About split P waves

We have read with great interest the article ‘Split P waves: marker of extreme interatrial delay’, recently published in Europace.¹ The authors showed the electrocardiographic findings of a 38-year-old-male patient with syncope and familial PRKAG2 cardiomyopathy due to R302Q mutation. It stands out on the electrocardiogram of his admission in 2004, just before implanting a sequential DDD permanent pacemaker, P waves in leads II, III, and aVF with a biphasic morphology and a duration ≥120 ms suggestive of advanced interatrial block (aIAB). In 2017, during the interrogation of the device, they observed a split P wave with a discreet negative mode, characteristic of aIAB during sinus rhythm. In addition, authors described a biatrial deformity obtained by longitudinal tissue Doppler strain imaging, highlighting that the pattern of left atrial (LA) deformation is consistent with Bachmann’s bundle block and inferior interatrial conduction. The right atrial contraction curve originates during the first P wave and the LA contraction after the second P wave, with a deformation curve earlier in the lateral wall compared to that of the interatrial septum. This is just the opposite of what happens during the contraction phase of a normal LA, where the first structure that deforms is the atrial septum; and the lateral and anterior wall the last.² However, it draws attention that in this patient with familial PRKAG2 cardiomyopathy due to R302Q mutation, the values of strain of the lateral wall of both atria during atrial booster pump function are normal, with a value in the lateral wall of LA > 20%. This observation contrasts with what was recently published by our group.³ We observed that the global longitudinal strain of the LA wall during atrial booster pump function, determined by speckle-tracking echocardiography in patients with IAB, is significantly decreased, both in partial IAB (pIAB) (15.1 ± 3.0%), and in aIAB (12.7 ± 4.0%), compared to patients who do not have IAB (18.0 ± 5.5%).

We congratulate the authors on opening up the possibility that ventricular conduction disorders already described in patients with familial PRKAG2 cardiomyopathy due to R302Q mutation, could also present atrial conduction disorders explained by the excess glycogen storage and/or ion channel remodelling,⁴ so that the decreased longitudinal echocardiographic strain is located in the interatrial septum. Nevertheless, in our series of patients with IAB, fibrosis affecting the Bachmann region is likely to be generalized to the full thickness and extension of the LA wall,⁵ and for this reason the overall values of strain both in the contraction phase and the reservoir of LA, is abnormally diminished. This fact would explain how, in this particular case (congenital condition), despite the abnormality in interatrial conduction velocity during 13 years of follow-up, the patient had presented with no clinical atrial fibrillation, a circumstance much more frequent in patients with IAB, who are usually older and with a more advanced atrial fibrosis process.⁵

Conflict of interest: none declared.

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