Influence of psychological stress on Systolic-Diastolic Interval (SDI) interaction characteristics measured from the electrocardiogram (ECG) signal

Stress affects the ventricular repolarization and the ventricular mechanical function by increasing the QT interval variability and changing left ventricular ejection fraction respectively. As QT and TQ intervals are considered as surrogates of mechanical systolic and diastolic durations, alteration of QT and TQ interval dynamics can be used to analyse stress related changes in the systolic and diastolic function of the heart. The ratio of QT to TQ interval within a cardiac cycle (i.e. QTTQ ratio) represents the synchronized contraction and relaxation operation of the heart. Besides QTTQ, the ratio of TQ to RR interval (i.e. TQRR ratio) can also be used as a non-invasive measure of the diastolic function to analyse ventricular dysfunction. The stress related alteration of ventricular function is reported in subjects with coronary heart diseases, but the same was not reported in healthy subjects widely. In this study, the effect of stress on systolic-diastolic interval (SDI) ratios is analysed to investigate the stress related alteration in ventricular repolarization in healthy subjects. The study results indicate that stress induction increases the mean QTTQ ratio (mSDIQT-TQ) and decreases the TQRR ratio (mSDITQ-RR) indicating the effect of stress on systolic and diastolic functions. The increase in mSDIQT-TQ indicates the increases in the probability of arrhythmogenesis. However, the difference between stressed and unstressed conditions for theses ratio parameters was not significant (p>0.05). Alternatively, the variability of SDI parameters (i.e. variance of QTTQ and TQRR ratios) increased significantly, which can detect the induced stress in healthy individuals and significantly (p<;0.05) differentiated the stressed condition form natural steady state relaxed condition of the same individual. The significant increase in variability in QTTQ and TQRR ratio indicate the increased probability of arrhythmogenesis due to sympathetic activation during stressed conditions.