Hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate in acute myocardial infarction
Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolitic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or...
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Veröffentlicht in: | The American journal of cardiology 1985-08, Vol.56 (4), p.266-269 |
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creator | Marchionni, Niccolò Conti, Alberto De Alfieri, Walter Di Bari, Mauro Ferrucci, Luigi Lombardi, Alessandra Moschi, Guya Pini, Riccardo Vannucci, Andrea |
description | Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolitic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or less) pulmonary artery (PA) wedge pressure and normal (35 g-m/m
2 or greater) left ventricular (LV) stroke work index; subset 2, elevated (more than 15 mm Hg) PA wedge pressure and normal LV stroke work index; subset 3, normal PA wedge pressure and reduced (less than 35 g-m/m
2) LV stroke work index; subset 4, elevated PA wedge pressure and LV stroke work index moderately reduced to a range between 16 and 34 g-m/m
2. Patients were randomized into an FDP (250 mg/kg body weight in isotonic saline solution intravenously in 20 minutes) and into a placebo group. Each subset contained 5 FDP- and 5 placebo-treated patients. After basal measurements, hemodynamic measurements were reassessed at 60, 90 and 120 minutes from the infusions, while a standard 12-lead electrocardiogram was recorded in the basal state and 120 minutes after infusion. Nonsignificant hemodynamic change was observed in the placebo subsets, and FDP failed to exert any effect in subsets 1, 2 and 3. A 24% (p < 0.02) increase in cardiac index occurred 60 minutes after FDP in subset 4. LV stroke work index also increased, while PA wedge pressure remained unchanged. Electrocardiographic markers of myocardial ischemia were not significantly reduced in any of the subsets, both in the control and in the treated group. Nevertheless, reduction was greater after FDP than after placebo administration in each subset, and it attained statistical significance when analyzed in the whole series of 20 FDP-treated patients. Two control patients died (1 from progressive LV failure) and 1 had a primary ventricular fibrillation successfully treated by direct-current shock. No FDP-treated patient died or had ventricular arrhythmias. |
doi_str_mv | 10.1016/0002-9149(85)90847-1 |
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2 or greater) left ventricular (LV) stroke work index; subset 2, elevated (more than 15 mm Hg) PA wedge pressure and normal LV stroke work index; subset 3, normal PA wedge pressure and reduced (less than 35 g-m/m
2) LV stroke work index; subset 4, elevated PA wedge pressure and LV stroke work index moderately reduced to a range between 16 and 34 g-m/m
2. Patients were randomized into an FDP (250 mg/kg body weight in isotonic saline solution intravenously in 20 minutes) and into a placebo group. Each subset contained 5 FDP- and 5 placebo-treated patients. After basal measurements, hemodynamic measurements were reassessed at 60, 90 and 120 minutes from the infusions, while a standard 12-lead electrocardiogram was recorded in the basal state and 120 minutes after infusion. Nonsignificant hemodynamic change was observed in the placebo subsets, and FDP failed to exert any effect in subsets 1, 2 and 3. A 24% (p < 0.02) increase in cardiac index occurred 60 minutes after FDP in subset 4. LV stroke work index also increased, while PA wedge pressure remained unchanged. Electrocardiographic markers of myocardial ischemia were not significantly reduced in any of the subsets, both in the control and in the treated group. Nevertheless, reduction was greater after FDP than after placebo administration in each subset, and it attained statistical significance when analyzed in the whole series of 20 FDP-treated patients. Two control patients died (1 from progressive LV failure) and 1 had a primary ventricular fibrillation successfully treated by direct-current shock. No FDP-treated patient died or had ventricular arrhythmias.