Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation
Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythm...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ahmed, Imdad [verfasserIn] Gertner, Elie [verfasserIn] Nelson, William B. [verfasserIn] House, Chad M. [verfasserIn] Zhu, Dennis W. X. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Journal of interventional cardiac electrophysiology - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997, 29(2010), 3 vom: 13. Okt., Seite 203-207 |
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| Übergeordnetes Werk: |
volume:29 ; year:2010 ; number:3 ; day:13 ; month:10 ; pages:203-207 |
| Links: |
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| DOI / URN: |
10.1007/s10840-010-9520-6 |
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| Katalog-ID: |
SPR013637223 |
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| 245 | 1 | 0 | |a Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
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| 520 | |a Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. | ||
| 650 | 4 | |a Anticoagulation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Warfarin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pacemaker |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Defibrillator |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Implantation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Gertner, Elie |e verfasserin |4 aut | |
| 700 | 1 | |a Nelson, William B. |e verfasserin |4 aut | |
| 700 | 1 | |a House, Chad M. |e verfasserin |4 aut | |
| 700 | 1 | |a Zhu, Dennis W. X. |e verfasserin |4 aut | |
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10.1007/s10840-010-9520-6 doi (DE-627)SPR013637223 (SPR)s10840-010-9520-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Ahmed, Imdad verfasserin aut Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. Anticoagulation (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Pacemaker (dpeaa)DE-He213 Defibrillator (dpeaa)DE-He213 Implantation (dpeaa)DE-He213 Gertner, Elie verfasserin aut Nelson, William B. verfasserin aut House, Chad M. verfasserin aut Zhu, Dennis W. X. verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 29(2010), 3 vom: 13. Okt., Seite 203-207 (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:29 year:2010 number:3 day:13 month:10 pages:203-207 https://dx.doi.org/10.1007/s10840-010-9520-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 29 2010 3 13 10 203-207 |
| spelling |
10.1007/s10840-010-9520-6 doi (DE-627)SPR013637223 (SPR)s10840-010-9520-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Ahmed, Imdad verfasserin aut Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. Anticoagulation (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Pacemaker (dpeaa)DE-He213 Defibrillator (dpeaa)DE-He213 Implantation (dpeaa)DE-He213 Gertner, Elie verfasserin aut Nelson, William B. verfasserin aut House, Chad M. verfasserin aut Zhu, Dennis W. X. verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 29(2010), 3 vom: 13. Okt., Seite 203-207 (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:29 year:2010 number:3 day:13 month:10 pages:203-207 https://dx.doi.org/10.1007/s10840-010-9520-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 29 2010 3 13 10 203-207 |
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10.1007/s10840-010-9520-6 doi (DE-627)SPR013637223 (SPR)s10840-010-9520-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Ahmed, Imdad verfasserin aut Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. Anticoagulation (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Pacemaker (dpeaa)DE-He213 Defibrillator (dpeaa)DE-He213 Implantation (dpeaa)DE-He213 Gertner, Elie verfasserin aut Nelson, William B. verfasserin aut House, Chad M. verfasserin aut Zhu, Dennis W. X. verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 29(2010), 3 vom: 13. Okt., Seite 203-207 (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:29 year:2010 number:3 day:13 month:10 pages:203-207 https://dx.doi.org/10.1007/s10840-010-9520-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 29 2010 3 13 10 203-207 |
| allfieldsGer |
10.1007/s10840-010-9520-6 doi (DE-627)SPR013637223 (SPR)s10840-010-9520-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Ahmed, Imdad verfasserin aut Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. Anticoagulation (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Pacemaker (dpeaa)DE-He213 Defibrillator (dpeaa)DE-He213 Implantation (dpeaa)DE-He213 Gertner, Elie verfasserin aut Nelson, William B. verfasserin aut House, Chad M. verfasserin aut Zhu, Dennis W. X. verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 29(2010), 3 vom: 13. Okt., Seite 203-207 (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:29 year:2010 number:3 day:13 month:10 pages:203-207 https://dx.doi.org/10.1007/s10840-010-9520-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 29 2010 3 13 10 203-207 |
| allfieldsSound |
10.1007/s10840-010-9520-6 doi (DE-627)SPR013637223 (SPR)s10840-010-9520-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Ahmed, Imdad verfasserin aut Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. Anticoagulation (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Pacemaker (dpeaa)DE-He213 Defibrillator (dpeaa)DE-He213 Implantation (dpeaa)DE-He213 Gertner, Elie verfasserin aut Nelson, William B. verfasserin aut House, Chad M. verfasserin aut Zhu, Dennis W. X. verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 29(2010), 3 vom: 13. Okt., Seite 203-207 (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:29 year:2010 number:3 day:13 month:10 pages:203-207 https://dx.doi.org/10.1007/s10840-010-9520-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 29 2010 3 13 10 203-207 |
| language |
English |
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Enthalten in Journal of interventional cardiac electrophysiology 29(2010), 3 vom: 13. Okt., Seite 203-207 volume:29 year:2010 number:3 day:13 month:10 pages:203-207 |
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Enthalten in Journal of interventional cardiac electrophysiology 29(2010), 3 vom: 13. Okt., Seite 203-207 volume:29 year:2010 number:3 day:13 month:10 pages:203-207 |
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Anticoagulation Warfarin Pacemaker Defibrillator Implantation |
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Journal of interventional cardiac electrophysiology |
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Ahmed, Imdad @@aut@@ Gertner, Elie @@aut@@ Nelson, William B. @@aut@@ House, Chad M. @@aut@@ Zhu, Dennis W. X. @@aut@@ |
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Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). 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Ahmed, Imdad |
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Ahmed, Imdad ddc 610 bkl 44.85 misc Anticoagulation misc Warfarin misc Pacemaker misc Defibrillator misc Implantation Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
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610 ASE 44.85 bkl Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation Anticoagulation (dpeaa)DE-He213 Warfarin (dpeaa)DE-He213 Pacemaker (dpeaa)DE-He213 Defibrillator (dpeaa)DE-He213 Implantation (dpeaa)DE-He213 |
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ddc 610 bkl 44.85 misc Anticoagulation misc Warfarin misc Pacemaker misc Defibrillator misc Implantation |
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Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
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Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
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Ahmed, Imdad Gertner, Elie Nelson, William B. House, Chad M. Zhu, Dennis W. X. |
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chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
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Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
| abstract |
Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. |
| abstractGer |
Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. |
| abstract_unstemmed |
Introduction The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery. Methods Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation. Results The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22–3.21; p = 0.03). Conclusion Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents. |
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Chronic kidney disease is an independent predictor of pocket hematoma after pacemaker and defibrillator implantation |
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https://dx.doi.org/10.1007/s10840-010-9520-6 |
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Gertner, Elie Nelson, William B. House, Chad M. Zhu, Dennis W. X. |
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10.1007/s10840-010-9520-6 |
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2024-07-03T21:07:31.914Z |
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| score |
7.400859 |