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Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children
The clinical manifestations of inherited disorders of fatty acid oxidation vary according to the enzymatic defect. They may present as isolated cardiomyopathy, sudden death, progressive skeletal myopathy, or hepatic failure. Arrhythmia is an unusual presenting symptom of fatty acid oxidation deficie...
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| Published in: | Circulation (New York, N.Y.) N.Y.), 1999-11, Vol.100 (22), p.2248-2253 |
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| cited_by | cdi_FETCH-LOGICAL-c557t-2f727783754822118d86c698d080d29dd9233a833f513afc914d56f8ebfe89093 |
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| container_end_page | 2253 |
| container_issue | 22 |
| container_start_page | 2248 |
| container_title | Circulation (New York, N.Y.) |
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| creator | BONNET, D MARTIN, D DE LONLAY, P VILLAIN, E JOUVET, P RABIER, D BRIVET, M SAUDUBRAY, J.-M |
| description | The clinical manifestations of inherited disorders of fatty acid oxidation vary according to the enzymatic defect. They may present as isolated cardiomyopathy, sudden death, progressive skeletal myopathy, or hepatic failure. Arrhythmia is an unusual presenting symptom of fatty acid oxidation deficiencies.
Over a period of 25 years, 107 patients were diagnosed with an inherited fatty acid oxidation disorder. Arrhythmia was the predominant presenting symptom in 24 cases. These 24 cases included 15 ventricular tachycardias, 4 atrial tachycardias, 4 sinus node dysfunctions with episodes of atrial tachycardia, 6 atrioventricular blocks, and 4 left bundle-branch blocks in newborn infants. Conduction disorders and atrial tachycardias were observed in patients with defects of long-chain fatty acid transport across the inner mitochondrial membrane (carnitine palmitoyl transferase type II deficiency and carnitine acylcarnitine translocase deficiency) and in patients with trifunctional protein deficiency. Ventricular tachycardias were observed in patients with any type of fatty acid oxidation deficiency. Arrhythmias were absent in patients with primary carnitine carrier, carnitine palmitoyl transferase I, and medium chain acyl coenzyme A dehydrogenase deficiencies.
The accumulation of arrhythmogenic intermediary metabolites of fatty acids, such as long-chain acylcarnitines, may be responsible for arrhythmias. Inborn errors of fatty acid oxidation should be considered in unexplained sudden death or near-miss in infants and in infants with conduction defects or ventricular tachycardia. Diagnosis can be easily ascertained by an acylcarnitine profile from blood spots on filter paper. |
| doi_str_mv | 10.1161/01.cir.100.22.2248 |
| format | article |
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Over a period of 25 years, 107 patients were diagnosed with an inherited fatty acid oxidation disorder. Arrhythmia was the predominant presenting symptom in 24 cases. These 24 cases included 15 ventricular tachycardias, 4 atrial tachycardias, 4 sinus node dysfunctions with episodes of atrial tachycardia, 6 atrioventricular blocks, and 4 left bundle-branch blocks in newborn infants. Conduction disorders and atrial tachycardias were observed in patients with defects of long-chain fatty acid transport across the inner mitochondrial membrane (carnitine palmitoyl transferase type II deficiency and carnitine acylcarnitine translocase deficiency) and in patients with trifunctional protein deficiency. Ventricular tachycardias were observed in patients with any type of fatty acid oxidation deficiency. Arrhythmias were absent in patients with primary carnitine carrier, carnitine palmitoyl transferase I, and medium chain acyl coenzyme A dehydrogenase deficiencies.
