Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators
OBJECTIVES The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury. BACKGROUND...
Gespeichert in:
| Veröffentlicht in: | Journal of the American College of Cardiology 1999-08, Vol.34 (2), p.402-408 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 408 |
|---|---|
| container_issue | 2 |
| container_start_page | 402 |
| container_title | Journal of the American College of Cardiology |
| container_volume | 34 |
| creator | Hurst, Tanja M Hinrichs, Michael Breidenbach, Christiane Katz, Norbert Waldecker, Bernd |
| description | OBJECTIVES
The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury.
BACKGROUND
During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury.
METHODS
Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation.
RESULTS
Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE ≥ 18 J and a recent MI were identified as strong risk factors for cTNI rise.
CONCLUSIONS
During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE ≥ 18 J seem to be prone to cTNI rise. |
| doi_str_mv | 10.1016/S0735-1097(99)00194-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69942000</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0735109799001941</els_id><sourcerecordid>69942000</sourcerecordid><originalsourceid>FETCH-LOGICAL-c537t-ea5dc413ac03bbe15a30582fda6cd6bc06a9dd4a522431dfe35ea5d79a9f3dc43</originalsourceid><addsrcrecordid>eNqFkctq4zAUQMUwpUnTfsIMXgylXbiVLMuOVsOQPqHQRdu1uJaui4JtZSQ5kL-v8pjHrishOEe6nEvIN0avGGXV9QutucgZlfWFlJeUMlnm7AuZMiHmORey_kqmf5EJOQlhSSmt5kwekwmjZUmZKKbk_QYj6mjdkLk26zdOgzcWuswOy9FvMjN6O7xn0cMQ1ji4MWS2X3UwRPgjwRhdn24627lujT6izw22tvG26yA6H07JUQtdwLPDOSNvd7evi4f86fn-cfHrKdeC1zFHEEaXjIOmvGmQCeBUzIvWQKVN1WhagTSmBFEUJWemRS62Si1BtjyZfEbO9--uvPs9Yoiqt0FjmmLANLyqpCyLFCKBYg9q70Lw2KqVtz34jWJUbQurXWG1zaekVLvCiiXv--GDsenR_GftkybgxwGAoKFrUzltwz-uYPWcb7GfewxTjbVFr4K2OGg01qeFKOPsJ5N8AKKOm5Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69942000</pqid></control><display><type>article</type><title>Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Hurst, Tanja M ; Hinrichs, Michael ; Breidenbach, Christiane ; Katz, Norbert ; Waldecker, Bernd</creator><creatorcontrib>Hurst, Tanja M ; Hinrichs, Michael ; Breidenbach, Christiane ; Katz, Norbert ; Waldecker, Bernd</creatorcontrib><description>OBJECTIVES
The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury.
BACKGROUND
During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury.
METHODS
Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation.
RESULTS
Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE ≥ 18 J and a recent MI were identified as strong risk factors for cTNI rise.
CONCLUSIONS
During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE ≥ 18 J seem to be prone to cTNI rise.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/S0735-1097(99)00194-1</identifier><identifier>PMID: 10440152</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Biological and medical sciences ; Biomarkers - blood ; Cardiac Pacing, Artificial - adverse effects ; Creatine Kinase - blood ; Defibrillators, Implantable - adverse effects ; Diseases of the cardiovascular system ; Female ; Heart Injuries - diagnosis ; Heart Injuries - etiology ; Humans ; Isoenzymes ; Male ; Medical sciences ; Middle Aged ; Myoglobin - blood ; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) ; Troponin I - blood ; Troponin T - blood</subject><ispartof>Journal of the American College of Cardiology, 1999-08, Vol.34 (2), p.402-408</ispartof><rights>1999 American College of Cardiology</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c537t-ea5dc413ac03bbe15a30582fda6cd6bc06a9dd4a522431dfe35ea5d79a9f3dc43</citedby><cites>FETCH-LOGICAL-c537t-ea5dc413ac03bbe15a30582fda6cd6bc06a9dd4a522431dfe35ea5d79a9f3dc43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0735-1097(99)00194-1$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1217832$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10440152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hurst, Tanja M</creatorcontrib><creatorcontrib>Hinrichs, Michael</creatorcontrib><creatorcontrib>Breidenbach, Christiane</creatorcontrib><creatorcontrib>Katz, Norbert</creatorcontrib><creatorcontrib>Waldecker, Bernd</creatorcontrib><title>Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>OBJECTIVES
The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury.
BACKGROUND
During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury.
METHODS
Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation.
RESULTS
Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE ≥ 18 J and a recent MI were identified as strong risk factors for cTNI rise.
