Effect of Captopril on Progressive Ventricular Dilatation after Anterior Myocardial Infarction
We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a rad...
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Veröffentlicht in: | The New England journal of medicine 1988-07, Vol.319 (2), p.80-86 |
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description | We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months.
No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [±SEM] of 21 ±8 ml (P |
doi_str_mv | 10.1056/NEJM198807143190204 |
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No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [±SEM] of 21 ±8 ml (P<0.02) in the placebo group, but by only 10±6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P<0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P<0.05). Patients given captopril also had increased exercise capacity (P<0.05).
This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance. (N Engl J Med 1988; 319:80–6.)
VENTRICULAR dilatation is an important expression of systolic dysfunction of diverse causes, and the extent of dilatation provides important prognostic information. In patients with coronary artery disease, left ventricular volume is the most powerful predictor of survival.
1
2
3
The left ventricle begins to dilate soon after myocardial infarction, and in the acute phase, such chamber enlargement is caused primarily by expansion of the infarct.
4
,
5
However, lengthening of the zone without an infarct also contributes to the overall increase in ventricular size.
6
,
7
The eventual volume of the ventricle with an infarct has been shown to be related to the size of the . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJM198807143190204</identifier><identifier>PMID: 2967917</identifier><identifier>CODEN: NEJMAG</identifier><language>eng</language><publisher>Boston, MA: Massachusetts Medical Society</publisher><subject>Antihypertensive agents ; Biological and medical sciences ; Captopril - pharmacology ; Captopril - therapeutic use ; Cardiomegaly - drug therapy ; Cardiomegaly - etiology ; Cardiomegaly - physiopathology ; Cardiovascular disease ; Cardiovascular system ; Catheterization ; Clinical trials ; Clinical Trials as Topic ; Congestive heart failure ; Coronary artery ; Coronary vessels ; Dilatation ; Electrocardiography ; Enzymes ; Exercise Test ; Female ; Fitness equipment ; Follow-Up Studies ; Heart attacks ; Heart failure ; Heart Ventricles ; Humans ; Intubation ; Ischemia ; Male ; Medical prognosis ; Medical sciences ; Middle Aged ; Myocardial infarction ; Myocardial Infarction - complications ; Myocardial Infarction - drug therapy ; Myocardial Infarction - physiopathology ; Occlusion ; Patients ; Pharmacology. Drug treatments ; Random Allocation ; Rodents ; Stroke Volume ; Time Factors ; Ventricle ; Womens health</subject><ispartof>The New England journal of medicine, 1988-07, Vol.319 (2), p.80-86</ispartof><rights>1990 INIST-CNRS</rights><rights>Copyright Massachusetts Medical Society Jul 14, 1988</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-326f7be46117305a7647fb9610355406c634146bfff482b22635afb80ba7ddac3</citedby><cites>FETCH-LOGICAL-c495t-326f7be46117305a7647fb9610355406c634146bfff482b22635afb80ba7ddac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1881507480?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,64383,64385,64387,72239</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6596971$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2967917$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pfeffer, Marc A</creatorcontrib><creatorcontrib>Lamas, Gervasio A</creatorcontrib><creatorcontrib>Vaughan, Douglas E</creatorcontrib><creatorcontrib>Parisi, Alfred F</creatorcontrib><creatorcontrib>Braunwald, Eugene</creatorcontrib><title>Effect of Captopril on Progressive Ventricular Dilatation after Anterior Myocardial Infarction</title><title>The New England journal of medicine</title><addtitle>N Engl J Med</addtitle><description>We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months.
No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [±SEM] of 21 ±8 ml (P<0.02) in the placebo group, but by only 10±6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P<0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P<0.05). Patients given captopril also had increased exercise capacity (P<0.05).
This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance. (N Engl J Med 1988; 319:80–6.)
VENTRICULAR dilatation is an important expression of systolic dysfunction of diverse causes, and the extent of dilatation provides important prognostic information. In patients with coronary artery disease, left ventricular volume is the most powerful predictor of survival.
