Wild-type (senile) amyloidosis electrocardiogram: Difference between revisions
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{{Wild-type (senile) amyloidosis}} | {{Wild-type (senile) amyloidosis}} | ||
{{CMG}} | {{CMG}}{{AE}}{{Sab}} | ||
==Overview== | ==Overview== | ||
[[The electrocardiogram|EKG]] findings encountered during the evaluation of a [[patient]] with wild-type (senile) amyloidosis include [[pseudoinfarct pattern]], [[Poor R Wave Progression|poor R wave progression]], [[atrial fibrillation]], [[first degree AV block]], and nonspecific ST-T wave abnormalities. Voltage-to-mass ratio, calculated by the sum of [[S wave]] in lead V1 plus [[R wave]] in lead V5 or V6 (SV1 + RV5 or V6) divided by the [[Echocardiography|echocardiographic]] muscle cross-sectional area, has been implicated to have high [[Sensitivity (tests)|sensitivity]] and [[Specificity (tests)|specificity]] for wild-type (senile) amyloidosis. | |||
==Electrocardiogram== | ==Electrocardiogram== | ||
*The [[The electrocardiogram|EKG]] findings in wild-type (senile) amyloidosis have low [[Sensitivity (tests)|sensitivity]] and [[Specificity (tests)|specificity]] for the condition.<ref>{{Cite journal | |||
| author = [[Ilia G. Halatchev]], [[Jingsheng Zheng]] & [[Jiafu Ou]] | |||
| title = Wild-type transthyretin cardiac amyloidosis (ATTRwt-CA), previously known as senile cardiac amyloidosis: clinical presentation, diagnosis, management and emerging therapies | |||
| journal = [[Journal of thoracic disease]] | |||
| volume = 10 | |||
| issue = 3 | |||
| pages = 2034–2045 | |||
| year = 2018 | |||
| month = March | |||
| doi = 10.21037/jtd.2018.03.134 | |||
| pmid = 29707360 | |||
}}</ref> | |||
*This is because the [[The electrocardiogram|EKG]] findings are also common in [[Ageing|aging]] patients suffering from comorbidities. | |||
*[[The electrocardiogram|EKG]] findings encountered during the evaluation of a [[patient]] with wild-type (senile) amyloidosis are given below: | |||
* | :*[[Pseudoinfarct pattern]]<ref>{{Cite journal | ||
| author = [[Thibaud Damy]], [[Mathew S. Maurer]], [[Claudio Rapezzi]], [[Violaine Plante-Bordeneuve]], [[Onur N. Karayal]], [[Rajiv Mundayat]], [[Ole B. Suhr]] & [[Arnt V. Kristen]] | |||
| title = Clinical, ECG and echocardiographic clues to the diagnosis of TTR-related cardiomyopathy | |||
| journal = [[Open heart]] | |||
| volume = 3 | |||
* | | issue = 1 | ||
* | | pages = e000289 | ||
* | | year = 2016 | ||
| month = | |||
| doi = 10.1136/openhrt-2015-000289 | |||
| pmid = 26870387 | |||
* Voltage-to-mass ratio, calculated by sum of S wave in lead V1 plus R wave in lead V5 or V6 (SV1 + RV5 or V6) divided by the echocardiographic muscle cross-sectional area has been | }}</ref><ref>{{Cite journal | ||
| author = [[Esther Gonzalez-Lopez]], [[Christian Gagliardi]], [[Fernando Dominguez]], [[Cristina Candida Quarta]], [[F. Javier de Haro-Del Moral]], [[Agnese Milandri]], [[Clara Salas]], [[Mario Cinelli]], [[Marta Cobo-Marcos]], [[Massimiliano Lorenzini]], [[Enrique Lara-Pezzi]], [[Serena Foffi]], [[Luis Alonso-Pulpon]], [[Claudio Rapezzi]] & [[Pablo Garcia-Pavia]] | |||
| title = Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths | |||
| journal = [[European heart journal]] | |||
| volume = 38 | |||
| issue = 24 | |||
| pages = 1895–1904 | |||
| year = 2017 | |||
| month = June | |||
| doi = 10.1093/eurheartj/ehx043 | |||