The accumulation of arrhythmogenic intermediary metabolites of fatty acids, such as long-chain acylcarnitines, may be responsible for arrhythmias. Inborn errors of fatty acid oxidation should be considered in unexplained sudden death or near-miss in infants and in infants with conduction defects or ventricular tachycardia. Diagnosis can be easily ascertained by an acylcarnitine profile from blood spots on filter paper.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.100.22.2248</identifier><identifier>PMID: 10577999</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>3-Hydroxyacyl CoA Dehydrogenases - deficiency ; 3-Hydroxyacyl CoA Dehydrogenases - genetics ; Acyl-CoA Dehydrogenase ; Acyl-CoA Dehydrogenase, Long-Chain ; Arrhythmias, Cardiac - etiology ; Biological and medical sciences ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Carnitine - analogs & derivatives ; Carnitine - blood ; Carnitine Acyltransferases - deficiency ; Carnitine Acyltransferases - genetics ; Carnitine O-Palmitoyltransferase - deficiency ; Carnitine O-Palmitoyltransferase - genetics ; Fatty Acid Desaturases - deficiency ; Fatty Acid Desaturases - genetics ; Fatty Acids - metabolism ; Female ; Heart ; Heart Conduction System - physiopathology ; Humans ; Infant ; Infant, Newborn ; Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase ; Male ; Medical sciences ; Mitochondria, Heart - metabolism ; Mitochondrial Myopathies - complications ; Mitochondrial Myopathies - diagnosis ; Mitochondrial Myopathies - genetics ; Mitochondrial Myopathies - physiopathology ; Models, Biological ; Oxidation-Reduction ; Sudden Infant Death - etiology ; Tachycardia, Ventricular - etiology</subject><ispartof>Circulation (New York, N.Y.), 1999-11, Vol.100 (22), p.2248-2253</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 30, 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-2f727783754822118d86c698d080d29dd9233a833f513afc914d56f8ebfe89093</citedby><cites>FETCH-LOGICAL-c557t-2f727783754822118d86c698d080d29dd9233a833f513afc914d56f8ebfe89093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1194458$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10577999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BONNET, D</creatorcontrib><creatorcontrib>MARTIN, D</creatorcontrib><creatorcontrib>DE LONLAY, P</creatorcontrib><creatorcontrib>VILLAIN, E</creatorcontrib><creatorcontrib>JOUVET, P</creatorcontrib><creatorcontrib>RABIER, D</creatorcontrib><creatorcontrib>BRIVET, M</creatorcontrib><creatorcontrib>SAUDUBRAY, J.-M</creatorcontrib><title>Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The clinical manifestations of inherited disorders of fatty acid oxidation vary according to the enzymatic defect. They may present as isolated cardiomyopathy, sudden death, progressive skeletal myopathy, or hepatic failure. Arrhythmia is an unusual presenting symptom of fatty acid oxidation deficiencies.
Over a period of 25 years, 107 patients were diagnosed with an inherited fatty acid oxidation disorder. Arrhythmia was the predominant presenting symptom in 24 cases. These 24 cases included 15 ventricular tachycardias, 4 atrial tachycardias, 4 sinus node dysfunctions with episodes of atrial tachycardia, 6 atrioventricular blocks, and 4 left bundle-branch blocks in newborn infants. Conduction disorders and atrial tachycardias were observed in patients with defects of long-chain fatty acid transport across the inner mitochondrial membrane (carnitine palmitoyl transferase type II deficiency and carnitine acylcarnitine translocase deficiency) and in patients with trifunctional protein deficiency. Ventricular tachycardias were observed in patients with any type of fatty acid oxidation deficiency. Arrhythmias were absent in patients with primary carnitine carrier, carnitine palmitoyl transferase I, and medium chain acyl coenzyme A dehydrogenase deficiencies.
