7 (2.9) to 19.9 (2.2) p = 0.01. Despite a fall in systemic vascular resistance from 1.540 (110) to 1.330 (76) dyn/s/cm and mean arterial pressure from 84.8 (3.9) to 76.7 (2.7) p = 0.001, changes in cardiac output were small3.8 (0.3) to 4.2 (0.3) NS. Angiotensin II fell in all patients even after only 3.125 mg to a mean of 3.6 (1.0). These improvements occurred whether basal angiotensin II was elevated or normal, and in the presence or absence of diuretic therapy. At 24 hours, seven patients received captopril in the maximum titrated dose of the previous day. Haemodynamic changes at one hour were of similar magnitude to those during incremental dosing. These results suggest that reduction of angiotensin II exerts beneficial haemodynamic effects in heart failure complicating acute myocardial infarction.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><identifier>DOI: 10.1097/00005344-198700002-00007</identifier><identifier>PMID: 2441196</identifier><language>eng</language><publisher>United States: Lippincott-Raven Publishers</publisher><subject>Angiotensin II - blood ; Blood Pressure ; Captopril - therapeutic use ; Female ; Heart Failure - blood ; Heart Failure - drug therapy ; Heart Failure - etiology ; Hemodynamics - drug effects ; Humans ; Male ; Middle Aged ; Myocardial Infarction - complications ; Pulmonary Wedge Pressure ; Renin - blood</subject><ispartof>Journal of cardiovascular pharmacology, 1987, Vol.9 Suppl 2, p.S25-S30</ispartof><rights>Lippincott-Raven Publishers.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2707-7d5c55f2ae226c72749a5348501a01a217f7f23169171cdea5c48065df0edce93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf><![CDATA[$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&PDF=y&D=ovft&AN=00005344-198700002-00007$$EPDF$$P50$$Gwolterskluwer$$H]]></linktopdf><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00005344-198700002-00007$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>314,780,784,4023,4608,27922,27923,27924,64565,65332</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2441196$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McAlpine, Howard M</creatorcontrib><creatorcontrib>Morton, James J</creatorcontrib><creatorcontrib>Leckie, Brenda</creatorcontrib><creatorcontrib>Dargie, Henry J</creatorcontrib><title>Haemodynamic Effects of Captopril in Acute Left Ventricular Failure Complicating Myocardial Infarction</title><title>Journal of cardiovascular pharmacology</title><addtitle>J Cardiovasc Pharmacol</addtitle><description>Activation of the renin-angiotensin system in acute myocardial infarction may have important haemodynamic consequences. The effects of captopril were assessed in nine patients with acute left ventricular failure complicating myocardial infarction. Plasma angiotensin II was elevated at 16.8 (3.6) pmol/1 (mean [SE]) including high levels in three of four patients in the absence of any previous therapy, including diuretics. Repeated low doses of captopril were administered to reduce pulmonary capillary wedge pressure <14 mm Hg or to a maximum total dose of 25 mg. Right atrial pressure fell from 12.4 (0.9) to 9.4 (0.7) mm Hg p < 0.001, pulmonary arterial pressure from 32.7 (3) to 26.4 (2.2) p = 0.01. and pulmonary capillary wedge pressure from 25.7 (2.9) to 19.9 (2.2) p = 0.01. Despite a fall in systemic vascular resistance from 1.540 (110) to 1.330 (76) dyn/s/cm and mean arterial pressure from 84.8 (3.9) to 76.7 (2.7) p = 0.001, changes in cardiac output were small3.8 (0.3) to 4.2 (0.3) NS. Angiotensin II fell in all patients even after only 3.125 mg to a mean of 3.6 (1.0). These improvements occurred whether basal angiotensin II was elevated or normal, and in the presence or absence of diuretic therapy. At 24 hours, seven patients received captopril in the maximum titrated dose of the previous day. Haemodynamic changes at one hour were of similar magnitude to those during incremental dosing. These results suggest that reduction of angiotensin II exerts beneficial haemodynamic effects in heart failure complicating acute myocardial infarction.