Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload
Aim To evaluate the role of atrial natriuretic peptide (ANP) in differentiating the aetiology of heart failure in children with left ventricular (LV) volume overload. Methods The study was conducted on 48 patients with LV volume overload (G one: rheumatic heart disease in failure; G2: compensated rh...
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creator | Kotby, Alyaa A Taman, Khaled H Sedky, Heba Tallah A Habeeb, Nevin MM El-Hadidi, Eman S Yosseif, Hanan S |
description | Aim
To evaluate the role of atrial natriuretic peptide (ANP) in differentiating the aetiology of heart failure in children with left ventricular (LV) volume overload.
Methods
The study was conducted on 48 patients with LV volume overload (G one: rheumatic heart disease in failure; G2: compensated rheumatic heart disease; G3: congenital left to right shunt; and G4: dilated cardiomyopathy). Twelve healthy children served as a control group. New York Heart Association (NYHA) class, LV dimensions and functions using Vivid 7 dimensions were evaluated. Serum ANP was measured using the ELISA technique, before and 3 months after treatment with angiotensin converting enzyme inhibitor.
Results
ANP was raised in all patients as compared to controls (G one: 28.33 ± 5.78, G2: 26.5 ± 4.11, G3: 28.5 ± 6.6, G4: 29.25 ± 4.5 pg/mL, control group: 5.54 ± 1.4 pg/mL, P < 0.001 for all) and varied significantly between different NYHA classes regardless of the underlying cardiac lesion. It was significantly higher in group 1 than 2 (P < 0.05). It decreased significantly after treatment (G1: 15.3 ± 5.3, G2: 10.7 ± 2.5, G3: 11.5 ± 3.8, G4: 15.7 ± 10.7 pg/mL, P < 0.001). The rate of change of ANP correlated with that of LV end diastolic diameter (r = 0.3, P < 0.05) irrespective of the underlying cause.
Conclusion
ANP increases in cases of LV volume overload irrespective of the aetiology of heart failure. It can differentiate between children in quiescent state from those in clinical failure even in the absence of echocardiographically detectable systolic dysfunction. Furthermore, it can monitor LV remodelling with treatment. |
doi_str_mv | 10.1111/jpc.12012 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1273593103</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2866149661</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3912-bd6f3d3e31dcbcf131e7097fe4fc66c2992e0bb718822a5d2fce26f47528441f3</originalsourceid><addsrcrecordid>eNp1kUFvFCEUgInR2Fo9-AcMiRc9TMsDZhiO7arVplFjNR4JwzyyrOzMCDNb--9Ft-3BRC6Pw_e-kA9CngM7hnJONpM7Bs6APyCHICWrQNXyYbkzISvZAjsgT3LeMMZ4XbePyQEXXGkm1CEJp3MKNtLBlrkknIOjE05z6JHaTC3d2vQDEx09XaNNM_U2xMLRMFC3DrFPONDrMK9pRD_THQ7F45ZoE92NcdkiHXeY4mj7p-SRtzHjs9t5RL69e_t19b66_HT-YXV6WTmhgVdd33jRCxTQu855EICKaeVRetc0jmvNkXWdgrbl3NY99w5546WqeSsleHFEXu29Uxp_Lphnsw3ZYYx2wHHJBrgStRalTUFf_oNuxiUN5XWFanTdag26UK_3lEtjzgm9mVIoWW4MMPOnvyn9zd_-hX1xa1y6Lfb35F3wApzsgesQ8eb_JnPxeXWnrPYbIc_4636jfItplFC1-f7x3MDVm9WF-HJmrsRvaSyeZQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1269589919</pqid></control><display><type>article</type><title>Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Kotby, Alyaa A ; Taman, Khaled H ; Sedky, Heba Tallah A ; Habeeb, Nevin MM ; El-Hadidi, Eman S ; Yosseif, Hanan S</creator><creatorcontrib>Kotby, Alyaa A ; Taman, Khaled H ; Sedky, Heba Tallah A ; Habeeb, Nevin MM ; El-Hadidi, Eman S ; Yosseif, Hanan S</creatorcontrib><description>Aim
To evaluate the role of atrial natriuretic peptide (ANP) in differentiating the aetiology of heart failure in children with left ventricular (LV) volume overload.
Methods
The study was conducted on 48 patients with LV volume overload (G one: rheumatic heart disease in failure; G2: compensated rheumatic heart disease; G3: congenital left to right shunt; and G4: dilated cardiomyopathy). Twelve healthy children served as a control group. New York Heart Association (NYHA) class, LV dimensions and functions using Vivid 7 dimensions were evaluated. Serum ANP was measured using the ELISA technique, before and 3 months after treatment with angiotensin converting enzyme inhibitor.
