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:


* EKG is one of the oldest, best described and most widely used cardiac diagnostic modalities worldwide. However, its use as diagnostic tool for ATTRwt-CA has likely lead to falsely reduced clinical suspicion and its underdiagnoses of the disease.
:*[[Pseudoinfarct pattern]]<ref>{{Cite journal
* This is largely from the “classical” teaching which dictates that cardiac amyloidosis is associated with low voltage
| author = [[Thibaud Damy]], [[Mathew S. Maurer]], [[Claudio Rapezzi]], [[Violaine Plante-Bordeneuve]], [[Onur N. Karayal]], [[Rajiv Mundayat]], [[Ole B. Suhr]] & [[Arnt V. Kristen]]
* In recent ATTRwt-CA studies, low voltage has been found to have poor independent sensitivity (~30%) for its diagnosis.
| title = Clinical, ECG and echocardiographic clues to the diagnosis of TTR-related cardiomyopathy
* There are numerous other EKG findings that are seen in patients with ATTRwt-CA but have low sensitivity and specificity for the disease because they are also common in age and comorbidities matched patient cohorts:
| journal = [[Open heart]]
** Pseudoinfarct pattern
| volume = 3
** Poor R-wave progression  
| issue = 1
** Atrial fibrillation
| pages = e000289
** First degree AV block  
| year = 2016
** Nonspecific ST-T-wave abnormalities  
| month =
** Left bundle branch block can be potentially useful to differentiate ATTRwt-CA and AL-CA.
| 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 shown to have high sensitivity and specificity for ATTRwt-CA.
}}</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:

References

  1. ↑ 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)
  2. ↑ 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.
  3. ↑ 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)
  4. ↑ 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)
  5. ↑ 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)
  6. ↑ 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)
  7. ↑ 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)
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ 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)
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