P-wave assessment is frequently used in clinical practice to recognize atrial abnormalities. However, the use of P-wave criteria to diagnose specific atrial abnormalities such as left atrial enlargement has shown to be of limited use since these abnormalities can be difficult to distinguish using P-wave criteria to date. Hence, a mechanistic understanding how specific atrial abnormalities affect the P-wave is desirable. In this study, we investigated the effect of left atrial hypertrophy on P-wave morphology using an in silico approach. In a cohort of four realistic patient models, we homogeneously increased left atrial wall thickness in up to seven degrees of left atrial hypertrophy. Excitation conduction was simulated using a monodomain finite element approach. Then, the resulting transmembrane voltage distribution was used to calculate the corresponding extracellular potential distribution on the torso by solving the forward problem of electrocardiography. In our simulation setup, left atrial wall thickening strongly correlated with an increased absolute value of the P-wave terminal force (PTF) in Wilson lead V1 due to an increased negative amplitude while P-wave duration was unaffected. Remarkably, an increased PTF-V1 has often been associated with left atrial enlargement which is defined as a rather increased left atrial volume than a solely thickened left atrium. Hence, the observed contribution of left atrial wall thickness changes to PTF-V1 might explain the poor empirical correlation of left atrial enlargement with PTF-V1.
P-wave morphology correlates with the risk for atrial fibrillation (AF). Left atrial (LA) enlargement could ex- plain both the higher risk for AF and higher P-wave ter- minal force (PTF) in ECG lead V1. However, PTF-V1 has been shown to correlate poorly with LA size. We hypoth- esize that LA hypertrophy, i.e. a thickening of the myocar- dial 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, atrial excitation propagation was simulated in a cohort of four anatomically individualized models in- cluding rule-based myocyte orientation and spatial elec- trophysiological heterogeneity using the monodomain ap- proach. 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 mod- els. During the early P-wave stemming from sources in the RA, no changes were observed. Once the LA got activated, the voltage in V1 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 neg- ative terminal phase increased. PTF-V1 and LA wall thick- ening showed a correlation of 0.95. The P-wave duration was almost unaffected by LA wall thickening (∆ ≤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.
R. Andlauer. Investigation of the effect of left atrial anatomy alterations on p-wave morphology in a computational model. Institute of Biomedical Engineering, Karlsruhe Institute of Technology (KIT). Bachelorarbeit. 2016
P-wave assessment can offer a simple and inexpensive means to diagnose left atrial enlargement, which is a predictor for atrial fibrillation. However, the underlying influence of left atrial enlargement on the P-wave is not fully understood. Furthermore, P-wave markers to assess left atrial enlargement show poor sensitivity or specificity - potentially due to other left atrial abnormalities similarly affecting P-wave morphology as left atrial enlargement. In an in silico approach, the left atrium was dilated by mechanical inflation. In another approach, the left atrial myocardium was homogeneously thickened in four patient models. To generate torso meshes containing the modified atria, an existing method to mesh tetrahedral torsos was applied for left atrial wall thickening. For left atrial dilation, a new method was developed to generate tetrahedral torso meshes from organ surfaces. Afterwards, the P-waves were simulated for the two different left atrial anatomical alterations. Left atrial wall thickening resulted in an increased P-terminal force in V1 and an increased P-wave area. For left atrial dilation, the resulting P-waves were not realistic, as the underlying electrophysiological simulation method was not es- tablished yet. Furthermore, left atrial dilation was only applied to a single model. Thus, the results were unreliable. Considering this, the results suggest a prolonged P-wave duration, P-wave notching and an increased P-wave amplitude in aV L to be correlated with left atrial dilation.