Inducible myocardial ischaemia in hypertrophic cardiomyopathy (HCM) may be detected on the stress electrocardiogram (ECG). However, how the ECG manifestation of ischaemia is affected by abnormal repolarisation at baseline in HCM, and the related electrophysiological mechanisms, are poorly understood.
Computational biventricular human HCM models (n = 20) were constructed of apical and asymmetric septal hypertrophy types, with regionally slowed repolarisation secondary to ionic remodelling, manifesting on the ECG as inverted T waves at baseline. Biventricular models were subjected to regionally ischaemic K+ accumulation in hypertrophied segments, and compared to cases with benign stress changes such as exercise-induced serum K+ accumulation and/or increased pacing frequency. Virtual 12-lead ECGs were computed from 520 simulations to analyse effects on ST segments, T wave polarity/amplitudes and QT intervals.
Correction of T wave polarity (T wave pseudonormalisation) occurred due to regionally ischaemic K+ accumulation in HCM models, with larger ischaemic ECG changes occurring in T waves than ST segments. In some anatomical and electrophysiological phenotypes, serum K+ accumulation and increased pacing rates also partially corrected inverted T waves.
Ischaemic T wave pseudonormalisation can occur and precede ischaemic ST segment changes on the stress ECG, such that correction to T wave polarity may sometimes be an early, or the only, ECG feature of myocardial ischaemia in HCM. Dynamic T wave abnormalities may signify ischaemia in HCM, but efforts are needed to discern ischaemic changes from those occurring secondary to exercise.