Results
ANP was raised in all patients as compared to controls (G one: 28.33 ± 5.78, G2: 26.5 ± 4.11, G3: 28.5 ± 6.6, G4: 29.25 ± 4.5 pg/mL, control group: 5.54 ± 1.4 pg/mL, P < 0.001 for all) and varied significantly between different NYHA classes regardless of the underlying cardiac lesion. It was significantly higher in group 1 than 2 (P < 0.05). It decreased significantly after treatment (G1: 15.3 ± 5.3, G2: 10.7 ± 2.5, G3: 11.5 ± 3.8, G4: 15.7 ± 10.7 pg/mL, P < 0.001). The rate of change of ANP correlated with that of LV end diastolic diameter (r = 0.3, P < 0.05) irrespective of the underlying cause.
Conclusion
ANP increases in cases of LV volume overload irrespective of the aetiology of heart failure. It can differentiate between children in quiescent state from those in clinical failure even in the absence of echocardiographically detectable systolic dysfunction. Furthermore, it can monitor LV remodelling with treatment.</description><identifier>ISSN: 1034-4810</identifier><identifier>EISSN: 1440-1754</identifier><identifier>DOI: 10.1111/jpc.12012</identifier><identifier>PMID: 23279037</identifier><language>eng</language><publisher>Australia: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; ANP ; Atrial Natriuretic Factor - blood ; Biomarkers ; Biomarkers - blood ; Cardiomyopathy, Dilated - blood ; Cardiomyopathy, Dilated - complications ; Cardiomyopathy, Dilated - drug therapy ; Case-Control Studies ; Child ; Child, Preschool ; Ductus Arteriosus, Patent - blood ; Ductus Arteriosus, Patent - complications ; Enzyme-Linked Immunosorbent Assay ; Female ; Follow-Up Studies ; Heart failure ; Heart Failure - blood ; Heart Failure - diagnosis ; Heart Failure - drug therapy ; Heart Failure - etiology ; Heart Septal Defects - blood ; Heart Septal Defects - complications ; Heart Valve Diseases - blood ; Heart Valve Diseases - complications ; Humans ; Infant ; Infant, Newborn ; left ventricular volume overload ; Male ; Pediatrics ; Peptides ; Prospective Studies ; Rheumatic Heart Disease - blood ; Rheumatic Heart Disease - complications ; Rheumatic Heart Disease - drug therapy ; Treatment Outcome ; Ventricular Dysfunction, Left - blood ; Ventricular Dysfunction, Left - complications ; Ventricular Dysfunction, Left - diagnosis ; Ventricular Remodeling</subject><ispartof>Journal of paediatrics and child health, 2013-01, Vol.49 (1), p.43-47</ispartof><rights>2012 The Authors. Journal of Paediatrics and Child Health © 2012 Paediatrics and Child Health Division (Royal Australasian College of Physicians)</rights><rights>2012 The Authors. Journal of Paediatrics and Child Health © 2012 Paediatrics and Child Health Division (Royal Australasian College of Physicians).</rights><rights>Journal of Paediatrics and Child Health © 2013 Paediatrics and Child Health Division (Royal Australasian College of Physicians)</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3912-bd6f3d3e31dcbcf131e7097fe4fc66c2992e0bb718822a5d2fce26f47528441f3</citedby><cites>FETCH-LOGICAL-c3912-bd6f3d3e31dcbcf131e7097fe4fc66c2992e0bb718822a5d2fce26f47528441f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjpc.12012$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjpc.12012$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23279037$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kotby, Alyaa A</creatorcontrib><creatorcontrib>Taman, Khaled H</creatorcontrib><creatorcontrib>Sedky, Heba Tallah A</creatorcontrib><creatorcontrib>Habeeb, Nevin MM</creatorcontrib><creatorcontrib>El-Hadidi, Eman S</creatorcontrib><creatorcontrib>Yosseif, Hanan S</creatorcontrib><title>Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload</title><title>Journal of paediatrics and child health</title><addtitle>J Paediatr Child Health</addtitle><description>Aim
To evaluate the role of atrial natriuretic peptide (ANP) in differentiating the aetiology of heart failure in children with left ventricular (LV) volume overload.
Methods
The study was conducted on 48 patients with LV volume overload (G one: rheumatic heart disease in failure; G2: compensated rheumatic heart disease; G3: congenital left to right shunt; and G4: dilated cardiomyopathy). Twelve healthy children served as a control group. New York Heart Association (NYHA) class, LV dimensions and functions using Vivid 7 dimensions were evaluated. Serum ANP was measured using the ELISA technique, before and 3 months after treatment with angiotensin converting enzyme inhibitor.
