QT‐interval abnormalities in hypertrophic cardiomyopathy

Abstract

Summary:To examine whether QTc and QTc dispersion across the leads of a surface electrocardiogram (ECG) are different in patients with hypertrophic cardiomyopathy (HCM) compared with normal subjects, we measured QT and calculated QTc in all 12 leads of a surface ECG in 24 patients with HCM and in 20 age-and sex-matched normal control subjects. Maximal QTc was prolonged in HCM patients (465 f 24 ms) compared with controls (410f20 ms) (p < 0.001). QTc dispersion defined as the difference of maximum-minimum QTc was also greater in HCM patients (71 f21 ms) compared with normals (35 f l l ms) (p <0.001). A correlation was found between the degree of left ventricular hypertrophy expressed by the maximal wall thickness and maximal QTc (r =0.48, p < 0.02). However, QTc dispersion did not correlate with maximal wall thickness. Thus, patients with HCM show a prolonged QTc (>440 ms) and increased QTc dispersion compared with normal subjects. In addition, the degree of left ventricular hypertrophy correlates with maximal QTc. The presence of a prolonged QT with increased regional dispersion may be associated with the occurrence of serious ventricular arrhythmia and sudden death in HCM.

Relation of ventricular repolarization to cardiac cycle length in normal subjects, hypertrophic cardiomyopathy, and patients with myocardial infarction

“…'~~ Is Like other investigators: 22 we noted significantly higher values of all intervals in patients with HC. In patients with MI, only the maximum values of QT interval differed significantly from those in normal subjects, which agrees with previous results observed in survivors ofML5.…”

Cardiac Pathology in Glycogen Storage Disease Type III

“…The mechanism of the VT was determined to be reentry which is often caused by myocardial fibrosis or fatty infiltration as a result of infarction or cardiomyopathy. Myocardial fibrosis is thought to possibly cause spatial dispersion of the cardiac impulse supporting reentrant arrhythmias (Dritsas et al 1992;Yi et al 1998;Shirani et al 2000;McDowell et al 2008). Tada et al speculated that the glycogen accumulation in the heart may have led to a ventricular conduction delay which drove the reentrant circuit and thereby caused the VT.…”

QT Dispersion Correlates with Systolic Rather than Diastolic Parameters in Patients Receiving Anthracycline Treatment

“…QT dispersion has been widely studied as a marker for arrhythmia risk and as a prognostic factor for some heart diseases (4)(5)(6)(7)(8). While these studies show that QT dispersion has some diagnostic capability, the clinical value of QT dispersion remains controversial and unclear.…”