Association between obstructive sleep apnoea and QTc at rest and during exercise test in patients with severe obesity

Obesity and obstructive sleep apnoea (OSA), both predictors of cardiovascular morbidity and mortality, has been independently associated with QTc interval (QTc) prolongation, as sign of a reduced repolarisation reserve, and arrythmias. Provocative manoeuvres, such as brisk standing and exercise testing, can be used to "unmask" these repolarisation abnormalities.

To evaluate the QTc and its adaptations to brisk standing and exercise testing in patients with severe obesity and moderate to severe OSA. The number of arrhythmic events during cardiopulmonary exercise testing and the influence of CPAP therapy on QTc were also investigated.

Observational cross-sectional study conducted on 126 patients with severe obesity and suspected OSA. All patients underwent cardiorespiratory sleep study, spirometry, brisk standing test, and cardiopulmonary exercise testing (CPET). QTc was measured at rest, at the stable heart rate after brisk standing (QTc return) and at the 4th minute of the recovery phase. QT interval correction was performed with the Bazett’s or Fridericia’s formulas depending on the heart rate. Patients with ECG abnormalities influencing QT interval measurement were excluded from the study population.

Age and anthropometric parameters were similar in patients with obesity and OSA (Ob-OSA) compared to those without OSA (Ob-noOSA), only waist circumference was significantly higher in the first group (140.8±14.7 cm vs. 133.0±16.0 cm; p 0.019). Ob-OSA compared to Ob-noOSA (Figure 1) had significantly longer QTc rest (QTc rest D2 427.1±23.3 ms vs. 414.3±24.9 ms; p 0.004), QTc return (Qtc return D2 421.8±19.3 ms vs. 410.0±24.4 ms; p 0.035), and QTc 4-min recovery (Qtc 4min recovery D2 421.0±21.3ms vs. 408.1±30.7 ms; p 0.007) despite none of these QTc parameters were prolonged enough to reach the cut-off value for the diagnosis of long QT syndrome. Moreover, there was a significant correlation between QTc rest and the apnoea-hypopnea index (AHI). The difference in the total number of premature supraventricular complexes (PSVCs) and premature ventricular complexes (PVCs) between Ob-OSA and Ob-noOSA was not statistically significant. Finally, in Ob-OSA, CPAP therapy did not influence the QTc both at rest and during provocative manoeuvres.

OSA is associated with a prolonged, despite not pathologic, QTc as a sign of the reduced repolarisation reserve. Nevertheless, we found no significant difference in the total number of PSVCs and PVCs during exercise testing between Ob-OSA and Ob-noOSA, nor a significant effect of CPAP therapy on QTc. These findings underline that patients with obesity, in particular if complicated by OSA, need careful cardiovascular evaluation in order to detect the obesity-related structural and electrophysiological remodelling of the heart.

QTc comparison: Ob-OSA vs. Ob-noOSA.