Hypoglycaemia and Cardiac Arrhythmias in Patients with Type 2 Diabetes Mellitus

Lindström, Torbjörn; Jorfeldt, L.; Tegler, Lennart; Arnqvist, Hans J.

doi:10.1111/j.1464-5491.1992.tb01834.x

Cited by 106 publications

(73 citation statements)

References 28 publications

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“…Arrhythmias and/or ECG abnormalities have been recorded during hypoglycaemia in patients with diabetes, either accidentally observed or during induced hypoglycaemia. These include ventricular ectopics and S-T depression [9], though this study involved only participants with type 2 diabetes and occult coronary artery disease is difficult to exclude.…”

Section: Discussionmentioning

confidence: 99%

Cardiac arrhythmia and nocturnal hypoglycaemia in type 1 diabetes—the ‘dead in bed’ syndrome revisited

et al. 2008

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Aims/hypothesis Sudden nocturnal death in type 1 diabetes ('dead in bed' syndrome) is thought to be due to ECG QT prolongation with subsequent ventricular tachyarrhythmia in response to nocturnal hypoglycaemia. We investigated this theoretical mechanism using continuous ECG and continuous glucose monitoring in a group of patients with type 1 diabetes. Methods Twenty-five patients with type 1 diabetes (age 20-50 years) underwent two separate 24 h ECG and continuous glucose monitoring periods. Patients were fully ambulant and carried out normal daily activities. Results There were 13 episodes (26% of recordings) of nocturnal hypoglycaemia, eight of <2.2 mmol/l and five of 2.2-3.4 mmol/l. Corrected QT interval (QTc) was longer during nocturnal hypoglycaemia compared with normoglycaemic control periods (445±40 vs 415±23 ms; p=0.037). Cardiac rate and rhythm disturbances (excluding sinus tachycardia) were seen in eight of the 13 nocturnal hypoglycaemia episodes (62%). These were sinus bradycardia (<40 beats/ min; three episodes), ventricular ectopics (three episodes), atrial ectopics (one) and P wave abnormalities (one). Conclusions/interpretation This study demonstrates QTc prolongation and cardiac rate/rhythm disturbances in response to episodes of nocturnal hypoglycaemia in ambulant patients with type 1 diabetes. This may support an arrhythmic basis for the 'dead in bed' syndrome.

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Section: Discussionmentioning

confidence: 99%

Cardiac arrhythmia and nocturnal hypoglycaemia in type 1 diabetes—the ‘dead in bed’ syndrome revisited

et al. 2008

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“…Arrhythmias were also observed in patients submitted to the Hollander test, a test used post- operatively after gastric vagotomy to measure the gastric acid response to hypoglycaemia in the 1960s [21]. In a more recent study, where hypoglycaemia was experimentally induced in patients with type 2 diabetes, two out of six patients developed arrhythmias [22]. Spontaneous hypoglycaemia has also been associated with arrhythmias in a number of case reports [23±27].…”

Section: Discussionmentioning

confidence: 99%

Increased QT dispersion during hypoglycaemia in patients with type 2 diabetes mellitus

Landstedt-Hallin

Englund

Adamson

et al. 1999

Journal of Internal Medicine

125

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Abstract. Landstedt-Hallin L, Englund A, Adamson U, Lins P-E (Karolinska Institute, Danderyd Hospital, Danderyd; and Uppsala University Hospital, Uppsala, Sweden). Increased QT dispersion during hypoglycaemia in patients with type 2 diabetes mellitus. J Intern Med 1999; 246: 299±307.Objectives. To study effects of insulin-induced hypoglycaemia on the cardiac repolarization, using QT interval measurements, in patients with type 2 diabetes. Design. Hypoglycaemia was induced by an i.v. insulin-infusion and blood glucose was clamped at 2.7 mmol L 21 for 60 min (T = 90±150 min) in two experiments, with (+GLIB) and without (±GLIB) glibenclamide. In a third experiment, with similar hyperinsulinaemia, glucose was clamped at a euglycaemic level (5 mmol L 21 ). ECG was continuously recorded for arrhythmia-monitoring, and 12-lead ECGs were recorded at T = 0 and 150 min. QT intervals were measured, and we determined QT dispersion (difference between the maximum and the minimum QT interval) reflecting interlead variability of repolarization.Subjects. Thirteen patients with type 2 diabetes, on combined insulin and glibenclamide treatment, were studied during hypoglycaemia, and eight of them participated in the euglycaemic experiment. Results. No significant arrhythmias were seen during hypoglycaemia but the mean QT intervals and QT dispersion increased significantly (P , 0.001), with no differences between ±GLIB and +GLIB. During the euglycaemic clamp all QT measurements remained unchanged. Serum potassium decreased significantly (P , 0.001) during all three clamps, but the decrease was more pronounced during hypoglycaemia. The change in potassium was not correlated to the degree of QT prolongation or QT dispersion. Conclusions. Significant changes in the repolarization of the heart can be seen during hypoglycaemia in patients with type 2 diabetes, indicating an increased risk of arrhythmia at low blood glucose levels.

