Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle
Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunc...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sternick, Eduardo Back [verfasserIn] Correa, Frederico [verfasserIn] Negri, Ricardo [verfasserIn] Scarpelli, Ricardo Baeta [verfasserIn] Gerken, Luiz Márcio [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
Papillary muscle ventricular arrhythmia |
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| Übergeordnetes Werk: |
Enthalten in: Journal of interventional cardiac electrophysiology - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997, 25(2009), 1 vom: 16. Jan. |
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| Übergeordnetes Werk: |
volume:25 ; year:2009 ; number:1 ; day:16 ; month:01 |
| Links: |
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| DOI / URN: |
10.1007/s10840-008-9341-z |
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| Katalog-ID: |
SPR013635611 |
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| 245 | 1 | 0 | |a Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle |
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| 520 | |a Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. | ||
| 650 | 4 | |a Papillary muscle ventricular arrhythmia |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ventricular premature beats |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ventricular premature beats induced cardiomyopathy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Reversible cardiomyopathy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a BNP |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Catheter ablation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Irrigated-tip |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Tachycardiomyopathy |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Correa, Frederico |e verfasserin |4 aut | |
| 700 | 1 | |a Negri, Ricardo |e verfasserin |4 aut | |
| 700 | 1 | |a Scarpelli, Ricardo Baeta |e verfasserin |4 aut | |
| 700 | 1 | |a Gerken, Luiz Márcio |e verfasserin |4 aut | |
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10.1007/s10840-008-9341-z doi (DE-627)SPR013635611 (SPR)s10840-008-9341-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Sternick, Eduardo Back verfasserin aut Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. Papillary muscle ventricular arrhythmia (dpeaa)DE-He213 Ventricular premature beats (dpeaa)DE-He213 Ventricular premature beats induced cardiomyopathy (dpeaa)DE-He213 Reversible cardiomyopathy (dpeaa)DE-He213 BNP (dpeaa)DE-He213 Catheter ablation (dpeaa)DE-He213 Irrigated-tip (dpeaa)DE-He213 Tachycardiomyopathy (dpeaa)DE-He213 Correa, Frederico verfasserin aut Negri, Ricardo verfasserin aut Scarpelli, Ricardo Baeta verfasserin aut Gerken, Luiz Márcio verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 25(2009), 1 vom: 16. Jan. (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:25 year:2009 number:1 day:16 month:01 https://dx.doi.org/10.1007/s10840-008-9341-z 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 25 2009 1 16 01 |
| spelling |
10.1007/s10840-008-9341-z doi (DE-627)SPR013635611 (SPR)s10840-008-9341-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Sternick, Eduardo Back verfasserin aut Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. Papillary muscle ventricular arrhythmia (dpeaa)DE-He213 Ventricular premature beats (dpeaa)DE-He213 Ventricular premature beats induced cardiomyopathy (dpeaa)DE-He213 Reversible cardiomyopathy (dpeaa)DE-He213 BNP (dpeaa)DE-He213 Catheter ablation (dpeaa)DE-He213 Irrigated-tip (dpeaa)DE-He213 Tachycardiomyopathy (dpeaa)DE-He213 Correa, Frederico verfasserin aut Negri, Ricardo verfasserin aut Scarpelli, Ricardo Baeta verfasserin aut Gerken, Luiz Márcio verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 25(2009), 1 vom: 16. Jan. (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:25 year:2009 number:1 day:16 month:01 https://dx.doi.org/10.1007/s10840-008-9341-z 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 25 2009 1 16 01 |
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10.1007/s10840-008-9341-z doi (DE-627)SPR013635611 (SPR)s10840-008-9341-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Sternick, Eduardo Back verfasserin aut Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. Papillary muscle ventricular arrhythmia (dpeaa)DE-He213 Ventricular premature beats (dpeaa)DE-He213 Ventricular premature beats induced cardiomyopathy (dpeaa)DE-He213 Reversible cardiomyopathy (dpeaa)DE-He213 BNP (dpeaa)DE-He213 Catheter ablation (dpeaa)DE-He213 Irrigated-tip (dpeaa)DE-He213 Tachycardiomyopathy (dpeaa)DE-He213 Correa, Frederico verfasserin aut Negri, Ricardo verfasserin aut Scarpelli, Ricardo Baeta verfasserin aut Gerken, Luiz Márcio verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 25(2009), 1 vom: 16. Jan. (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:25 year:2009 number:1 day:16 month:01 https://dx.doi.org/10.1007/s10840-008-9341-z 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 25 2009 1 16 01 |
