Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest
In patients with shock after acute myocardial infarction (AMI), the optimal level of pharmacologic support is unknown. Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary perfusion and increase infarct size. This study aim...
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| Veröffentlicht in: | Journal of the American College of Cardiology 2020-08, Vol.76 (7), p.812-824 |
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| creator | Ameloot, Koen Jakkula, Pekka Hästbacka, Johanna Reinikainen, Matti Pettilä, Ville Loisa, Pekka Tiainen, Marjaana Bendel, Stepani Birkelund, Thomas Belmans, Ann Palmers, Pieter-Jan Bogaerts, Eline Lemmens, Robin De Deyne, Cathy Ferdinande, Bert Dupont, Matthias Janssens, Stefan Dens, Joseph Skrifvars, Markus B |
| description | In patients with shock after acute myocardial infarction (AMI), the optimal level of pharmacologic support is unknown. Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary perfusion and increase infarct size.
This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest.
This study used patient-level pooled analysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) trials who were randomized to MAP 65 mm Hg or MAP 80/85 to 100 mm Hg targets during the first 36 h after admission. The primary endpoint was the area under the 72-h high-sensitivity troponin-T curve.
Of 235 patients originally randomized, 120 patients had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 ± 9 mm Hg vs. 72 ± 10 mm Hg, p |
| doi_str_mv | 10.1016/j.jacc.2020.06.043 |
| format | Article |
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This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest.
This study used patient-level pooled analysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) trials who were randomized to MAP 65 mm Hg or MAP 80/85 to 100 mm Hg targets during the first 36 h after admission. The primary endpoint was the area under the 72-h high-sensitivity troponin-T curve.
Of 235 patients originally randomized, 120 patients had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 ± 9 mm Hg vs. 72 ± 10 mm Hg, p < 0.001). Whereas admission hemodynamics and angiographic findings were all well-balanced and revascularization was performed equally effective, the area under the 72-h high-sensitivity troponin-T curve was lower in patients assigned to the higher MAP target (median: 1.14 μg.72 h/l [interquartile range: 0.35 to 2.31 μg.72 h/l] vs. median: 1.56 μg.72 h/l [interquartile range: 0.61 to 4.72 μg. 72 h/l]; p = 0.04). Additional pharmacologic support did not increase the risk of a new cardiac arrest (p = 0.88) or atrial fibrillation (p = 0.94). Survival with good neurologic outcome at 180 days was not different between both groups (64% vs. 53%, odds ratio: 1.55; 95% confidence interval: 0.74 to 3.22).
In post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 and 100 mm Hg with additional use of inotropes and vasopressors was associated with smaller myocardial injury.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2020.06.043</identifier><identifier>PMID: 32792079</identifier><language>eng</language><publisher>United States</publisher><subject>Arterial Pressure - drug effects ; Atrial Fibrillation - etiology ; Atrial Fibrillation - physiopathology ; Atrial Fibrillation - prevention & control ; Blood Pressure Determination - methods ; Cardiotonic Agents - administration & dosage ; Coronary Angiography - methods ; Female ; Heart Arrest - complications ; Heart Arrest - physiopathology ; Heart Arrest - therapy ; Hemodynamics - drug effects ; Humans ; Male ; Middle Aged ; Myocardial Infarction - blood ; Myocardial Infarction - etiology ; Myocardial Infarction - physiopathology ; Myocardial Infarction - prevention & control ; Outcome Assessment, Health