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Left atrial hypertrophy increases P-wave terminal force through amplitude but not duration

Loewe, Axel; Andlauer, Robin; Platonov, Pyotr G. LU ; Dossel, Olaf and Seemann, Gunnar (2017) 43rd Computing in Cardiology Conference, CinC 2016 In Computing in Cardiology Conference, CinC 2016 43. p.1-4
Abstract

P-wave morphology correlates with the risk for a trial fibrillation (AF). Left atrial (LA) enlargement could explain both the higher risk for AF and higher P-wave terminal force (PTF) in ECG lead V1. However, PTF-V1 has been shown to correlate poorly with LA size. We hypothesize that LA hypertrophy, i.e. a thickening of the myocardial wall, also contributes to increased PTF-V1 and is part of the reason for the rather low specificity of increased PTF-V1 regarding LA enlargement. To show this, a trial excitation propagation was simulated in a cohort of four anatomically individualized models including rule-based myocyte orientation and spatial electrophysiological heterogeneity using the mono... (More)

P-wave morphology correlates with the risk for a trial fibrillation (AF). Left atrial (LA) enlargement could explain both the higher risk for AF and higher P-wave terminal force (PTF) in ECG lead V1. However, PTF-V1 has been shown to correlate poorly with LA size. We hypothesize that LA hypertrophy, i.e. a thickening of the myocardial wall, also contributes to increased PTF-V1 and is part of the reason for the rather low specificity of increased PTF-V1 regarding LA enlargement. To show this, a trial excitation propagation was simulated in a cohort of four anatomically individualized models including rule-based myocyte orientation and spatial electrophysiological heterogeneity using the mono domain approach. The LA wall was thickened symmetrically in steps of 0.66mm by up to 3.96mm. Interatrial conduction was possible via discrete connections at the coronary sinus, Bachmann's bundle and posteriorly. Body surface ECGs were computed using realistic, heterogeneous torso models. During the early P-wave stemming from sources in the RA, no changes were observed. Once the LA got activated, the voltage in Vi tended to lower values for higher degrees of hypertrophy. Thus, the amplitude of the late positive P-wave decreased while the amplitude of the subsequent negative terminal phase increased. PTF-V1 and LA wall thickening showed a correlation of 0.95. The P-wave duration was almost unaffected by LA wall thickening (Δ <2 ms). Our results show that PTF-V1 is a sensitive marker for LA wall thickening and elucidate why it is superior to P-wave area. The interplay of LA hypertrophy and dilation might cause the poor empirical correlation of LA size and PTF-V1.

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author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
Left atrial hypertrophy, P-wave terminal force
in
Computing in Cardiology Conference, CinC 2016
volume
43
pages
4 pages
publisher
IEEE Computer Society
conference name
43rd Computing in Cardiology Conference, CinC 2016
external identifiers
  • scopus:85016093960
ISBN
9781509008964
language
English
LU publication?
yes
id
57257b01-d170-4a08-86f6-a584c5722736
date added to LUP
2017-04-24 11:01:30
date last changed
2018-01-07 12:00:35
@inproceedings{57257b01-d170-4a08-86f6-a584c5722736,
  abstract     = {<p>P-wave morphology correlates with the risk for a trial fibrillation (AF). Left atrial (LA) enlargement could explain both the higher risk for AF and higher P-wave terminal force (PTF) in ECG lead V<sub>1</sub>. However, PTF-V<sub>1</sub> has been shown to correlate poorly with LA size. We hypothesize that LA hypertrophy, i.e. a thickening of the myocardial wall, also contributes to increased PTF-V<sub>1</sub> and is part of the reason for the rather low specificity of increased PTF-V<sub>1</sub> regarding LA enlargement. To show this, a trial excitation propagation was simulated in a cohort of four anatomically individualized models including rule-based myocyte orientation and spatial electrophysiological heterogeneity using the mono domain approach. The LA wall was thickened symmetrically in steps of 0.66mm by up to 3.96mm. Interatrial conduction was possible via discrete connections at the coronary sinus, Bachmann's bundle and posteriorly. Body surface ECGs were computed using realistic, heterogeneous torso models. During the early P-wave stemming from sources in the RA, no changes were observed. Once the LA got activated, the voltage in Vi tended to lower values for higher degrees of hypertrophy. Thus, the amplitude of the late positive P-wave decreased while the amplitude of the subsequent negative terminal phase increased. PTF-V<sub>1</sub> and LA wall thickening showed a correlation of 0.95. The P-wave duration was almost unaffected by LA wall thickening (Δ &lt;2 ms). Our results show that PTF-V<sub>1</sub> is a sensitive marker for LA wall thickening and elucidate why it is superior to P-wave area. The interplay of LA hypertrophy and dilation might cause the poor empirical correlation of LA size and PTF-V<sub>1</sub>.</p>},
  author       = {Loewe, Axel and Andlauer, Robin and Platonov, Pyotr G. and Dossel, Olaf and Seemann, Gunnar},
  booktitle    = {Computing in Cardiology Conference, CinC 2016},
  isbn         = {9781509008964},
  keyword      = {Left atrial hypertrophy,P-wave terminal force },
  language     = {eng},
  month        = {03},
  pages        = {1--4},
  publisher    = {IEEE Computer Society},
  title        = {Left atrial hypertrophy increases P-wave terminal force through amplitude but not duration},
  volume       = {43},
  year         = {2017},
}