Wild-type (senile) amyloidosis electrocardiogram
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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)