Natural evolution of left ventricular haemodynamics following uncomplicated acute myocardial infarction
In an attempt to investigate the changes in left ventricular haemodynamics following uncomplicated myocardial infarction 95 patients with definite electrocardiographic signs of infarction, without clinical signs of cardiac failure, were monitored with a Swan Ganz catheter for the first 24 hours afte...
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Veröffentlicht in: | International journal of cardiology 1986-05, Vol.11 (2), p.175-186 |
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container_title | International journal of cardiology |
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creator | Murray, D.P. Corbeij, H.M.A. Dunselman, P.H.J.M. Held, P.H. Hjalmarson, A. Swedberg, K. |
description | In an attempt to investigate the changes in left ventricular haemodynamics following uncomplicated myocardial infarction 95 patients with definite electrocardiographic signs of infarction, without clinical signs of cardiac failure, were monitored with a Swan Ganz catheter for the first 24 hours after admission to hospital. The median delay from onset of symptoms was 6.8 hours.
Mean heart rate increased (83–86 beats/min;
P < 0.05) while stroke volume index fell (38.4-36.6 ml/m
2;
P < 0.05); cardiac index therefore remained unchanged during the observation period. As a result of a fall in arterial pressure both systemic vascular resistance and left ventricular stroke work index fell significantly (
P < 0.01). Pulmonary wedge pressure also fell (13.6-10.5 mm Hg;
P < 0.001), but this fall was confined to patients whose initial reading was above the median of 13 mm Hg. Pulmonary wedge pressure fell both among the 41 patients who required some medical therapy (15.6-10.8 mm Hg;
P < 0.001) and the 54 who received no medication throughout the 24 hours (12.0-9.8 mm Hg;
P < 0.05).
The 39 patients with anterior wall infarction had higher baseline pulmonary wedge pressure and systemic vascular resistance than the 42 with inferior wall infarction. Later the stroke volume and stroke work index were persistently lower reflecting the greater degree of impairment of left ventricular function in anterior wall infarction.
In conclusion, following an uncomplicated myocardial infarction, cardiac index was maintained, despite a fall in stroke volume, by an increase in heart rate. Pulmonary wedge pressure showed both a spontaneous fall and a fall in those patients given additional medical therapy during the study period. |
doi_str_mv | 10.1016/0167-5273(86)90177-4 |
format | Article |
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Mean heart rate increased (83–86 beats/min;
P < 0.05) while stroke volume index fell (38.4-36.6 ml/m
2;
P < 0.05); cardiac index therefore remained unchanged during the observation period. As a result of a fall in arterial pressure both systemic vascular resistance and left ventricular stroke work index fell significantly (
P < 0.01). Pulmonary wedge pressure also fell (13.6-10.5 mm Hg;
P < 0.001), but this fall was confined to patients whose initial reading was above the median of 13 mm Hg. Pulmonary wedge pressure fell both among the 41 patients who required some medical therapy (15.6-10.8 mm Hg;
P < 0.001) and the 54 who received no medication throughout the 24 hours (12.0-9.8 mm Hg;
P < 0.05).
The 39 patients with anterior wall infarction had higher baseline pulmonary wedge pressure and systemic vascular resistance than the 42 with inferior wall infarction. Later the stroke volume and stroke work index were persistently lower reflecting the greater degree of impairment of left ventricular function in anterior wall infarction.
