P wave dispersion on 12-lead electrocardiography in adolescents with neurocardiogenic syncope

Abstract

PurposeNeurocardiogenic syncope (NCS) is the most frequent cause of fainting during adolescence. Inappropriate cardiovascular autonomic control may be responsible for this clinical event. The head-up tilt test has been considered a diagnostic standard, but it is cumbersome and has a high false-positive rate. We performed a study to evaluate whether P-wave dispersion (PWD) could be a useful electrocardiographic parameter of cardiac autonomic dysfunction in children with NCS.MethodsFifty-four patients with NCS (28 boys and 26 girls; mean age, 12.3±1.4 years) and 55 age- and sex-matched healthy controls were enrolled. PWD was obtained as the difference between maximum and minimum durations of the P wave on standard 12-lead electrocardiography in all patients and controlsResultsThe value of PWD was significantly higher in the syncope group than in the control group (69.7±19.6 msec vs. 45.5±17.1 msec, respectively; P<0.001). The minimum duration of P wave was shorter in the syncope group than in the control group (43.8±16.8 msec vs. 53.5±10.7 msec, respectively; P<0.001). Left atrial volume was not different between the groups on transthoracic echocardiographyConclusionPWD on echocardiography could be used as a clinical parameter in patients with NCS.

Features of vitamin B6 profile in children and adolescents with vasovagal syncope

“…Зменшення рівня вітамі ну В6 асоціювалося зі збільшенням моди (r= 0,38; p=0,04) та середнього значення інтер валу P Q (r= 0,48; p=0,01), а також моди інтер валу Q T (r= 0,40; p=0,03). Станом на сьогодні доведено, що подовження інтервалів P Q та Q T є одним із проявів автономної дисфунк ції в дітей та підлітків [19,22]. Отримані резуль тати підтверджують опосередковану роль дефі циту вітаміну В6 у ґенезі автономної дисфунк ції [32].…”

Left atrial function evaluation by 2D speckle‐tracking echocardiography in patients with vasovagal syncope

“…The current evidence, however, suggests that changes in the volume or function of the heart chambers may be implicated in VVS recurrences. [5][6][7][8][9][10][11] The left atrium (LA) appears to play a part in VVS, probably as a consequence of decreased LA volumes, 5,7 LA hypocontractility during HUTT, 6,8 increased P-wave dispersions as an LA electrical activity index, 12 and lengthened atrial conduction times or intra-atrial delays as a marker of LA electromechanical function. 10 Evidence also indicates an association between syncope and atrial fibrillation.…”