| pmid = 28329248 | |||
}}</ref> | |||
:*[[Poor R Wave Progression|Poor R wave progression]]<ref>{{Cite journal | |||
| author = [[Esther Gonzalez-Lopez]], [[Christian Gagliardi]], [[Fernando Dominguez]], [[Cristina Candida Quarta]], [[F. Javier de Haro-Del Moral]], [[Agnese Milandri]], [[Clara Salas]], [[Mario Cinelli]], [[Marta Cobo-Marcos]], [[Massimiliano Lorenzini]], [[Enrique Lara-Pezzi]], [[Serena Foffi]], [[Luis Alonso-Pulpon]], [[Claudio Rapezzi]] & [[Pablo Garcia-Pavia]] | |||
| title = Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths | |||
| journal = [[European heart journal]] | |||
| volume = 38 | |||
| issue = 24 | |||
| pages = 1895–1904 | |||
| year = 2017 | |||
| month = June | |||
| doi = 10.1093/eurheartj/ehx043 | |||
| pmid = 28329248 | |||
}}</ref> | |||
:*[[Atrial fibrillation]]<ref>{{Cite journal | |||
| author = [[Christoph Rocken]], [[Brigitte Peters]], [[Gina Juenemann]], [[Wolfgang Saeger]], [[Helmut U. Klein]], [[Christof Huth]], [[Albert Roessner]] & [[Andreas Goette]] | |||
| title = Atrial amyloidosis: an arrhythmogenic substrate for persistent atrial fibrillation | |||
| journal = [[Circulation]] | |||
| volume = 106 | |||
| issue = 16 | |||
| pages = 2091–2097 | |||
| year = 2002 | |||
| month = October | |||
| doi = 10.1161/01.cir.0000034511.06350.df | |||
| pmid = 12379579 | |||
}}</ref><ref>{{Cite journal | |||
| author = [[Nicole B. Cyrille]], [[Jeff Goldsmith]], [[Julissa Alvarez]] & [[Mathew S. Maurer]] | |||
| title = Prevalence and prognostic significance of low QRS voltage among the three main types of cardiac amyloidosis | |||
| journal = [[The American journal of cardiology]] | |||
| volume = 114 | |||
| issue = 7 | |||
| pages = 1089–1093 | |||
| year = 2014 | |||
| month = October | |||
| doi = 10.1016/j.amjcard.2014.07.026 | |||
| pmid = 25212550 | |||
}}</ref> | |||
:*[[First degree AV block]]<ref>{{Cite journal | |||
| author = [[Blaithnead Murtagh]], [[Stephen C. Hammill]], [[Morie A. Gertz]], [[Robert A. Kyle]], [[A. Jamil Tajik]] & [[Martha Grogan]] | |||
| title = Electrocardiographic findings in primary systemic amyloidosis and biopsy-proven cardiac involvement | |||
| journal = [[The American journal of cardiology]] | |||
| volume = 95 | |||
| issue = 4 | |||
| pages = 535–537 | |||
| year = 2005 | |||
| month = February | |||
| doi = 10.1016/j.amjcard.2004.10.028 | |||
| pmid = 15695149 | |||
}}</ref> | |||
:*Nonspecific ST-T wave abnormalities<ref>{{Cite journal | |||
| author = [[Blaithnead Murtagh]], [[Stephen C. Hammill]], [[Morie A. Gertz]], [[Robert A. Kyle]], [[A. Jamil Tajik]] & [[Martha Grogan]] | |||
| title = Electrocardiographic findings in primary systemic amyloidosis and biopsy-proven cardiac involvement | |||
| journal = [[The American journal of cardiology]] | |||
| volume = 95 | |||
| issue = 4 | |||
| pages = 535–537 | |||
| year = 2005 | |||
| month = February | |||
| doi = 10.1016/j.amjcard.2004.10.028 | |||
| pmid = 15695149 | |||
}}</ref> | |||
*Voltage-to-mass ratio, calculated by the sum of [[S wave]] in lead V1 plus [[R wave]] in lead V5 or V6 (SV1 + RV5 or V6) divided by the [[Echocardiography|echocardiographic]] muscle cross-sectional area, has been implicated to have high [[Sensitivity (tests)|sensitivity]] and [[Specificity (tests)|specificity]] for wild-type (senile) amyloidosis.<ref>{{Cite journal | |||
