Effects of controlled hypoglycaemia on cardiac repolarisation in patients with type 1 diabetes
Aims/hypothesis Nocturnal hypoglycaemia may contribute to sudden death in diabetic patients. However, it is not well known why hypoglycaemia makes these patients prone to death. Methods We assessed the effects of controlled hypoglycaemia on cardiac repolarisation using novel electrocardiographic des...
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Published in | Diabetologia Vol. 51; no. 3; pp. 426 - 435 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Berlin/Heidelberg : Springer-Verlag
01.03.2008
Springer-Verlag Springer Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Aims/hypothesis Nocturnal hypoglycaemia may contribute to sudden death in diabetic patients. However, it is not well known why hypoglycaemia makes these patients prone to death. Methods We assessed the effects of controlled hypoglycaemia on cardiac repolarisation using novel electrocardiographic descriptors of T-wave and QRS complex morphology in 16 type 1 diabetic patients and eight healthy counterparts. Several electrocardiographic variables characterising repolarisation were analysed from digitised 12-lead electrocardiograms during a euglycaemic and a hypoglycaemic clamp. Results Hypoglycaemia did not result in significant changes either in the QT interval corrected for heart rate by the nomogram method or in QT dispersion. However, the morphology of the T-wave changed significantly during hypoglycaemia. The T-wave amplitude and area in precordial leads decreased significantly in both groups (p < 0.05 to p < 0.001). The spatial QRS-T angle (total cosine R to T) (p < 0.05) and the height and the width of the T-wave loop (p < 0.05 and p < 0.01, respectively) were also reduced in the diabetic patients. The changes in the repolarisation parameters did not exhibit any significant association with changes in catecholamine levels or in heart rate variability in either group. Conclusions/interpretation Hypoglycaemia results in distinct alterations in cardiac repolarisation, which may increase the vulnerability to arrhythmic events. |
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Bibliography: | http://dx.doi.org/10.1007/s00125-007-0902-y ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0012-186X 1432-0428 |
DOI: | 10.1007/s00125-007-0902-y |