In conclusion, following an uncomplicated myocardial infarction, cardiac index was maintained, despite a fall in stroke volume, by an increase in heart rate. Pulmonary wedge pressure showed both a spontaneous fall and a fall in those patients given additional medical therapy during the study period.]]></description><identifier>ISSN: 0167-5273</identifier><identifier>EISSN: 1874-1754</identifier><identifier>DOI: 10.1016/0167-5273(86)90177-4</identifier><identifier>PMID: 3710624</identifier><identifier>CODEN: IJCDD5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Aged ; Biological and medical sciences ; Blood Pressure - drug effects ; Cardiac Catheterization ; Cardiac Output - drug effects ; Cardiology. Vascular system ; Coronary heart disease ; Drug Therapy, Combination ; Electrocardiography ; Female ; haemodynamics ; Heart ; Heart Rate - drug effects ; Heart Ventricles - drug effects ; Heart Ventricles - physiopathology ; Hemodynamics - drug effects ; Humans ; Male ; Medical sciences ; Metoprolol - therapeutic use ; myocardial infarction ; Myocardial Infarction - drug therapy ; Myocardial Infarction - physiopathology ; Pulmonary Wedge Pressure - drug effects ; Random Allocation ; Vascular Resistance - drug effects</subject><ispartof>International journal of cardiology, 1986-05, Vol.11 (2), p.175-186</ispartof><rights>1986</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c250t-80e244cb5ebfbe9850a5849ddabd2946ba26e04968d4f3f996968676dea996e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0167-5273(86)90177-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8659349$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3710624$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murray, D.P.</creatorcontrib><creatorcontrib>Corbeij, H.M.A.</creatorcontrib><creatorcontrib>Dunselman, P.H.J.M.</creatorcontrib><creatorcontrib>Held, P.H.</creatorcontrib><creatorcontrib>Hjalmarson, A.</creatorcontrib><creatorcontrib>Swedberg, K.</creatorcontrib><title>Natural evolution of left ventricular haemodynamics following uncomplicated acute myocardial infarction</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description><![CDATA[In an attempt to investigate the changes in left ventricular haemodynamics following uncomplicated myocardial infarction 95 patients with definite electrocardiographic signs of infarction, without clinical signs of cardiac failure, were monitored with a Swan Ganz catheter for the first 24 hours after admission to hospital. The median delay from onset of symptoms was 6.8 hours.
Mean heart rate increased (83–86 beats/min;
P < 0.05) while stroke volume index fell (38.4-36.6 ml/m
2;
P < 0.05); cardiac index therefore remained unchanged during the observation period. As a result of a fall in arterial pressure both systemic vascular resistance and left ventricular stroke work index fell significantly (
P < 0.01). Pulmonary wedge pressure also fell (13.6-10.5 mm Hg;
P < 0.001), but this fall was confined to patients whose initial reading was above the median of 13 mm Hg. Pulmonary wedge pressure fell both among the 41 patients who required some medical therapy (15.6-10.8 mm Hg;
P < 0.001) and the 54 who received no medication throughout the 24 hours (12.0-9.8 mm Hg;
P < 0.05).
The 39 patients with anterior wall infarction had higher baseline pulmonary wedge pressure and systemic vascular resistance than the 42 with inferior wall infarction. Later the stroke volume and stroke work index were persistently lower reflecting the greater degree of impairment of left ventricular function in anterior wall infarction.
In conclusion, following an uncomplicated myocardial infarction, cardiac index was maintained, despite a fall in stroke volume, by an increase in heart rate. Pulmonary wedge pressure showed both a spontaneous fall and a fall in those patients given additional medical therapy during the study period.]]></description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiac Catheterization</subject><subject>Cardiac Output - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Drug Therapy, Combination</subject><subject>Electrocardiography</subject><subject>Female</subject><subject>haemodynamics</subject><subject>Heart</subject><subject>Heart Rate - drug effects</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metoprolol - therapeutic use</subject><subject>myocardial infarction</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Pulmonary Wedge Pressure - drug effects</subject><subject>Random Allocation</subject><subject>Vascular Resistance - drug effects</subject><issn>0167-5273</issn><issn>1874-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhoMo67j6DxT6IKKH1nR3Op1cFmTxCxa96DlUJ5U1kk7GJD0y_960M8zRQ0hBvfVQ9RDyvKNvO9rxd_VN7dhPw2vB30jaTVPLHpBdJybWdtPIHpLdJfKYPMn5F6WUSSmuyNUwdZT3bEfuv0JZE_gGD9GvxcXQRNt4tKU5YCjJ6dVDan4CLtEcAyxO58ZG7-MfF-6bNei47L3TUNA0oNeCzXKMGpJxFeqChaQ36lPyyILP-Oz8X5MfHz98v_3c3n379OX2_V2r-5GWVlDsGdPziLOdUYqRwiiYNAZm00vGZ-g51iO4MMwOVkpeSz5xg1BrlMM1eXXi7lP8vWIuanFZo_cQMK5ZTbwye8FqkJ2COsWcE1q1T26BdFQdVZtftclTmzwluPrnV21jL878dV7QXIbOQmv_5bkPWYO3CYJ2-RITfJQD29a8OcWwujg4TCprh0GjcQl1USa6_-_xF6oPmTs</recordid><startdate>198605</startdate><enddate>198605</enddate><creator>Murray, D.P.