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

Abstract

Aims 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. Methods 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 (ΔTamp_mean and ΔTamp_SD) were calculated. To investigate the modulatory effects of desaturation severity, the data were divided into subgroups based on the desaturation duration (Tdes; 10 s≤Tdes<20 s, 20 s≤Tdes<30 s, 30 s≤Tdes<45 s and Tdes≥45 s) and magnitude of blood oxygen saturation drop (change in peripheral oxygen saturation (ΔSpO2); 3%≤ΔSpO2<4.5%, 4.5%≤ΔSpO2<6%, 6%≤ΔSpO2<7.5% and ΔSpO2≥7.5%) for men and women. Results Desaturations caused significant (p<0.01) changes in ΔTamp_mean during and after desaturations. In men, the median ΔTamp_mean during and after deep (ΔSpO2≥7.5%) desaturations were 21 µV and 24 µV, respectively. In women, the median ΔTamp_mean in deep desaturations was 15 µV during and 21 µV after desaturations. Similarly, the ΔTamp_SD increased during and after deep desaturations. In regression analysis, the desaturation depth was an independent predictor for ventricular repolarisation instability. Conclusion 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.