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“…Type I diabetic patients present a lengthened Q-T interval [1,2,3]. Depression of the S-T segment has been observed in derivations V2 and V6 only in patients with Type II diabetes during hypoglycaemic episodes [22].…”

Section: Discussionmentioning

confidence: 99%

Effects of diabetic cardiomyopathy on regional electrophysiologic characteristics of rat ventricle

Casis

Gallego

Iriarte³

et al. 2000

Diabetologia

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The electrocardiogram of diabetic patients shows a series of deviations from normal patterns, most of which involve the QT interval and the T wave. The QT interval is longer in patients with diabetes mellitus than in normal people [1]. Diabetic patients show a corrected QT interval (QTc), measured using Bazett's formula, longer than 0.44 s [2,3]. Using Holter ECG monitoring, the appearance of ventricular late potentials is more frequent in patients with Type I (insulin-dependent) diabetes mellitus than in healthy people, and even more frequent in patients with Type II (non-insulin-dependent) diabetes mellitus [4,5]. Nearly all these changes are related to repolarisation. The QRS complex lasts longer in diabetic patients than in control subjects, suggesting intracardiac conduction disorders, but this type of change has only been described in children [6].Various studies report a lengthening of the duration of the rat ventricular action potential (APD) stemming from diabetic cardiomyopathy as a possible cause of these changes [7±9]. None took into account, however, the regional variability in the duration of the action potential under control conditions [10,11]. Various reports pointed to a lowering of the transient outward current, I to [9,12,13] and, to a lesser extent, the delayed rectifying outward current, I K [9,12], as the main cause of the lengthening of APD. Initial studies did not take into account regional variations in the distribution of the repolarising outward Diabetologia (2000) Abstract Aims/hypothesis. To identify the possible causes of the lengthening of the action potential duration described in patients affected by diabetes mellitus. Methods. We studied the effects of streptozotocininduced diabetes on the current density of the repolarising potassium currents I to , I K , I ss and I K1 in enzymatically isolated myocytes from three different regions of rat heart: total right ventricle, subepicardium at the apex of the left ventricle and subendocardium at the base of the left ventricle. Results. No changes in I K1 were found due to diabetes, but there was a uniform decrease in I to (50 %) and I ss (40 %) current densities in the three regions.In contrast, I K diminished unevenly, with the greatest decrease in the subendocardium at the base of the left ventricle (48 %), followed by the subepicardium at the apex of the left ventricle (32 %) and right ventricle (10 %). Conclusion/interpretation. These findings suggest the existence of regional differences in ion channel expression associated with diabetes. The decrease of these repolarising currents could account for the lengthening of action potential and the consequent change in the Q-T interval of the ECG observed in diabetic rats. [Diabetologia (2000)

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Hypoglycaemia and Cardiac Arrhythmias in Patients with Type 2 Diabetes Mellitus

Cited by 106 publications

References 28 publications

Cardiac arrhythmia and nocturnal hypoglycaemia in type 1 diabetes—the ‘dead in bed’ syndrome revisited

Cardiac arrhythmia and nocturnal hypoglycaemia in type 1 diabetes—the ‘dead in bed’ syndrome revisited

Increased QT dispersion during hypoglycaemia in patients with type 2 diabetes mellitus

Effects of diabetic cardiomyopathy on regional electrophysiologic characteristics of rat ventricle

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