THE FRONTAL PLANAR QRS/T ANGLE IN NEWLY DIAGNOSED OBSTRUCTIVE SLEEP APNEA PATIENTS

MUTLU GUNGOR*, MURAT CELIK**, OZCAN OZEKE***, YALCIN GOKOGLAN**, ERKAN YILDIRIM**, DENIZ DOGAN*****, UYGAR CAGDAS YUKSEL**, SALIM YASAR**, EROL GURSOY**, MUSTAFA KOKLU**, ALPER TOLGA POLAT*, HAZIM DINCER*

*Bayindir Hospital, Cardiology Clinic, Ankara,Turkey - **Gulhane Military Medical Academy, Department of Cardiology, Ankara, Turkey - ***Yuksek Ihtisas Heart-Education and Research Hospital, Department of Cardiology, Ankara, Turkey - ****Aksaz Military Hospital, Service of Cardiology, Mugla, Turkey - *****Gulhane Military Medical Academy, Department of Pulmonary Medicine, Ankara, Turkey

Introduction: Obstructive sleep apnea syndrome might have a deleterious effect on ventricular repolarization, reflected by an altered frontal planar QRS/T angle.

Material and method: We retrospectively analyzed the medical records of a total 120 patients underwent overnight polysomnography test. Patients were divided into 4 groups according to apnea hypopnea index (AHI) values (< 5/h, 5-15/h, 15-30/h, and > 30/h). The frontal planar QRS/T angle was defined as absolute difference between the frontal QRS wave axis and T-wave axis on resting 12-lead surface electrocardiography (ECG).

Results: The average frontal planar QRS-T angle of all participants was 42.79 ± 38.75°. The frontal planar QRS-T angle is increased with the severity of obstructive sleep apnea syndrome (OSAS) and significantly highest in severe OSAS group (AHI >30/h) (p< 0.001). In post hoc analysis, we found statistically significant differences as regard mean frontal planar QRS-T angle between normal (AHI 0-5/h) and severe OSAS (AHI > 30/h) (p = 0.002), and between mild OSAS (AHI 5-15/h) and severe OSAS (AHI > 30/h) (p = 0.002). Age, male sex, left ventricular ejection fraction and obstructive apnea index showed significant association with frontal planar QRS/T angle in multivariate linear regression analysis (for all, p < 0.005).

Conclusion: The frontal planar QRS/T angle is significantly widened in patients with newly diagnosed OSAS compared with controls and increased by the severity of the disease determined by AHI. This finding might help the underlying pathophysiological mechanism of life-threatening ventricular arrhythmic susceptibility in OSAS patients.