1
2
3
The left ventricle begins to dilate soon after myocardial infarction, and in the acute phase, such chamber enlargement is caused primarily by expansion of the infarct.
4
,
5
However, lengthening of the zone without an infarct also contributes to the overall increase in ventricular size.
6
,
7
The eventual volume of the ventricle with an infarct has been shown to be related to the size of the . . .</description><subject>Antihypertensive agents</subject><subject>Biological and medical sciences</subject><subject>Captopril - pharmacology</subject><subject>Captopril - therapeutic use</subject><subject>Cardiomegaly - drug therapy</subject><subject>Cardiomegaly - etiology</subject><subject>Cardiomegaly - physiopathology</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular system</subject><subject>Catheterization</subject><subject>Clinical trials</subject><subject>Clinical Trials as Topic</subject><subject>Congestive heart failure</subject><subject>Coronary artery</subject><subject>Coronary vessels</subject><subject>Dilatation</subject><subject>Electrocardiography</subject><subject>Enzymes</subject><subject>Exercise Test</subject><subject>Female</subject><subject>Fitness equipment</subject><subject>Follow-Up Studies</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Heart Ventricles</subject><subject>Humans</subject><subject>Intubation</subject><subject>Ischemia</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - complications</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Occlusion</subject><subject>Patients</subject><subject>Pharmacology. Drug treatments</subject><subject>Random Allocation</subject><subject>Rodents</subject><subject>Stroke Volume</subject><subject>Time Factors</subject><subject>Ventricle</subject><subject>Womens health</subject><issn>0028-4793</issn><issn>1533-4406</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp90M9LHDEUB_BQLLra_gUiBBQvMjaZ_D4u2221qO2h7dHhTTaRLDOTNZkp-N83sosHEXNIDu_zXpIvQseUXFIi5Je75Y9barQminJGDakJ_4BmVDBWcU7kHpoRUuuKK8MO0GHOa1IW5WYf7ddGKkPVDN0vvXd2xNHjBWzGuEmhw3HAv1J8SC7n8M_hv24YU7BTBwl_DR2MMIZCwI8u4flQ9hATvn2KFtIqQIevBw_JPqNP6KOHLrvPu_MI_fm2_L24qm5-fr9ezG8qy40YK1ZLr1rHJaWKEQFKcuVbIylhQpSvWMk45bL13nNdt3UtmQDfatKCWq3AsiN0vp27SfFxcnls-pCt6zoYXJxyo3QtjCCmwNNXcB2nNJS3NVRrKojimhTFtsqmmHNyvim59JCeGkqa5-ybN7IvXSe72VPbu9VLzy7sUj_b1SFb6HyCwYb8wqQw0iha2MWW9X1uBrfu3730P0cKlz8</recordid><startdate>19880714</startdate><enddate>19880714</enddate><creator>Pfeffer, Marc A</creator><creator>Lamas, Gervasio A</creator><creator>Vaughan, Douglas E</creator><creator>Parisi, Alfred F</creator><creator>Braunwald, Eugene</creator><general>Massachusetts Medical Society</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>0TZ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K0Y</scope><scope>LK8</scope><scope>M0R</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>19880714</creationdate><title>Effect of Captopril on Progressive Ventricular Dilatation after Anterior Myocardial Infarction</title><author>Pfeffer, Marc A ; Lamas, Gervasio A ; Vaughan, Douglas E ; Parisi, Alfred F ; Braunwald, Eugene</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-326f7be46117305a7647fb9610355406c634146bfff482b22635afb80ba7ddac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Antihypertensive agents</topic><topic>Biological and medical sciences</topic><topic>Captopril - pharmacology</topic><topic>Captopril - therapeutic use</topic><topic>Cardiomegaly - drug therapy</topic><topic>Cardiomegaly - etiology</topic><topic>Cardiomegaly - physiopathology</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular system</topic><topic>Catheterization</topic><topic>Clinical trials</topic><topic>Clinical Trials as Topic</topic><topic>Congestive heart failure</topic><topic>Coronary artery</topic><topic>Coronary vessels</topic><topic>Dilatation</topic><topic>Electrocardiography</topic><topic>Enzymes</topic><topic>Exercise Test</topic><topic>Female</topic><topic>Fitness equipment</topic><topic>Follow-Up Studies</topic><topic>Heart