Diabetic patients have an excess risk of dying from cardiovascular diseases. Recently, several studies have reported a high prevalence of QT prolongation and increased QT dispersion (QTd) in patients with diabetes. These abnormalities have been shown to be associated with sudden death and poor survival in both type 1 (1) and type 2 (2) diabetes. QTd, i.e., the difference between the maximum and minimum QT intervals on the 12-lead electrocardiogram (ECG) (QTd = QT max − QT min), is claimed to reflect the degree of inhomogeneity of myocardial repolarization. The role of hyperglycemia in causing QT abnormalities in people with diabetes is not clear. The present study was therefore undertaken to assess the effect of controlling hyperglycemia on QT intervals and dispersion.
A total of 26 newly diagnosed type 2 diabetic patients with no coronary artery disease or autonomic dysfunction were recruited. Each was examined and had three ECGs recorded before and after 8 weeks of dietary intervention. All ECGs were analyzed automatically by the previously validated Glasgow program (3). The Hodges formula [corrected QT (QTc) = QT + 1.75 (rate − 60)] was used to correct QT interval. The mean of the three estimates of QTc and QTd before and after intervention was used to improve accuracy. QTc >440 ms and QTd >50 ms were considered as abnormally prolonged (4).
The mean age of 10 men and 16 women was 55.6 ± 12.0 years. Four patients (15.4%) had QTc >440 ms but none had increased QTd at baseline. After dietary intervention, even though glycemic control improved (HbA1c 8.1 ± 1.9% to 7.2 ± 1.3%, P < 0.01), no significant change was noticed in QTc (415.7 ± 19 to 415.1 ± 16.3 ms, P = NS) or QTd (25 ± 7.5 to 23.5 ± 6.7 ms, P = NS). Individual changes in QTc and QTd were not significantly correlated with corresponding initial levels or change in HbA1c. The subset of patients who had prolonged QTc or microalbuminuria at baseline did not show statistically significant differences postintervention. There was no correlation between HbA1c or fasting blood glucose and QTc or QTd before or after intervention. However, a significant correlation was observed between QTc and QTd before (r = 0.590, P < 0.05) and after (r = 0.405, P < 0.05) intervention.
It is surprising that despite the conservative criterion for the diagnosis of increased QTd (many previous studies have considered QTd >80 ms as abnormally prolonged), no patient was found to have prolonged QTd. This contrasts with other studies that have reported a high prevalence of QT abnormalities in diabetes (5).
In conclusion, this is the first prospective interventional study in a well-defined cohort of newly diagnosed type 2 diabetic patients to demonstrate that dietary treatment does not influence QT abnormalities in the short term. This study also shows that the prevalence of abnormal QTc and QTd in type 2 diabetes may not be as high as previously thought.
We are thankful to E. Cameron (diabetes specialist nurse), Bernie Quinn (dietitian), Jean Watts and Kathryn Maclaren (ECG technicians), and Julie Kennedy (ECG coder) for all their assistance.