Results
ANP was raised in all patients as compared to controls (G one: 28.33 ± 5.78, G2: 26.5 ± 4.11, G3: 28.5 ± 6.6, G4: 29.25 ± 4.5 pg/mL, control group: 5.54 ± 1.4 pg/mL, P < 0.001 for all) and varied significantly between different NYHA classes regardless of the underlying cardiac lesion. It was significantly higher in group 1 than 2 (P < 0.05). It decreased significantly after treatment (G1: 15.3 ± 5.3, G2: 10.7 ± 2.5, G3: 11.5 ± 3.8, G4: 15.7 ± 10.7 pg/mL, P < 0.001). The rate of change of ANP correlated with that of LV end diastolic diameter (r = 0.3, P < 0.05) irrespective of the underlying cause.
Conclusion
ANP increases in cases of LV volume overload irrespective of the aetiology of heart failure. It can differentiate between children in quiescent state from those in clinical failure even in the absence of echocardiographically detectable systolic dysfunction. Furthermore, it can monitor LV remodelling with treatment.</description><subject>Adolescent</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>ANP</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Cardiomyopathy, Dilated - blood</subject><subject>Cardiomyopathy, Dilated - complications</subject><subject>Cardiomyopathy, Dilated - drug therapy</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Ductus Arteriosus, Patent - blood</subject><subject>Ductus Arteriosus, Patent - complications</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Heart failure</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - diagnosis</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - etiology</subject><subject>Heart Septal Defects - blood</subject><subject>Heart Septal Defects - complications</subject><subject>Heart Valve Diseases - blood</subject><subject>Heart Valve Diseases - complications</subject><subject>Humans</subject><subject>Infant</subject><subject>Infant, Newborn</subject><subject>left ventricular volume overload</subject><subject>Male</subject><subject>Pediatrics</subject><subject>Peptides</subject><subject>Prospective Studies</subject><subject>Rheumatic Heart Disease - blood</subject><subject>Rheumatic Heart Disease - complications</subject><subject>Rheumatic Heart Disease - drug therapy</subject><subject>Treatment Outcome</subject><subject>Ventricular Dysfunction, Left - blood</subject><subject>Ventricular Dysfunction, Left - complications</subject><subject>Ventricular Dysfunction, Left - diagnosis</subject><subject>Ventricular Remodeling</subject><issn>1034-4810</issn><issn>1440-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUFvFCEUgInR2Fo9-AcMiRc9TMsDZhiO7arVplFjNR4JwzyyrOzMCDNb--9Ft-3BRC6Pw_e-kA9CngM7hnJONpM7Bs6APyCHICWrQNXyYbkzISvZAjsgT3LeMMZ4XbePyQEXXGkm1CEJp3MKNtLBlrkknIOjE05z6JHaTC3d2vQDEx09XaNNM_U2xMLRMFC3DrFPONDrMK9pRD_THQ7F45ZoE92NcdkiHXeY4mj7p-SRtzHjs9t5RL69e_t19b66_HT-YXV6WTmhgVdd33jRCxTQu855EICKaeVRetc0jmvNkXWdgrbl3NY99w5546WqeSsleHFEXu29Uxp_Lphnsw3ZYYx2wHHJBrgStRalTUFf_oNuxiUN5XWFanTdag26UK_3lEtjzgm9mVIoWW4MMPOnvyn9zd_-hX1xa1y6Lfb35F3wApzsgesQ8eb_JnPxeXWnrPYbIc_4636jfItplFC1-f7x3MDVm9WF-HJmrsRvaSyeZQ</recordid><startdate>201301</startdate><enddate>201301</enddate><creator>Kotby, Alyaa A</creator><creator>Taman, Khaled H</creator><creator>Sedky, Heba Tallah A</creator><creator>Habeeb, Nevin MM</creator><creator>El-Hadidi, Eman S</creator><creator>Yosseif, Hanan S</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>ASE</scope><scope>FPQ</scope><scope>K6X</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>201301</creationdate><title>Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload</title><author>Kotby, Alyaa A ; Taman, Khaled H ; Sedky, Heba Tallah A ; Habeeb, Nevin MM ; El-Hadidi, Eman S ; Yosseif, Hanan S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3912-bd6f3d3e31dcbcf131e7097fe4fc66c2992e0bb718822a5d2fce26f47528441f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adolescent</topic><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>ANP</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>Biomarkers</topic><topic>Biomarkers - blood</topic><topic>Cardiomyopathy, Dilated - blood</topic><topic>Cardiomyopathy, Dilated - complications</topic><topic>Cardiomyopathy, Dilated - drug therapy</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Ductus Arteriosus, Patent - blood</topic><topic>Ductus Arteriosus, Patent - complications</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Heart failure</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - diagnosis</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - etiology</topic><topic>Heart Septal Defects - blood</topic><topic>Heart Septal Defects - complications</topic><topic>Heart Valve Diseases - blood</topic><topic>Heart Valve Diseases - complications</topic><topic>Humans</topic><topic>Infant</topic><topic>Infant, Newborn</topic><topic>left