| allfieldsGer |
10.1007/s10840-008-9341-z doi (DE-627)SPR013635611 (SPR)s10840-008-9341-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Sternick, Eduardo Back verfasserin aut Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. Papillary muscle ventricular arrhythmia (dpeaa)DE-He213 Ventricular premature beats (dpeaa)DE-He213 Ventricular premature beats induced cardiomyopathy (dpeaa)DE-He213 Reversible cardiomyopathy (dpeaa)DE-He213 BNP (dpeaa)DE-He213 Catheter ablation (dpeaa)DE-He213 Irrigated-tip (dpeaa)DE-He213 Tachycardiomyopathy (dpeaa)DE-He213 Correa, Frederico verfasserin aut Negri, Ricardo verfasserin aut Scarpelli, Ricardo Baeta verfasserin aut Gerken, Luiz Márcio verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 25(2009), 1 vom: 16. Jan. (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:25 year:2009 number:1 day:16 month:01 https://dx.doi.org/10.1007/s10840-008-9341-z 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 25 2009 1 16 01 |
| allfieldsSound |
10.1007/s10840-008-9341-z doi (DE-627)SPR013635611 (SPR)s10840-008-9341-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Sternick, Eduardo Back verfasserin aut Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. Papillary muscle ventricular arrhythmia (dpeaa)DE-He213 Ventricular premature beats (dpeaa)DE-He213 Ventricular premature beats induced cardiomyopathy (dpeaa)DE-He213 Reversible cardiomyopathy (dpeaa)DE-He213 BNP (dpeaa)DE-He213 Catheter ablation (dpeaa)DE-He213 Irrigated-tip (dpeaa)DE-He213 Tachycardiomyopathy (dpeaa)DE-He213 Correa, Frederico verfasserin aut Negri, Ricardo verfasserin aut Scarpelli, Ricardo Baeta verfasserin aut Gerken, Luiz Márcio verfasserin aut Enthalten in Journal of interventional cardiac electrophysiology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 25(2009), 1 vom: 16. Jan. (DE-627)320457869 (DE-600)2006887-6 1572-8595 nnns volume:25 year:2009 number:1 day:16 month:01 https://dx.doi.org/10.1007/s10840-008-9341-z 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 25 2009 1 16 01 |
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Enthalten in Journal of interventional cardiac electrophysiology 25(2009), 1 vom: 16. Jan. volume:25 year:2009 number:1 day:16 month:01 |
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Papillary muscle ventricular arrhythmia Ventricular premature beats Ventricular premature beats induced cardiomyopathy Reversible cardiomyopathy BNP Catheter ablation Irrigated-tip Tachycardiomyopathy |
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Sternick, Eduardo Back @@aut@@ Correa, Frederico @@aut@@ Negri, Ricardo @@aut@@ Scarpelli, Ricardo Baeta @@aut@@ Gerken, Luiz Márcio @@aut@@ |
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The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. 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Sternick, Eduardo Back |
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610 ASE 44.85 bkl Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle Papillary muscle ventricular arrhythmia (dpeaa)DE-He213 Ventricular premature beats (dpeaa)DE-He213 Ventricular premature beats induced cardiomyopathy (dpeaa)DE-He213 Reversible cardiomyopathy (dpeaa)DE-He213 BNP (dpeaa)DE-He213 Catheter ablation (dpeaa)DE-He213 Irrigated-tip (dpeaa)DE-He213 Tachycardiomyopathy (dpeaa)DE-He213 |
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Sternick, Eduardo Back Correa, Frederico Negri, Ricardo Scarpelli, Ricardo Baeta Gerken, Luiz Márcio |
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Sternick, Eduardo Back |
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10.1007/s10840-008-9341-z |
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reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle |
| title_auth |
Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle |
| abstract |
Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. |
| abstractGer |
Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. |
| abstract_unstemmed |
Background A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. Case report We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX® system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Conclusion Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB. |
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Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle |
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| score |
7.4001484 |