The accumulation of arrhythmogenic intermediary metabolites of fatty acids, such as long-chain acylcarnitines, may be responsible for arrhythmias. Inborn errors of fatty acid oxidation should be considered in unexplained sudden death or near-miss in infants and in infants with conduction defects or ventricular tachycardia. Diagnosis can be easily ascertained by an acylcarnitine profile from blood spots on filter paper.</description><subject>3-Hydroxyacyl CoA Dehydrogenases - deficiency</subject><subject>3-Hydroxyacyl CoA Dehydrogenases - genetics</subject><subject>Acyl-CoA Dehydrogenase</subject><subject>Acyl-CoA Dehydrogenase, Long-Chain</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Biological and medical sciences</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Carnitine - analogs & derivatives</subject><subject>Carnitine - blood</subject><subject>Carnitine Acyltransferases - deficiency</subject><subject>Carnitine Acyltransferases - genetics</subject><subject>Carnitine O-Palmitoyltransferase - deficiency</subject><subject>Carnitine O-Palmitoyltransferase - genetics</subject><subject>Fatty Acid Desaturases - deficiency</subject><subject>Fatty Acid Desaturases - genetics</subject><subject>Fatty Acids - metabolism</subject><subject>Female</subject><subject>Heart</subject><subject>Heart Conduction System - physiopathology</subject><subject>Humans</subject><subject>Infant</subject><subject>Infant, Newborn</subject><subject>Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Mitochondrial Myopathies - complications</subject><subject>Mitochondrial Myopathies - diagnosis</subject><subject>Mitochondrial Myopathies - genetics</subject><subject>Mitochondrial Myopathies - physiopathology</subject><subject>Models, Biological</subject><subject>Oxidation-Reduction</subject><subject>Sudden Infant Death - etiology</subject><subject>Tachycardia, Ventricular - etiology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNpdkVuLFDEQhYMo7jj6B3yQIOJbj7l2J4_L4GVhQRB9DtlcdrJ0J2MqDTv_3iwzoAgFxSm-cyiqEHpLyY7SkX4idOdS3VFCdoz1EuoZ2lDJxCAk18_RhhCih4kzdoVeATx0OfJJvkRXlMhp0lpv0P11rYdTOyzJArbZY1eyX11LJWMfYnCtjwEfa4CQW8r3GE7LsZUFcIk42tZO2LrkcXlM3p5tCUr1oQJOGbtDmn0N-TV6Ee0M4c2lb9GvL59_7r8Nt9-_3uyvbwcn5dQGFic2TapvKRRjlCqvRjdq5YkinmnvNePcKs6jpNxGp6nwcowq3MWgNNF8iz6ec4-1_F4DNLMkcGGebQ5lBTNqzgURooPv_wMfylpz380wysaR0E5uETtDrhaAGqI51rTYejKUmKcfGELN_uZHl8QwZp5-0E3vLsnr3RL8P5bz0Tvw4QJYcHaO1WaX4C9HtRBS8T9A3Y89</recordid><startdate>19991130</startdate><enddate>19991130</enddate><creator>BONNET, D</creator><creator>MARTIN, D</creator><creator>DE LONLAY, P</creator><creator>VILLAIN, E</creator><creator>JOUVET, P</creator><creator>RABIER, D</creator><creator>BRIVET, M</creator><creator>SAUDUBRAY, J.-M</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19991130</creationdate><title>Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children</title><author>BONNET, D ; MARTIN, D ; DE LONLAY, P ; VILLAIN, E ; JOUVET, P ; RABIER, D ; BRIVET, M ; SAUDUBRAY, J.-M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-2f727783754822118d86c698d080d29dd9233a833f513afc914d56f8ebfe89093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>3-Hydroxyacyl CoA Dehydrogenases - deficiency</topic><topic>3-Hydroxyacyl CoA Dehydrogenases - genetics</topic><topic>Acyl-CoA Dehydrogenase</topic><topic>Acyl-CoA Dehydrogenase, Long-Chain</topic><topic>Arrhythmias, Cardiac - etiology</topic><topic>Biological and medical sciences</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Carnitine - analogs & derivatives</topic><topic>Carnitine - blood</topic><topic>Carnitine Acyltransferases - deficiency</topic><topic>Carnitine Acyltransferases - genetics</topic><topic>Carnitine O-Palmitoyltransferase - deficiency</topic><topic>Carnitine O-Palmitoyltransferase - genetics</topic><topic>Fatty Acid Desaturases - deficiency</topic><topic>Fatty Acid Desaturases - genetics</topic><topic>Fatty Acids - metabolism</topic><topic>Female</topic><topic>Heart</topic><topic>Heart Conduction System - physiopathology</topic><topic>Humans</topic><topic>Infant</topic><topic>Infant, Newborn</topic><topic>Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Mitochondrial Myopathies - complications</topic><topic>Mitochondrial