Care ; Shock - complications ; Shock - physiopathology ; Shock - therapy ; Survivors ; Troponin T - analysis ; Vasoconstrictor Agents - administration & dosage</subject><ispartof>Journal of the American College of Cardiology, 2020-08, Vol.76 (7), p.812-824</ispartof><rights>Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c347t-ab68f27e4c9ba20a7cbae747380c83be10767bb832119a070ec212fe92f56f53</citedby><cites>FETCH-LOGICAL-c347t-ab68f27e4c9ba20a7cbae747380c83be10767bb832119a070ec212fe92f56f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32792079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ameloot, Koen</creatorcontrib><creatorcontrib>Jakkula, Pekka</creatorcontrib><creatorcontrib>Hästbacka, Johanna</creatorcontrib><creatorcontrib>Reinikainen, Matti</creatorcontrib><creatorcontrib>Pettilä, Ville</creatorcontrib><creatorcontrib>Loisa, Pekka</creatorcontrib><creatorcontrib>Tiainen, Marjaana</creatorcontrib><creatorcontrib>Bendel, Stepani</creatorcontrib><creatorcontrib>Birkelund, Thomas</creatorcontrib><creatorcontrib>Belmans, Ann</creatorcontrib><creatorcontrib>Palmers, Pieter-Jan</creatorcontrib><creatorcontrib>Bogaerts, Eline</creatorcontrib><creatorcontrib>Lemmens, Robin</creatorcontrib><creatorcontrib>De Deyne, Cathy</creatorcontrib><creatorcontrib>Ferdinande, Bert</creatorcontrib><creatorcontrib>Dupont, Matthias</creatorcontrib><creatorcontrib>Janssens, Stefan</creatorcontrib><creatorcontrib>Dens, Joseph</creatorcontrib><creatorcontrib>Skrifvars, Markus B</creatorcontrib><title>Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>In patients with shock after acute myocardial infarction (AMI), the optimal level of pharmacologic support is unknown. Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary perfusion and increase infarct size.
This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest.
This study used patient-level pooled analysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) trials who were randomized to MAP 65 mm Hg or MAP 80/85 to 100 mm Hg targets during the first 36 h after admission. The primary endpoint was the area under the 72-h high-sensitivity troponin-T curve.
Of 235 patients originally randomized, 120 patients had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 ± 9 mm Hg vs. 72 ± 10 mm Hg, p < 0.001). Whereas admission hemodynamics and angiographic findings were all well-balanced and revascularization was performed equally effective, the area under the 72-h high-sensitivity troponin-T curve was lower in patients assigned to the higher MAP target (median: 1.14 μg.72 h/l [interquartile range: 0.35 to 2.31 μg.72 h/l] vs. median: 1.56 μg.72 h/l [interquartile range: 0.61 to 4.72 μg. 72 h/l]; p = 0.04). Additional pharmacologic support did not increase the risk of a new cardiac arrest (p = 0.88) or atrial fibrillation (p = 0.94). Survival with good neurologic outcome at 180 days was not different between both groups (64% vs. 53%, odds ratio: 1.55; 95% confidence interval: 0.74 to 3.22).
In post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 and 100 mm Hg with additional use of inotropes and vasopressors was associated with smaller myocardial injury.</description><subject>Arterial Pressure - drug effects</subject><subject>Atrial Fibrillation - etiology</subject><subject>Atrial Fibrillation - physiopathology</subject><subject>Atrial Fibrillation - prevention & control</subject><subject>Blood Pressure Determination - methods</subject><subject>Cardiotonic Agents - administration & dosage</subject><subject>Coronary Angiography - methods</subject><subject>Female</subject><subject>Heart Arrest - complications</subject><subject>Heart Arrest - physiopathology</subject><subject>Heart Arrest - therapy</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Infarction - prevention & control</subject><subject>Outcome Assessment, Health