Hypoxaemic load in sleep apnoea is associated with acute changes in T-wave amplitude

Obstructive sleep apnoea (OSA) imposes significant stress on the cardiovascular system and the heart. While long-term cardiac effects are understood, the immediate impact of hypoxaemia on the heart's electrophysiology lacks understanding. Our study aims to explore desaturation severity on cardiovascular repolarisation.

We retrospectively analysed ECGs from full diagnostic polysomnographies from 492 patients with suspected OSA. The analyses were conducted before, during and after 9137 nocturnal apnoea- or hypopnoea-related desaturations. The mean and sd of T-wave amplitude change from the baseline level to the level during and after desaturations (ΔT_{amp_mean} and ΔT_{amp_SD}) were calculated. To investigate the modulatory effects of desaturation severity, the data were divided into subgroups based on the desaturation duration (T_des; 10 s≤T_des<20 s, 20 s≤T_des<30 s, 30 s≤T_des<45 s and T_des≥45 s) and magnitude of blood oxygen saturation drop (change in peripheral oxygen saturation (ΔS _pO ); 3%≤ΔS _pO <4.5%, 4.5%≤ΔS _pO <6%, 6%≤ΔS _pO <7.5% and ΔS _pO ≥7.5%) for men and women.

Desaturations caused significant (p<0.01) changes in ΔT_{amp_mean} during and after desaturations. In men, the median ΔT_{amp_mean} during and after deep (ΔS _pO ≥7.5%) desaturations were 21 µV and 24 µV, respectively. In women, the median ΔT_{amp_mean} in deep desaturations was 15 µV during and 21 µV after desaturations. Similarly, the ΔT_{amp_SD} increased during and after deep desaturations. In regression analysis, the desaturation depth was an independent predictor for ventricular repolarisation instability.

We found an association between the severity of nocturnal desaturations and cardiac repolarisation instability. These findings hold particular importance, as repolarisation instability has been linked with cardiovascular morbidity and could potentially serve as a trigger for arrhythmias and sudden cardiac death.