attacks</topic><topic>Heart failure</topic><topic>Heart Ventricles</topic><topic>Humans</topic><topic>Intubation</topic><topic>Ischemia</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - complications</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Occlusion</topic><topic>Patients</topic><topic>Pharmacology. Drug treatments</topic><topic>Random Allocation</topic><topic>Rodents</topic><topic>Stroke Volume</topic><topic>Time Factors</topic><topic>Ventricle</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pfeffer, Marc A</creatorcontrib><creatorcontrib>Lamas, Gervasio A</creatorcontrib><creatorcontrib>Vaughan, Douglas E</creatorcontrib><creatorcontrib>Parisi, Alfred F</creatorcontrib><creatorcontrib>Braunwald, Eugene</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>Pharma and Biotech Premium PRO</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>SciTech Premium Collection</collection><collection>New England Journal of Medicine</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The New England journal of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pfeffer, Marc A</au><au>Lamas, Gervasio A</au><au>Vaughan, Douglas E</au><au>Parisi, Alfred F</au><au>Braunwald, Eugene</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Captopril on Progressive Ventricular Dilatation after Anterior Myocardial Infarction</atitle><jtitle>The New England journal of medicine</jtitle><addtitle>N Engl J Med</addtitle><date>1988-07-14</date><risdate>1988</risdate><volume>319</volume><issue>2</issue><spage>80</spage><epage>86</epage><pages>80-86</pages><issn>0028-4793</issn><eissn>1533-4406</eissn><coden>NEJMAG</coden><abstract>We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months.
No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [±SEM] of 21 ±8 ml (P<0.02) in the placebo group, but by only 10±6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P<0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P<0.05). Patients given captopril also had increased exercise capacity (P<0.05).
This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance. (N Engl J Med 1988; 319:80–6.)
VENTRICULAR dilatation is an important expression of systolic dysfunction of diverse causes, and the extent of dilatation provides important prognostic information. In patients with coronary artery disease, left ventricular volume is the most powerful predictor of survival.
1
2
3
The left ventricle begins to dilate soon after myocardial infarction, and in the acute phase, such chamber enlargement is caused primarily by expansion of the infarct.
4
,
5
However, lengthening of the zone without an infarct also contributes to the overall increase in ventricular size.
6
,
7
The eventual volume of the ventricle with an infarct has been shown to be related to the size of the . . .</abstract><cop>Boston, MA</cop><pub>Massachusetts Medical Society</pub><pmid>2967917</pmid><doi>10.1056/NEJM198807143190204</doi><tpages>7</tpages></addata></record> |
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subjects | Antihypertensive agents Biological and medical sciences Captopril - pharmacology Captopril - therapeutic use Cardiomegaly - drug therapy Cardiomegaly - etiology Cardiomegaly - physiopathology Cardiovascular disease Cardiovascular system Catheterization Clinical trials Clinical Trials as Topic Congestive heart failure Coronary artery Coronary vessels Dilatation Electrocardiography Enzymes Exercise Test Female Fitness equipment Follow-Up Studies Heart attacks Heart failure Heart Ventricles Humans Intubation Ischemia Male Medical prognosis Medical sciences Middle Aged Myocardial infarction Myocardial Infarction - complications Myocardial Infarction - drug therapy Myocardial Infarction - physiopathology Occlusion Patients Pharmacology. Drug treatments Random Allocation Rodents Stroke Volume Time Factors Ventricle Womens health |
title | Effect of Captopril on Progressive Ventricular Dilatation after Anterior Myocardial Infarction |
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