Myopathies - diagnosis</topic><topic>Mitochondrial Myopathies - genetics</topic><topic>Mitochondrial Myopathies - physiopathology</topic><topic>Models, Biological</topic><topic>Oxidation-Reduction</topic><topic>Sudden Infant Death - etiology</topic><topic>Tachycardia, Ventricular - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BONNET, D</creatorcontrib><creatorcontrib>MARTIN, D</creatorcontrib><creatorcontrib>DE LONLAY, P</creatorcontrib><creatorcontrib>VILLAIN, E</creatorcontrib><creatorcontrib>JOUVET, P</creatorcontrib><creatorcontrib>RABIER, D</creatorcontrib><creatorcontrib>BRIVET, M</creatorcontrib><creatorcontrib>SAUDUBRAY, J.-M</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BONNET, D</au><au>MARTIN, D</au><au>DE LONLAY, P</au><au>VILLAIN, E</au><au>JOUVET, P</au><au>RABIER, D</au><au>BRIVET, M</au><au>SAUDUBRAY, J.-M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1999-11-30</date><risdate>1999</risdate><volume>100</volume><issue>22</issue><spage>2248</spage><epage>2253</epage><pages>2248-2253</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The clinical manifestations of inherited disorders of fatty acid oxidation vary according to the enzymatic defect. They may present as isolated cardiomyopathy, sudden death, progressive skeletal myopathy, or hepatic failure. Arrhythmia is an unusual presenting symptom of fatty acid oxidation deficiencies.
Over a period of 25 years, 107 patients were diagnosed with an inherited fatty acid oxidation disorder. Arrhythmia was the predominant presenting symptom in 24 cases. These 24 cases included 15 ventricular tachycardias, 4 atrial tachycardias, 4 sinus node dysfunctions with episodes of atrial tachycardia, 6 atrioventricular blocks, and 4 left bundle-branch blocks in newborn infants. Conduction disorders and atrial tachycardias were observed in patients with defects of long-chain fatty acid transport across the inner mitochondrial membrane (carnitine palmitoyl transferase type II deficiency and carnitine acylcarnitine translocase deficiency) and in patients with trifunctional protein deficiency. Ventricular tachycardias were observed in patients with any type of fatty acid oxidation deficiency. Arrhythmias were absent in patients with primary carnitine carrier, carnitine palmitoyl transferase I, and medium chain acyl coenzyme A dehydrogenase deficiencies.
The accumulation of arrhythmogenic intermediary metabolites of fatty acids, such as long-chain acylcarnitines, may be responsible for arrhythmias. Inborn errors of fatty acid oxidation should be considered in unexplained sudden death or near-miss in infants and in infants with conduction defects or ventricular tachycardia. Diagnosis can be easily ascertained by an acylcarnitine profile from blood spots on filter paper.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10577999</pmid><doi>10.1161/01.cir.100.22.2248</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1999-11, Vol.100 (22), p.2248-2253 |
| issn | 0009-7322 1524-4539 |
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| subjects | 3-Hydroxyacyl CoA Dehydrogenases - deficiency 3-Hydroxyacyl CoA Dehydrogenases - genetics Acyl-CoA Dehydrogenase Acyl-CoA Dehydrogenase, Long-Chain Arrhythmias, Cardiac - etiology Biological and medical sciences Cardiac dysrhythmias Cardiology. Vascular system Carnitine - analogs & derivatives Carnitine - blood Carnitine Acyltransferases - deficiency Carnitine Acyltransferases - genetics Carnitine O-Palmitoyltransferase - deficiency Carnitine O-Palmitoyltransferase - genetics Fatty Acid Desaturases - deficiency Fatty Acid Desaturases - genetics Fatty Acids - metabolism Female Heart Heart Conduction System - physiopathology Humans Infant Infant, Newborn Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase Male Medical sciences Mitochondria, Heart - metabolism Mitochondrial Myopathies - complications Mitochondrial Myopathies - diagnosis Mitochondrial Myopathies - genetics Mitochondrial Myopathies - physiopathology Models, Biological Oxidation-Reduction Sudden Infant Death - etiology Tachycardia, Ventricular - etiology |
| title | Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children |
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