Rate-corrected QT-interval (QTc) and QT-dispersion (QTdisp) are two related electrocardiographic variables that, apart from assessing the autonomic dysfunction, can also predict cardiac death in diabetic patients. Several studies have suggested that change of QTdisp reflects the “dynamic pathological process” in a variety of cardiac diseases. Particularly, QTdisp was found to increase significantly during ischemia and to decrease after anti-ischemic treatment during acute coronary syndromes (ACS) (1).
The beneficial effect of optimal metabolic control achieved by intensive insulin therapy on the outcome of diabetic patients suffering from acute myocardial infarction has already been reported (2). Nevertheless, hyperinsulinemia has also been reported to increase QTc and QTdisp in healthy subjects (3). The potential effect of intensive insulin administration during ACS on the electrocardiographic ventricular repolarization variables remains to be elucidated.
We studied 66 non-insulin-treated type 2 diabetic patients with ACS without ST-segment elevation and no previous myocardial infarction. A total of 31 patients were randomized to receive conventional anti-ischemic therapy plus intensive insulin treatment (group A), and 35 received conventional therapy only (group B). Group A patients received soluble insulin by infusion for 72 h according to a predefined protocol aiming to maintain near-normal glycemia (4). Group B patients were treated according to coronary care unit usual care, with oral hypoglycemic drugs or two daily doses of intermediate-acting insulin.
QT-interval variables were determined on two occasions: admission and 72 h later. A single investigator with no knowledge of the clinical data interpreted QT-intervals manually. QT-values were corrected for heart rate using Bazett’s formula (QTc = QT/RR−1). QTdisp was calculated as the difference between the longest and shortest measured QT-interval. Informed consent was obtained from all patients.
The two groups were comparable according to baseline clinical and investigative characteristics. In group A, glucose values were maintained within near normoglycemic range during the study period (group A versus B: 7.1 ± 1.6 vs. 10.9 ± 2.7 mmol/l−1, P < 0.001). At 72 h, QTdisp decreased significantly only in group A patients (QTdisp 72 h: 46 ± 24 vs. 58 ± 19 m/s, P < 0.05), supporting the hypothesis that a more homogeneous electrical recovery state of myocardium was achieved by optimal glycemic control. Conversely, QTc showed a trend to increased values in intensively treated patients (QTc 72 h: 429 ± 37 vs. 409 ± 45 m/s, P = 0.072). This observation was rather disappointing, since QTc prolongation is another key factor that predisposes to cardiac arrhythmias, especially in ischemic conditions. Importantly, the change in potassium was not correlated to the degree of QT prolongation.
Our findings stress that the impact of intensive insulin treatment on repolarization of the diabetic heart during ACS is rather controversial. One may remember the phrase of Hippocrates in one of his writings 25 centuries ago, “As to diseases, make a habit of two things—to help, or at least to do no harm” (5).
Address correspondence to Alexander Stefanidis, Cardiology Department, Tzanio Hospital, 1 Afentouli and Zanni str, PC: 185-36, Piraeus, Greece. E-mail: firstname.lastname@example.org.