Left Atrial Hypertrophy Increases P:Wave Terminal Force Through Amplitude but not Duration

Abstract

P-wave morphology correlates with the risk for atrial 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 1 . However, PTF-V 1 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 1 and is part of the reason for the rather low specificity of increased PTF-V 1 regarding LA enlargement. To show this, atrial excitation propagation was simulated in a cohort of four anatomically individualized models including rule-based myocyte orientation and spatial electrophysiological heterogeneity using the monodomain approach. The LA wall was thickened symmetrically in steps of 0.66 mm by up to 3.96 mm. 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 V 1 tended to lower values for higher degrees of hypertrophy. Thus, the amplitude of the late positive Pwave decreased while the amplitude of the subsequent negative terminal phase increased. PTF-V 1 and LA wall thickening showed a correlation of 0.95. The P-wave duration was almost unaffected by LA wall thickening (∆ ≤2 ms). Our results show that PTF-V 1 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 1 . IntroductionThe P-wave in the body surface ECG has long been used to gain insight into anatomy, function and dysfunction of the atria [1]. As a 12-lead ECG is routinely acquired non-invasively as part of a large number of examinations, ECG-derived measures represent ideal risk markers due to their availability and low associated costs [2]. These properties render ECG-based markers more attractive than alternatives like ultrasound, magnetic resonance imaging, electroanatomical mapping, or ECG imaging. Therefore, clinicians aim to stratify arrhythmia risk based on P-wave markers [3]. The assessment of morphological features of the P-wave is recommended in current guidelines for ECG interpretation [4] regarding the diagnosis of atrial abnormalities such as left or right atrial enlargement. The anatomy of the left atrium (LA) is of particular interest regarding the risk to develop atrial fibrillation (AF) as larger atria are more vulnerable to reentry in general. Therefore, left atrial enlargement (LAE) could explain both the higher risk to develop AF and higher P-wave terminal force (PTF) in ECG lead V 1 defined as the product of the duration and the amplitude of the terminal negative part of the P-wave. However, the criterion PTF-V 1 > 4 mVms correlates rather poorly with LA size in empirical studies. Truong et al. reported an accuracy of 51% using compute...

Maximization of Left Atrial Information through the Optimization of ECG Lead Systems

“…Particularly optimized linear combinations of standard 12-lead signals amplified LRR by more than one order of magnitude and can in future be used to optimize diagnostic tools. Important examples are ECG markers as surrogate measures to assess LA anatomy and function [10][11][12]. The sensitivity and specificity of classifiers derived from these markers regarding risk stratification and disease classification are currently not satisfactory.…”