CONCLUSIONS
During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE ≥ 18 J seem to be prone to cTNI rise.</description><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Cardiac Pacing, Artificial - adverse effects</subject><subject>Creatine Kinase - blood</subject><subject>Defibrillators, Implantable - adverse effects</subject><subject>Diseases of the cardiovascular system</subject><subject>Female</subject><subject>Heart Injuries - diagnosis</subject><subject>Heart Injuries - etiology</subject><subject>Humans</subject><subject>Isoenzymes</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myoglobin - blood</subject><subject>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)</subject><subject>Troponin I - blood</subject><subject>Troponin T - blood</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctq4zAUQMUwpUnTfsIMXgylXbiVLMuOVsOQPqHQRdu1uJaui4JtZSQ5kL-v8pjHrishOEe6nEvIN0avGGXV9QutucgZlfWFlJeUMlnm7AuZMiHmORey_kqmf5EJOQlhSSmt5kwekwmjZUmZKKbk_QYj6mjdkLk26zdOgzcWuswOy9FvMjN6O7xn0cMQ1ji4MWS2X3UwRPgjwRhdn24627lujT6izw22tvG26yA6H07JUQtdwLPDOSNvd7evi4f86fn-cfHrKdeC1zFHEEaXjIOmvGmQCeBUzIvWQKVN1WhagTSmBFEUJWemRS62Si1BtjyZfEbO9--uvPs9Yoiqt0FjmmLANLyqpCyLFCKBYg9q70Lw2KqVtz34jWJUbQurXWG1zaekVLvCiiXv--GDsenR_GftkybgxwGAoKFrUzltwz-uYPWcb7GfewxTjbVFr4K2OGg01qeFKOPsJ5N8AKKOm5Q</recordid><startdate>19990801</startdate><enddate>19990801</enddate><creator>Hurst, Tanja M</creator><creator>Hinrichs, Michael</creator><creator>Breidenbach, Christiane</creator><creator>Katz, Norbert</creator><creator>Waldecker, Bernd</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>6I.</scope><scope>AAFTH</scope><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>19990801</creationdate><title>Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators</title><author>Hurst, Tanja M ; Hinrichs, Michael ; Breidenbach, Christiane ; Katz, Norbert ; Waldecker, Bernd</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c537t-ea5dc413ac03bbe15a30582fda6cd6bc06a9dd4a522431dfe35ea5d79a9f3dc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Cardiac Pacing, Artificial - adverse effects</topic><topic>Creatine Kinase - blood</topic><topic>Defibrillators, Implantable - adverse effects</topic><topic>Diseases of the cardiovascular system</topic><topic>Female</topic><topic>Heart Injuries - diagnosis</topic><topic>Heart Injuries - etiology</topic><topic>Humans</topic><topic>Isoenzymes</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myoglobin - blood</topic><topic>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)</topic><topic>Troponin I - blood</topic><topic>Troponin T - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hurst, Tanja M</creatorcontrib><creatorcontrib>Hinrichs, Michael</creatorcontrib><creatorcontrib>Breidenbach, Christiane</creatorcontrib><creatorcontrib>Katz, Norbert</creatorcontrib><creatorcontrib>Waldecker, Bernd</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hurst, Tanja M</au><au>Hinrichs, Michael</au><au>Breidenbach, Christiane</au><au>Katz, Norbert</au><au>Waldecker, Bernd</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>1999-08-01</date><risdate>1999</risdate><volume>34</volume><issue>2</issue><spage>402</spage><epage>408</epage><pages>402-408</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>OBJECTIVES
The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury.
BACKGROUND
During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury.
METHODS
Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation.
RESULTS
Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE ≥ 18 J and a recent MI were identified as strong risk factors for cTNI rise.
CONCLUSIONS
During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE ≥ 18 J seem to be prone to cTNI rise.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10440152</pmid><doi>10.1016/S0735-1097(99)00194-1</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0735-1097 |
| ispartof | Journal of the American College of Cardiology, 1999-08, Vol.34 (2), p.402-408 |
| issn | 0735-1097 1558-3597 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69942000 |
| source | MEDLINE; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Biological and medical sciences Biomarkers - blood Cardiac Pacing, Artificial - adverse effects Creatine Kinase - blood Defibrillators, Implantable - adverse effects Diseases of the cardiovascular system Female Heart Injuries - diagnosis Heart Injuries - etiology Humans Isoenzymes Male Medical sciences Middle Aged Myoglobin - blood Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) Troponin I - blood Troponin T - blood |
| title | Detection of myocardial injury during transvenous implantation of automatic cardioverter-defibrillators |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-20T08%3A22%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Detection%20of%20myocardial%20injury%20during%20transvenous%20implantation%20of%20automatic%20cardioverter-defibrillators&rft.jtitle=Journal%20of%20the%20American%20College%20of%20Cardiology&rft.au=Hurst,%20Tanja%20M&rft.date=1999-08-01&rft.volume=34&rft.issue=2&rft.spage=402&rft.epage=408&rft.pages=402-408&rft.issn=0735-1097&rft.eissn=1558-3597&rft.coden=JACCDI&rft_id=info:doi/10.1016/S0735-1097(99)00194-1&rft_dat=%3Cproquest_cross%3E69942000%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=69942000&rft_id=info:pmid/10440152&rft_els_id=S0735109799001941&rfr_iscdi=true |