</description><identifier>ISSN: 0002-9149</identifier><identifier>EISSN: 1879-1913</identifier><identifier>DOI: 10.1016/0002-9149(85)90847-1</identifier><identifier>PMID: 4025164</identifier><identifier>CODEN: AJCDAG</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Aged ; Antianginal agents. Coronary vasodilator agents ; Biological and medical sciences ; Cardiovascular system ; Electrocardiography ; Female ; Fructosediphosphates - pharmacology ; Fructosediphosphates - therapeutic use ; Hemodynamics - drug effects ; Hexosediphosphates - pharmacology ; Humans ; Male ; Medical sciences ; Middle Aged ; Myocardial Contraction - drug effects ; Myocardial Infarction - drug therapy ; Myocardial Infarction - physiopathology ; Pharmacology. Drug treatments ; Pulmonary Wedge Pressure - drug effects ; Stroke Volume - drug effects</subject><ispartof>The American journal of cardiology, 1985-08, Vol.56 (4), p.266-269</ispartof><rights>1985</rights><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-f6ab3b18375c69114438164f0c519554ab9543f57789d555bfee14d4a0e81b343</citedby><cites>FETCH-LOGICAL-c452t-f6ab3b18375c69114438164f0c519554ab9543f57789d555bfee14d4a0e81b343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0002-9149(85)90847-1$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9283308$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/4025164$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marchionni, Niccolò</creatorcontrib><creatorcontrib>Conti, Alberto</creatorcontrib><creatorcontrib>De Alfieri, Walter</creatorcontrib><creatorcontrib>Di Bari, Mauro</creatorcontrib><creatorcontrib>Ferrucci, Luigi</creatorcontrib><creatorcontrib>Lombardi, Alessandra</creatorcontrib><creatorcontrib>Moschi, Guya</creatorcontrib><creatorcontrib>Pini, Riccardo</creatorcontrib><creatorcontrib>Vannucci, Andrea</creatorcontrib><title>Hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate in acute myocardial infarction</title><title>The American journal of cardiology</title><addtitle>Am J Cardiol</addtitle><description>Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolitic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or less) pulmonary artery (PA) wedge pressure and normal (35 g-m/m
2 or greater) left ventricular (LV) stroke work index; subset 2, elevated (more than 15 mm Hg) PA wedge pressure and normal LV stroke work index; subset 3, normal PA wedge pressure and reduced (less than 35 g-m/m
2) LV stroke work index; subset 4, elevated PA wedge pressure and LV stroke work index moderately reduced to a range between 16 and 34 g-m/m
2. Patients were randomized into an FDP (250 mg/kg body weight in isotonic saline solution intravenously in 20 minutes) and into a placebo group. Each subset contained 5 FDP- and 5 placebo-treated patients. After basal measurements, hemodynamic measurements were reassessed at 60, 90 and 120 minutes from the infusions, while a standard 12-lead electrocardiogram was recorded in the basal state and 120 minutes after infusion. Nonsignificant hemodynamic change was observed in the placebo subsets, and FDP failed to exert any effect in subsets 1, 2 and 3. A 24% (p < 0.02) increase in cardiac index occurred 60 minutes after FDP in subset 4. LV stroke work index also increased, while PA wedge pressure remained unchanged. Electrocardiographic markers of myocardial ischemia were not significantly reduced in any of the subsets, both in the control and in the treated group. Nevertheless, reduction was greater after FDP than after placebo administration in each subset, and it attained statistical significance when analyzed in the whole series of 20 FDP-treated patients. Two control patients died (1 from progressive LV failure) and 1 had a primary ventricular fibrillation successfully treated by direct-current shock. No FDP-treated patient died or had ventricular arrhythmias.</description><subject>Adult</subject><subject>Aged</subject><subject>Antianginal agents. Coronary vasodilator agents</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular system</subject><subject>Electrocardiography</subject><subject>Female</subject><subject>Fructosediphosphates - pharmacology</subject><subject>Fructosediphosphates - therapeutic use</subject><subject>Hemodynamics - drug effects</subject><subject>Hexosediphosphates - pharmacology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Pharmacology. 