OBJECTIVE: Several risk factors are established for prediction of sudden cardiac death caused by ventricular arrhythmias in patients with hypertrophic cardiomyopathy (HCM). QT dispersion (QTd) is thought to reflect the heterogeneity of ventricular repolarization. The relation of QTd with ventricular arrhythmias and sudden cardiac death has been shown by several studies. The aim of this study is to examine whether there is a relationship between QTd and established risk factors of sudden cardiac death in patients with HCM. METHODS: In the present study 48 patients with HCM and 30 normal subjects were studied. The patients with electrocardiographic changes that could affect QT interval measurements and those in whom QTd was calculated in less than 9 leads were excluded from the study. A family history of sudden death due to HCM, a history of ventricular fibrillation, nonsustained ventricular tachycardia on Holter monitoring and a history of recurrent syncope were accepted as risk factors for sudden cardiac death. RESULTS: QTd was significantly greater in patients with HCM than in normal controls (55+/-22 ms vs 34+/-13 ms, p<0.001). There was no significant difference in QTd between patients with and without risk factors (57+/-22 ms vs 53+/-20 ms, p>0.05). There was also no significant difference in QTd between patients with and without left ventricular outflow gradient p>30 mmHg (57+/-23 ms vs 53+/-19 ms, p>0.05). CONCLUSION: Although QTd was significantly greater in patients with HCM than in normal controls, its relation to risk factors of sudden death could not be established.
OBJECTIVE: Several risk factors are established for prediction of sudden cardiac death caused by ventricular arrhythmias in patients with hypertrophic cardiomyopathy (HCM). QT dispersion (QTd) is thought to reflect the heterogeneity of ventricular repolarization. The relation of QTd with ventricular arrhythmias and sudden cardiac death has been shown by several studies. The aim of this study is to examine whether there is a relationship between QTd and established risk factors of sudden cardiac death in patients with HCM. METHODS: In the present study 48 patients with HCM and 30 normal subjects were studied. The patients with electrocardiographic changes that could affect QT interval measurements and those in whom QTd was calculated in less than 9 leads were excluded from the study. A family history of sudden death due to HCM, a history of ventricular fibrillation, nonsustained ventricular tachycardia on Holter monitoring and a history of recurrent syncope were accepted as risk factors for sudden cardiac death. RESULTS: QTd was significantly greater in patients with HCM than in normal controls (55+/-22 ms vs 34+/-13 ms, p<0.001). There was no significant difference in QTd between patients with and without risk factors (57+/-22 ms vs 53+/-20 ms, p>0.05). There was also no significant difference in QTd between patients with and without left ventricular outflow gradient p>30 mmHg (57+/-23 ms vs 53+/-19 ms, p>0.05). CONCLUSION: Although QTd was significantly greater in patients with HCM than in normal controls, its relation to risk factors of sudden death could not be established.