</description><subject>Angiotensin II - blood</subject><subject>Blood Pressure</subject><subject>Captopril - therapeutic use</subject><subject>Female</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - etiology</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - complications</subject><subject>Pulmonary Wedge Pressure</subject><subject>Renin - blood</subject><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1UcFu2zAMFYoNWdrtEwro1JtXSZas-BgE6Rogwy7brgInU4062UolGUX-fk6T5jaCIEHykQQfCaGcfeWs1fdsElVLWfF2oY-BqI5WX5E5V3VdSSbqD2TOeMMqIWXziVzn_MwYl0o3MzKbcpy3zZy4R8A-docBem_p2jm0JdPo6Ar2Je6TD9QPdGnHgnSLrtDfOJTk7Rgg0QfwYUxIV7HfB2-h-OGJfj9EC6nzEOhmcJBs8XH4TD46CBm_nP0N-fWw_rl6rLY_vm1Wy21lhWa60p2ySjkBKERjtdCyhenMhWIcJhVcO-1EzZuWa247BGXlgjWqcww7i219Q-5Oc_cpvoyYi-l9thgCDBjHbLRuat4KPgEXJ6BNMeeEzky39pAOhjNzpNi8U2wuFL-l9NR6e94x_umxuzSeOZ3q8lR_jaFgyn_D-IrJ7BBC2Zn_fa7-B7cHhnY</recordid><startdate>1987</startdate><enddate>1987</enddate><creator>McAlpine, Howard M</creator><creator>Morton, James J</creator><creator>Leckie, Brenda</creator><creator>Dargie, Henry J</creator><general>Lippincott-Raven Publishers</general><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>7X8</scope></search><sort><creationdate>1987</creationdate><title>Haemodynamic Effects of Captopril in Acute Left Ventricular Failure Complicating Myocardial Infarction</title><author>McAlpine, Howard M ; Morton, James J ; Leckie, Brenda ; Dargie, Henry J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2707-7d5c55f2ae226c72749a5348501a01a217f7f23169171cdea5c48065df0edce93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Angiotensin II - blood</topic><topic>Blood Pressure</topic><topic>Captopril - therapeutic use</topic><topic>Female</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - etiology</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - complications</topic><topic>Pulmonary Wedge Pressure</topic><topic>Renin - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McAlpine, Howard M</creatorcontrib><creatorcontrib>Morton, James J</creatorcontrib><creatorcontrib>Leckie, Brenda</creatorcontrib><creatorcontrib>Dargie, Henry J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McAlpine, Howard M</au><au>Morton, James J</au><au>Leckie, Brenda</au><au>Dargie, Henry J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Haemodynamic Effects of Captopril in Acute Left Ventricular Failure Complicating Myocardial Infarction</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><addtitle>J Cardiovasc Pharmacol</addtitle><date>1987</date><risdate>1987</risdate><volume>9 Suppl 2</volume><spage>S25</spage><epage>S30</epage><pages>S25-S30</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><abstract>Activation of the renin-angiotensin system in acute myocardial infarction may have important haemodynamic consequences. The effects of captopril were assessed in nine patients with acute left ventricular failure complicating myocardial infarction. Plasma angiotensin II was elevated at 16.8 (3.6) pmol/1 (mean [SE]) including high levels in three of four patients in the absence of any previous therapy, including diuretics. Repeated low doses of captopril were administered to reduce pulmonary capillary wedge pressure <14 mm Hg or to a maximum total dose of 25 mg. Right atrial pressure fell from 12.4 (0.9) to 9.4 (0.7) mm Hg p < 0.001, pulmonary arterial pressure from 32.7 (3) to 26.4 (2.2) p = 0.01. and pulmonary capillary wedge pressure from 25.7 (2.9) to 19.9 (2.2) p = 0.01. Despite a fall in systemic vascular resistance from 1.540 (110) to 1.330 (76) dyn/s/cm and mean arterial pressure from 84.8 (3.9) to 76.7 (2.7) p = 0.001, changes in cardiac output were small3.8 (0.3) to 4.2 (0.3) NS. Angiotensin II fell in all patients even after only 3.125 mg to a mean of 3.6 (1.0). These improvements occurred whether basal angiotensin II was elevated or normal, and in the presence or absence of diuretic therapy. At 24 hours, seven patients received captopril in the maximum titrated dose of the previous day. Haemodynamic changes at one hour were of similar magnitude to those during incremental dosing. These results suggest that reduction of angiotensin II exerts beneficial haemodynamic effects in heart failure complicating acute myocardial infarction.</abstract><cop>United States</cop><pub>Lippincott-Raven Publishers</pub><pmid>2441196</pmid><doi>10.1097/00005344-198700002-00007</doi></addata></record> |
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subjects | Angiotensin II - blood Blood Pressure Captopril - therapeutic use Female Heart Failure - blood Heart Failure - drug therapy Heart Failure - etiology Hemodynamics - drug effects Humans Male Middle Aged Myocardial Infarction - complications Pulmonary Wedge Pressure Renin - blood |
title | Haemodynamic Effects of Captopril in Acute Left Ventricular Failure Complicating Myocardial Infarction |
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