| author = [[Claudio Rapezzi]], [[Giampaolo Merlini]], [[Candida C. Quarta]], [[Letizia Riva]], [[Simone Longhi]], [[Ornella Leone]], [[Fabrizio Salvi]], [[Paolo Ciliberti]], [[Francesca Pastorelli]], [[Elena Biagini]], [[Fabio Coccolo]], [[Robin M. T. Cooke]], [[Letizia Bacchi-Reggiani]], [[Diego Sangiorgi]], [[Alessandra Ferlini]], [[Michele Cavo]], [[Elena Zamagni]], [[Maria Luisa Fonte]], [[Giovanni Palladini]], [[Francesco Salinaro]], [[Francesco Musca]], [[Laura Obici]], [[Angelo Branzi]] & [[Stefano Perlini]] | |||
| title = Systemic cardiac amyloidoses: disease profiles and clinical courses of the 3 main types | |||
| journal = [[Circulation]] | |||
| volume = 120 | |||
| issue = 13 | |||
| pages = 1203–1212 | |||
| year = 2009 | |||
| month = September | |||
| doi = 10.1161/CIRCULATIONAHA.108.843334 | |||
| pmid = 19752327 | |||
}}</ref><ref>{{Cite journal | |||
| author = [[J. D. Carroll]], [[W. H. Gaasch]] & [[K. P. McAdam]] | |||
| title = Amyloid cardiomyopathy: characterization by a distinctive voltage/mass relation | |||
| journal = [[The American journal of cardiology]] | |||
| volume = 49 | |||
| issue = 1 | |||
| pages = 9–13 | |||
| year = 1982 | |||
| month = January | |||
| doi = 10.1016/0002-9149(82)90270-3 | |||
| pmid = 6459025 | |||
}}</ref> | |||
==References== | ==References== |
Latest revision as of 22:35, 17 December 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]
Overview
EKG findings encountered during the evaluation of a patient with wild-type (senile) amyloidosis include pseudoinfarct pattern, poor R wave progression, atrial fibrillation, first degree AV block, and nonspecific ST-T wave abnormalities. Voltage-to-mass ratio, calculated by the sum of S wave in lead V1 plus R wave in lead V5 or V6 (SV1 + RV5 or V6) divided by the echocardiographic muscle cross-sectional area, has been implicated to have high sensitivity and specificity for wild-type (senile) amyloidosis.
Electrocardiogram
- The EKG findings in wild-type (senile) amyloidosis have low sensitivity and specificity for the condition.[1]
- This is because the EKG findings are also common in aging patients suffering from comorbidities.
- EKG findings encountered during the evaluation of a patient with wild-type (senile) amyloidosis are given below:
- Pseudoinfarct pattern[2][3]
- Poor R wave progression[4]
- Atrial fibrillation[5][6]
- First degree AV block[7]
- Nonspecific ST-T wave abnormalities[8]
- Voltage-to-mass ratio, calculated by the sum of S wave in lead V1 plus R wave in lead V5 or V6 (SV1 + RV5 or V6) divided by the echocardiographic muscle cross-sectional area, has been implicated to have high sensitivity and specificity for wild-type (senile) amyloidosis.[9][10]
References
- ↑ Ilia G. Halatchev, Jingsheng Zheng & Jiafu Ou (2018). "Wild-type transthyretin cardiac amyloidosis (ATTRwt-CA), previously known as senile cardiac amyloidosis: clinical presentation, diagnosis, management and emerging therapies". Journal of thoracic disease. 10 (3): 2034–2045. doi:10.21037/jtd.2018.03.134. PMID 29707360. Unknown parameter
|month=
ignored (help) - ↑ Thibaud Damy, Mathew S. Maurer, Claudio Rapezzi, Violaine Plante-Bordeneuve, Onur N. Karayal, Rajiv Mundayat, Ole B. Suhr & Arnt V. Kristen (2016). "Clinical, ECG and echocardiographic clues to the diagnosis of TTR-related cardiomyopathy". Open heart. 3 (1): e000289. doi:10.1136/openhrt-2015-000289. PMID 26870387.