ventricular volume overload</topic><topic>Male</topic><topic>Pediatrics</topic><topic>Peptides</topic><topic>Prospective Studies</topic><topic>Rheumatic Heart Disease - blood</topic><topic>Rheumatic Heart Disease - complications</topic><topic>Rheumatic Heart Disease - drug therapy</topic><topic>Treatment Outcome</topic><topic>Ventricular Dysfunction, Left - blood</topic><topic>Ventricular Dysfunction, Left - complications</topic><topic>Ventricular Dysfunction, Left - diagnosis</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kotby, Alyaa A</creatorcontrib><creatorcontrib>Taman, Khaled H</creatorcontrib><creatorcontrib>Sedky, Heba Tallah A</creatorcontrib><creatorcontrib>Habeeb, Nevin MM</creatorcontrib><creatorcontrib>El-Hadidi, Eman S</creatorcontrib><creatorcontrib>Yosseif, Hanan S</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>British Nursing Index</collection><collection>British Nursing Index (BNI) (1985 to Present)</collection><collection>British Nursing Index</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of paediatrics and child health</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kotby, Alyaa A</au><au>Taman, Khaled H</au><au>Sedky, Heba Tallah A</au><au>Habeeb, Nevin MM</au><au>El-Hadidi, Eman S</au><au>Yosseif, Hanan S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload</atitle><jtitle>Journal of paediatrics and child health</jtitle><addtitle>J Paediatr Child Health</addtitle><date>2013-01</date><risdate>2013</risdate><volume>49</volume><issue>1</issue><spage>43</spage><epage>47</epage><pages>43-47</pages><issn>1034-4810</issn><eissn>1440-1754</eissn><abstract>Aim
To evaluate the role of atrial natriuretic peptide (ANP) in differentiating the aetiology of heart failure in children with left ventricular (LV) volume overload.
Methods
The study was conducted on 48 patients with LV volume overload (G one: rheumatic heart disease in failure; G2: compensated rheumatic heart disease; G3: congenital left to right shunt; and G4: dilated cardiomyopathy). Twelve healthy children served as a control group. New York Heart Association (NYHA) class, LV dimensions and functions using Vivid 7 dimensions were evaluated. Serum ANP was measured using the ELISA technique, before and 3 months after treatment with angiotensin converting enzyme inhibitor.
Results
ANP was raised in all patients as compared to controls (G one: 28.33 ± 5.78, G2: 26.5 ± 4.11, G3: 28.5 ± 6.6, G4: 29.25 ± 4.5 pg/mL, control group: 5.54 ± 1.4 pg/mL, P < 0.001 for all) and varied significantly between different NYHA classes regardless of the underlying cardiac lesion. It was significantly higher in group 1 than 2 (P < 0.05). It decreased significantly after treatment (G1: 15.3 ± 5.3, G2: 10.7 ± 2.5, G3: 11.5 ± 3.8, G4: 15.7 ± 10.7 pg/mL, P < 0.001). The rate of change of ANP correlated with that of LV end diastolic diameter (r = 0.3, P < 0.05) irrespective of the underlying cause.
Conclusion
ANP increases in cases of LV volume overload irrespective of the aetiology of heart failure. It can differentiate between children in quiescent state from those in clinical failure even in the absence of echocardiographically detectable systolic dysfunction. Furthermore, it can monitor LV remodelling with treatment.</abstract><cop>Australia</cop><pub>Blackwell Publishing Ltd</pub><pmid>23279037</pmid><doi>10.1111/jpc.12012</doi><tpages>5</tpages></addata></record> |
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subjects | Adolescent Angiotensin-Converting Enzyme Inhibitors - therapeutic use ANP Atrial Natriuretic Factor - blood Biomarkers Biomarkers - blood Cardiomyopathy, Dilated - blood Cardiomyopathy, Dilated - complications Cardiomyopathy, Dilated - drug therapy Case-Control Studies Child Child, Preschool Ductus Arteriosus, Patent - blood Ductus Arteriosus, Patent - complications Enzyme-Linked Immunosorbent Assay Female Follow-Up Studies Heart failure Heart Failure - blood Heart Failure - diagnosis Heart Failure - drug therapy Heart Failure - etiology Heart Septal Defects - blood Heart Septal Defects - complications Heart Valve Diseases - blood Heart Valve Diseases - complications Humans Infant Infant, Newborn left ventricular volume overload Male Pediatrics Peptides Prospective Studies Rheumatic Heart Disease - blood Rheumatic Heart Disease - complications Rheumatic Heart Disease - drug therapy Treatment Outcome Ventricular Dysfunction, Left - blood Ventricular Dysfunction, Left - complications Ventricular Dysfunction, Left - diagnosis Ventricular Remodeling |
title | Atrial natriuretic peptide as a marker of heart failure in children with left ventricular volume overload |
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