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Coronary vasodilator agents</topic><topic>Biological and medical sciences</topic><topic>Cardiovascular system</topic><topic>Electrocardiography</topic><topic>Female</topic><topic>Fructosediphosphates - pharmacology</topic><topic>Fructosediphosphates - therapeutic use</topic><topic>Hemodynamics - drug effects</topic><topic>Hexosediphosphates - pharmacology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pulmonary Wedge Pressure - drug effects</topic><topic>Stroke Volume - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marchionni, Niccolò</creatorcontrib><creatorcontrib>Conti, Alberto</creatorcontrib><creatorcontrib>De Alfieri, Walter</creatorcontrib><creatorcontrib>Di Bari, Mauro</creatorcontrib><creatorcontrib>Ferrucci, Luigi</creatorcontrib><creatorcontrib>Lombardi, Alessandra</creatorcontrib><creatorcontrib>Moschi, Guya</creatorcontrib><creatorcontrib>Pini, Riccardo</creatorcontrib><creatorcontrib>Vannucci, Andrea</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>The American journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marchionni, Niccolò</au><au>Conti, Alberto</au><au>De Alfieri, Walter</au><au>Di Bari, Mauro</au><au>Ferrucci, Luigi</au><au>Lombardi, Alessandra</au><au>Moschi, Guya</au><au>Pini, Riccardo</au><au>Vannucci, Andrea</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate in acute myocardial infarction</atitle><jtitle>The American journal of cardiology</jtitle><addtitle>Am J Cardiol</addtitle><date>1985-08-01</date><risdate>1985</risdate><volume>56</volume><issue>4</issue><spage>266</spage><epage>269</epage><pages>266-269</pages><issn>0002-9149</issn><eissn>1879-1913</eissn><coden>AJCDAG</coden><abstract>Acute hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate (FDP), an agent that is supposed to restore anaerobic glycolitic flux in the ischemic myocardium, were studied in 40 patients with acute myocardial infarction who were grouped into 4 subsets: subset 1, normal (15 mm Hg or less) pulmonary artery (PA) wedge pressure and normal (35 g-m/m
2 or greater) left ventricular (LV) stroke work index; subset 2, elevated (more than 15 mm Hg) PA wedge pressure and normal LV stroke work index; subset 3, normal PA wedge pressure and reduced (less than 35 g-m/m
2) LV stroke work index; subset 4, elevated PA wedge pressure and LV stroke work index moderately reduced to a range between 16 and 34 g-m/m
2. Patients were randomized into an FDP (250 mg/kg body weight in isotonic saline solution intravenously in 20 minutes) and into a placebo group. Each subset contained 5 FDP- and 5 placebo-treated patients. After basal measurements, hemodynamic measurements were reassessed at 60, 90 and 120 minutes from the infusions, while a standard 12-lead electrocardiogram was recorded in the basal state and 120 minutes after infusion. Nonsignificant hemodynamic change was observed in the placebo subsets, and FDP failed to exert any effect in subsets 1, 2 and 3. A 24% (p < 0.02) increase in cardiac index occurred 60 minutes after FDP in subset 4. LV stroke work index also increased, while PA wedge pressure remained unchanged. Electrocardiographic markers of myocardial ischemia were not significantly reduced in any of the subsets, both in the control and in the treated group. Nevertheless, reduction was greater after FDP than after placebo administration in each subset, and it attained statistical significance when analyzed in the whole series of 20 FDP-treated patients. Two control patients died (1 from progressive LV failure) and 1 had a primary ventricular fibrillation successfully treated by direct-current shock. No FDP-treated patient died or had ventricular arrhythmias.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>4025164</pmid><doi>10.1016/0002-9149(85)90847-1</doi><tpages>4</tpages></addata></record> |
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subjects | Adult Aged Antianginal agents. Coronary vasodilator agents Biological and medical sciences Cardiovascular system Electrocardiography Female Fructosediphosphates - pharmacology Fructosediphosphates - therapeutic use Hemodynamics - drug effects Hexosediphosphates - pharmacology Humans Male Medical sciences Middle Aged Myocardial Contraction - drug effects Myocardial Infarction - drug therapy Myocardial Infarction - physiopathology Pharmacology. Drug treatments Pulmonary Wedge Pressure - drug effects Stroke Volume - drug effects |
title | Hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate in acute myocardial infarction |
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