We propose an image scoring method to improve the quality and the reproducibility of measurement of the AV interval before establishing reference tables of the measurements and studies on the prevention and treatment of first-degree AV block especially if the first child has been diagnosed AV block.

The RHOA-ROCK signaling pathway is involved in numerous developmental processes, including cell proliferation, differentiation and migration. RHOA is expressed in the atrioventricular node (AVN) and altered expression of RHOA results in atrioventricular (AV) conduction disorders in mice. The current study aims to detect functional AVN disorders after disturbing RHOA-ROCK signaling in chicken embryos. RHOA-ROCK signaling was inhibited chemically by using the Rho-kinase inhibitor compound Y-27632 in avian embryos (20 experimental and 29 control embryos). Morphological examination of control embryos show a myocardial sinus venosus to atrioventricular canal continuity, contributing to the transitional zone of the AVN. ROCK inhibited embryos revealed lateralization and diminished myocardial sinus venosus to atrioventricular canal continuity and at the severe end of the phenotype hypoplasia of the AVN region. Ex ovo micro-electrode recordings showed an AV conduction delay in all treated embryos as well as cases with first, second (Wenkebach and Mobitz type) and third-degree AV block which could be explained by the spectrum of severity of the morphological phenotype. Laser capture microdissection and subsequent qPCR of tissue collected from this region revealed disturbed expression of HCN1, ISL1, and SHOX2. We conclude that RHOA-ROCK signaling is essential for normal morphological development of the myocardial continuity between the sinus venosus and AVN, contributing to the transitional zone, and possibly the compact AVN region. Disturbing the RHOA-ROCK signaling pathway results in AV conduction disturbances including AV block. The RHOA-ROCK inhibition model can be used to further study the pathophysiology and therapeutic strategies for AV block. Anat Rec, 2018. © 2018 Wiley Periodicals, Inc.

A 48-year-old athletic man with history of dyslipidemia and second-degree atrioventricular block (Mobitz type I 2:1 atrioventricular block) endorses sleep-related difficulties at his annual physical examination. Mobitz type I block was diagnosed 11 years earlier when the patient presented to his primary care physician with left-sided chest pain for 2 months. He was evaluated by cardiology, with a normal stress echocardiogram. The impression was that the chest pain was nonanginal. He describes sleeping for only a few hours at a time and has nighttime awakenings. He does not wake up feeling refreshed. He experiences passive daytime sleepiness and evening somnolence. He is very active, runs every day, and has participated in several half-marathons. He currently undergoes high-intensity interval training, including running and lifting. Per his wife, the patient snores loudly and has apneic episodes during sleep. One of his siblings has OSA. He denies excessive sleepiness, with an Epworth Sleepiness Scale score of 2.