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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.

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