Care</subject><subject>Shock - complications</subject><subject>Shock - physiopathology</subject><subject>Shock - therapy</subject><subject>Survivors</subject><subject>Troponin T - analysis</subject><subject>Vasoconstrictor Agents - administration & dosage</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM9LwzAYhoMobk7_AQ-So5fWL0nbtMc5_DGYbODAY0jTlKW2zUzSw_57O52ePnh53-eDB6FbAjEBkj00cSOViilQiCGLIWFnaErSNI9YWvBzNAXO0ohAwSfoyvsGALKcFJdowigvKPBiisr1Pphu6PBja22FN057PziNTY83MhjdB48_TNjh951Vn3heB-3wXA1B47eDVdJVRrZ42dfSqWBsj2Vf4cVPrPDcjbhwjS5q2Xp9c7oztH1-2i5eo9X6ZbmYryLFEh4iWWZ5TblOVFFKCpKrUmqecJaDylmpCfCMl2XOKCGFBA5aUUJrXdA6zeqUzdD9L3bv7Ncw_hWd8Uq3rey1HbygCUuSPIWUjVX6W1XOeu90LfbOdNIdBAFxVCsacVQrjmoFZGJUO47uTvyh7HT1P_lzyb4BbMB12A</recordid><startdate>20200818</startdate><enddate>20200818</enddate><creator>Ameloot, Koen</creator><creator>Jakkula, Pekka</creator><creator>Hästbacka, Johanna</creator><creator>Reinikainen, Matti</creator><creator>Pettilä, Ville</creator><creator>Loisa, Pekka</creator><creator>Tiainen, Marjaana</creator><creator>Bendel, Stepani</creator><creator>Birkelund, Thomas</creator><creator>Belmans, Ann</creator><creator>Palmers, Pieter-Jan</creator><creator>Bogaerts, Eline</creator><creator>Lemmens, Robin</creator><creator>De Deyne, Cathy</creator><creator>Ferdinande, Bert</creator><creator>Dupont, Matthias</creator><creator>Janssens, Stefan</creator><creator>Dens, Joseph</creator><creator>Skrifvars, Markus B</creator><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>20200818</creationdate><title>Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest</title><author>Ameloot, Koen ; Jakkula, Pekka ; Hästbacka, Johanna ; Reinikainen, Matti ; Pettilä, Ville ; Loisa, Pekka ; Tiainen, Marjaana ; Bendel, Stepani ; Birkelund, Thomas ; Belmans, Ann ; Palmers, Pieter-Jan ; Bogaerts, Eline ; Lemmens, Robin ; De Deyne, Cathy ; Ferdinande, Bert ; Dupont, Matthias ; Janssens, Stefan ; Dens, Joseph ; Skrifvars, Markus B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c347t-ab68f27e4c9ba20a7cbae747380c83be10767bb832119a070ec212fe92f56f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Arterial Pressure - drug effects</topic><topic>Atrial Fibrillation - etiology</topic><topic>Atrial Fibrillation - physiopathology</topic><topic>Atrial Fibrillation - prevention & control</topic><topic>Blood Pressure Determination - methods</topic><topic>Cardiotonic Agents - administration & dosage</topic><topic>Coronary Angiography - methods</topic><topic>Female</topic><topic>Heart Arrest - complications</topic><topic>Heart Arrest - physiopathology</topic><topic>Heart Arrest - therapy</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Infarction - prevention & control</topic><topic>Outcome Assessment, Health Care</topic><topic>Shock - complications</topic><topic>Shock - physiopathology</topic><topic>Shock - therapy</topic><topic>Survivors</topic><topic>Troponin T - analysis</topic><topic>Vasoconstrictor Agents - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ameloot, Koen</creatorcontrib><creatorcontrib>Jakkula, Pekka</creatorcontrib><creatorcontrib>Hästbacka, Johanna</creatorcontrib><creatorcontrib>Reinikainen, Matti</creatorcontrib><creatorcontrib>Pettilä, Ville</creatorcontrib><creatorcontrib>Loisa, Pekka</creatorcontrib><creatorcontrib>Tiainen, Marjaana</creatorcontrib><creatorcontrib>Bendel, Stepani</creatorcontrib><creatorcontrib>Birkelund, Thomas</creatorcontrib><creatorcontrib>Belmans, Ann</creatorcontrib><creatorcontrib>Palmers, Pieter-Jan</creatorcontrib><creatorcontrib>Bogaerts, Eline</creatorcontrib><creatorcontrib>Lemmens, Robin</creatorcontrib><creatorcontrib>De Deyne, Cathy</creatorcontrib><creatorcontrib>Ferdinande, Bert</creatorcontrib><creatorcontrib>Dupont, Matthias</creatorcontrib><creatorcontrib>Janssens, Stefan</creatorcontrib><creatorcontrib>Dens, Joseph</creatorcontrib><creatorcontrib>Skrifvars, Markus