</creator><creator>Corbeij, H.M.A.</creator><creator>Dunselman, P.H.J.M.</creator><creator>Held, P.H.</creator><creator>Hjalmarson, A.</creator><creator>Swedberg, K.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>7X8</scope></search><sort><creationdate>198605</creationdate><title>Natural evolution of left ventricular haemodynamics following uncomplicated acute myocardial infarction</title><author>Murray, D.P. ; Corbeij, H.M.A. ; Dunselman, P.H.J.M. ; Held, P.H. ; Hjalmarson, A. ; Swedberg, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c250t-80e244cb5ebfbe9850a5849ddabd2946ba26e04968d4f3f996968676dea996e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiac Catheterization</topic><topic>Cardiac Output - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Drug Therapy, Combination</topic><topic>Electrocardiography</topic><topic>Female</topic><topic>haemodynamics</topic><topic>Heart</topic><topic>Heart Rate - drug effects</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metoprolol - therapeutic use</topic><topic>myocardial infarction</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Pulmonary Wedge Pressure - drug effects</topic><topic>Random Allocation</topic><topic>Vascular Resistance - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Murray, D.P.</creatorcontrib><creatorcontrib>Corbeij, H.M.A.</creatorcontrib><creatorcontrib>Dunselman, P.H.J.M.</creatorcontrib><creatorcontrib>Held, P.H.</creatorcontrib><creatorcontrib>Hjalmarson, A.</creatorcontrib><creatorcontrib>Swedberg, K.</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>MEDLINE - Academic</collection><jtitle>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murray, D.P.</au><au>Corbeij, H.M.A.</au><au>Dunselman, P.H.J.M.</au><au>Held, P.H.</au><au>Hjalmarson, A.</au><au>Swedberg, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Natural evolution of left ventricular haemodynamics following uncomplicated acute myocardial infarction</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>1986-05</date><risdate>1986</risdate><volume>11</volume><issue>2</issue><spage>175</spage><epage>186</epage><pages>175-186</pages><issn>0167-5273</issn><eissn>1874-1754</eissn><coden>IJCDD5</coden><abstract><![CDATA[In an attempt to investigate the changes in left ventricular haemodynamics following uncomplicated myocardial infarction 95 patients with definite electrocardiographic signs of infarction, without clinical signs of cardiac failure, were monitored with a Swan Ganz catheter for the first 24 hours after admission to hospital. The median delay from onset of symptoms was 6.8 hours.
Mean heart rate increased (83–86 beats/min;
P < 0.05) while stroke volume index fell (38.4-36.6 ml/m
2;
P < 0.05); cardiac index therefore remained unchanged during the observation period. As a result of a fall in arterial pressure both systemic vascular resistance and left ventricular stroke work index fell significantly (
P < 0.01). Pulmonary wedge pressure also fell (13.6-10.5 mm Hg;
P < 0.001), but this fall was confined to patients whose initial reading was above the median of 13 mm Hg. Pulmonary wedge pressure fell both among the 41 patients who required some medical therapy (15.6-10.8 mm Hg;
P < 0.001) and the 54 who received no medication throughout the 24 hours (12.0-9.8 mm Hg;
P < 0.05).
The 39 patients with anterior wall infarction had higher baseline pulmonary wedge pressure and systemic vascular resistance than the 42 with inferior wall infarction. Later the stroke volume and stroke work index were persistently lower reflecting the greater degree of impairment of left ventricular function in anterior wall infarction.
In conclusion, following an uncomplicated myocardial infarction, cardiac index was maintained, despite a fall in stroke volume, by an increase in heart rate. Pulmonary wedge pressure showed both a spontaneous fall and a fall in those patients given additional medical therapy during the study period.]]></abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>3710624</pmid><doi>10.1016/0167-5273(86)90177-4</doi><tpages>12</tpages></addata></record> |
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subjects | Aged Biological and medical sciences Blood Pressure - drug effects Cardiac Catheterization Cardiac Output - drug effects Cardiology. Vascular system Coronary heart disease Drug Therapy, Combination Electrocardiography Female haemodynamics Heart Heart Rate - drug effects Heart Ventricles - drug effects Heart Ventricles - physiopathology Hemodynamics - drug effects Humans Male Medical sciences Metoprolol - therapeutic use myocardial infarction Myocardial Infarction - drug therapy Myocardial Infarction - physiopathology Pulmonary Wedge Pressure - drug effects Random Allocation Vascular Resistance - drug effects |
title | Natural evolution of left ventricular haemodynamics following uncomplicated acute myocardial infarction |
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