- ↑ Esther Gonzalez-Lopez, Christian Gagliardi, Fernando Dominguez, Cristina Candida Quarta, F. Javier de Haro-Del Moral, Agnese Milandri, Clara Salas, Mario Cinelli, Marta Cobo-Marcos, Massimiliano Lorenzini, Enrique Lara-Pezzi, Serena Foffi, Luis Alonso-Pulpon, Claudio Rapezzi & Pablo Garcia-Pavia (2017). "Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths". European heart journal. 38 (24): 1895–1904. doi:10.1093/eurheartj/ehx043. PMID 28329248. Unknown parameter
|month=
ignored (help) - ↑ Esther Gonzalez-Lopez, Christian Gagliardi, Fernando Dominguez, Cristina Candida Quarta, F. Javier de Haro-Del Moral, Agnese Milandri, Clara Salas, Mario Cinelli, Marta Cobo-Marcos, Massimiliano Lorenzini, Enrique Lara-Pezzi, Serena Foffi, Luis Alonso-Pulpon, Claudio Rapezzi & Pablo Garcia-Pavia (2017). "Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths". European heart journal. 38 (24): 1895–1904. doi:10.1093/eurheartj/ehx043. PMID 28329248. Unknown parameter
|month=
ignored (help) - ↑ Christoph Rocken, Brigitte Peters, Gina Juenemann, Wolfgang Saeger, Helmut U. Klein, Christof Huth, Albert Roessner & Andreas Goette (2002). "Atrial amyloidosis: an arrhythmogenic substrate for persistent atrial fibrillation". Circulation. 106 (16): 2091–2097. doi:10.1161/01.cir.0000034511.06350.df. PMID 12379579. Unknown parameter
|month=
ignored (help) - ↑ Nicole B. Cyrille, Jeff Goldsmith, Julissa Alvarez & Mathew S. Maurer (2014). "Prevalence and prognostic significance of low QRS voltage among the three main types of cardiac amyloidosis". The American journal of cardiology. 114 (7): 1089–1093. doi:10.1016/j.amjcard.2014.07.026. PMID 25212550. Unknown parameter
|month=
ignored (help) - ↑ Blaithnead Murtagh, Stephen C. Hammill, Morie A. Gertz, Robert A. Kyle, A. Jamil Tajik & Martha Grogan (2005). "Electrocardiographic findings in primary systemic amyloidosis and biopsy-proven cardiac involvement". The American journal of cardiology. 95 (4): 535–537. doi:10.1016/j.amjcard.2004.10.028. PMID 15695149. Unknown parameter
|month=
ignored (help) - ↑ Blaithnead Murtagh, Stephen C. Hammill, Morie A. Gertz, Robert A. Kyle, A. Jamil Tajik & Martha Grogan (2005). "Electrocardiographic findings in primary systemic amyloidosis and biopsy-proven cardiac involvement". The American journal of cardiology. 95 (4): 535–537. doi:10.1016/j.amjcard.2004.10.028. PMID 15695149. Unknown parameter
|month=
ignored (help) - ↑ Claudio Rapezzi, Giampaolo Merlini, Candida C. Quarta, Letizia Riva, Simone Longhi, Ornella Leone, Fabrizio Salvi, Paolo Ciliberti, Francesca Pastorelli, Elena Biagini, Fabio Coccolo, Robin M. T. Cooke, Letizia Bacchi-Reggiani, Diego Sangiorgi, Alessandra Ferlini, Michele Cavo, Elena Zamagni, Maria Luisa Fonte, Giovanni Palladini, Francesco Salinaro, Francesco Musca, Laura Obici, Angelo Branzi & Stefano Perlini (2009). "Systemic cardiac amyloidoses: disease profiles and clinical courses of the 3 main types". Circulation. 120 (13): 1203–1212. doi:10.1161/CIRCULATIONAHA.108.843334. PMID 19752327. Unknown parameter
|month=
ignored (help) - ↑ J. D. Carroll, W. H. Gaasch & K. P. McAdam (1982). "Amyloid cardiomyopathy: characterization by a distinctive voltage/mass relation". The American journal of cardiology. 49 (1): 9–13. doi:10.1016/0002-9149(82)90270-3. PMID 6459025. Unknown parameter
|month=
ignored (help)