Relationship of mechanical dyssynchrony to QT interval prolongation in hypertrophic cardiomyopathy

Abstract

QT interval prolongation on surface ECG shows significant association with mechanical dyssynchrony and LV dysfunction in HCM. This may add pathophysiological insight into understanding ECG changes in such myocardial disease.

Spatial QT Dispersion Predicts Nonsustained Ventricular Tachycardia and Correlates with Confined Systodiastolic Dysfunction in Hypertrophic Cardiomyopathy

“…We confirm a marginal or absent correlation between this parameter and MWT or LV mass, respectively [33,34,35,36,37,38], whereas, given that all patients enrolled had a similar distribution of LV hypertrophy (i.e. interventricular septum with or without a LV anterior wall involvement), we cannot add data about a possible impact of this echocardiographic feature on spatial QT dispersion [43,44]. Thus, it can be assumed that, at least in our sample, spatial QT dispersion might be affected by the myocardium properties more than from the hypertrophy severity per se.…”

“…In such a homogenous study sample, our data suggest the whole QT e dispersion as the best 12-lead surface ECG marker of NSVT risk compared with all the other QT subsegment dispersion values (QRS, QT p , T p T e , JT p , and JT e ). This finding, albeit original, was not fully unexpected given that the QT e accounts for the myocardial repolarization as well as for the intra-LV electromechanical conduction (QRS segment), the latter also known to be significantly impaired in HCM patients [42,43,44]. Nonetheless, we should acknowledge our finding as a merely descriptive one given that although NSVT is a major risk factor for SCD in these patients, its positive predictive accuracy is modest [3,5].…”

Fibrosis and wall thickness affect ventricular repolarization dynamics in hypertrophic cardiomyopathy

“…The action potential is prolonged as the net repolarizing current is diminished by increased late‐type Na and Ca 2+ currents ( I NaL and I CaL ) and selective down regulation of the outward rectifying current ( I Kr )(Coppini et al., ; Crocini et al., ; Passini et al., ). The repolarization in the myocardium is also delayed due to hypertrophy (Badran et al., ) and global repolarization is spatially dispersed due to the asymmetric location of hypertrophy (Sakata et al., ). The pathophysiological abnormalities in potassium‐currents, especially the reduction in I Kr , resemble those found in type 2 LQTS patients and in agreement we found the prolongation of heart rate‐adapted QTe and the prolongation of TPE interval mimicking the findings in type 2 LQTS patients (Viitasalo, Oikarinen, Swan et al., ; Viitasalo, Oikarinen, Väänänen et al., ).…”

Evaluation of Prolonged QT Interval: Structural Heart Disease Mimicking Long QT Syndrome

“…Cardiomyopathic conditions, mainly those causing ventricular hypertrophy and/or dilatation, have been shown to be associated with abnormalities in ventricular repolarization . Hypertrophied and failing myocardium has been shown to exhibit functional downregulation of K currents (I to , I k1 , I kr , and I ks currents) resulting in QTc prolongation .…”

“…33 Cardiomyopathic conditions, mainly those causing ventricular hypertrophy and/or dilatation, have been shown to be associated with abnormalities in ventricular repolarization. [34][35][36][37][38][39] Hypertrophied and failing myocardium has been shown to exhibit functional downregulation of K currents (I to , I k1 , I kr , and I ks currents) resulting in QTc prolongation. [40][41][42] Repolarization duration measured by the QTc interval was shown to be inversely correlated with heart failure severity measured by peak VO2 and independent of LV loading conditions in patients with severe heart failure.…”