B</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 the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ameloot, Koen</au><au>Jakkula, Pekka</au><au>Hästbacka, Johanna</au><au>Reinikainen, Matti</au><au>Pettilä, Ville</au><au>Loisa, Pekka</au><au>Tiainen, Marjaana</au><au>Bendel, Stepani</au><au>Birkelund, Thomas</au><au>Belmans, Ann</au><au>Palmers, Pieter-Jan</au><au>Bogaerts, Eline</au><au>Lemmens, Robin</au><au>De Deyne, Cathy</au><au>Ferdinande, Bert</au><au>Dupont, Matthias</au><au>Janssens, Stefan</au><au>Dens, Joseph</au><au>Skrifvars, Markus B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2020-08-18</date><risdate>2020</risdate><volume>76</volume><issue>7</issue><spage>812</spage><epage>824</epage><pages>812-824</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>In patients with shock after acute myocardial infarction (AMI), the optimal level of pharmacologic support is unknown. Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, diastolic hypotension may reduce coronary perfusion and increase infarct size.
This study aimed to determine the optimal mean arterial pressure (MAP) in patients with AMI and shock after cardiac arrest.
This study used patient-level pooled analysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuroprotective Goal Directed Hemodynamic Optimization in Post-cardiac Arrest Patients; NCT02541591) and COMACARE (Carbon Dioxide, Oxygen and Mean Arterial Pressure After Cardiac Arrest and Resuscitation; NCT02698917) trials who were randomized to MAP 65 mm Hg or MAP 80/85 to 100 mm Hg targets during the first 36 h after admission. The primary endpoint was the area under the 72-h high-sensitivity troponin-T curve.
Of 235 patients originally randomized, 120 patients had AMI with shock. Patients assigned to the higher MAP target (n = 58) received higher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 ± 9 mm Hg vs. 72 ± 10 mm Hg, p < 0.001). Whereas admission hemodynamics and angiographic findings were all well-balanced and revascularization was performed equally effective, the area under the 72-h high-sensitivity troponin-T curve was lower in patients assigned to the higher MAP target (median: 1.14 μg.72 h/l [interquartile range: 0.35 to 2.31 μg.72 h/l] vs. median: 1.56 μg.72 h/l [interquartile range: 0.61 to 4.72 μg. 72 h/l]; p = 0.04). Additional pharmacologic support did not increase the risk of a new cardiac arrest (p = 0.88) or atrial fibrillation (p = 0.94). Survival with good neurologic outcome at 180 days was not different between both groups (64% vs. 53%, odds ratio: 1.55; 95% confidence interval: 0.74 to 3.22).
In post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 and 100 mm Hg with additional use of inotropes and vasopressors was associated with smaller myocardial injury.</abstract><cop>United States</cop><pmid>32792079</pmid><doi>10.1016/j.jacc.2020.06.043</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Arterial Pressure - drug effects Atrial Fibrillation - etiology Atrial Fibrillation - physiopathology Atrial Fibrillation - prevention & control Blood Pressure Determination - methods Cardiotonic Agents - administration & dosage Coronary Angiography - methods Female Heart Arrest - complications Heart Arrest - physiopathology Heart Arrest - therapy Hemodynamics - drug effects Humans Male Middle Aged Myocardial Infarction - blood Myocardial Infarction - etiology Myocardial Infarction - physiopathology Myocardial Infarction - prevention & control Outcome Assessment, Health Care Shock - complications Shock - physiopathology Shock - therapy Survivors Troponin T - analysis Vasoconstrictor Agents - administration & dosage |
| title | Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest |
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