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The interlead variability of QT interval in the 12-lead electrocardiogram, QT dispersion (QTd), has been shown to reflect dispersion of ventricular refractoriness and may provide a measure of arrhythmogenic potential in diabetic patients. QTd and heart rate corrected QTd (QTcd) were also proposed to be accurate predictors of cardiac death in patients with diabetes. In recent years, experimental and clinical evidence demonstrates that statins exert antiarrhythmic properties. Therefore, in the present study, we have examined whether simvastatin treatment has any effect on the QTd and QTcd in patients with diabetes mellitus. Sixty type 2 diabetic patients without known coronary artery disease and low-density lipoprotein cholesterol >100mg/dl and 30 age and sex-matched non-diabetic controls were included in a prospective study. Out of 60 diabetic patients, 30 were treated with simvastatin 40 mg/day for 1 year and the remaining 30 subjects were served as diabetic controls. No lipid lowering therapy was administered to the diabetic and the non-diabetic controls. QTd and QTcd of treated diabetics and the non-diabetic controls were measured at baseline, 6, 12 weeks and at 1 year. QTd and QTcd of the diabetic controls were obtained at baseline, 6 and 12 weeks. Both QTd and QTcd were significantly greater in patients with the diabetes than in the non-diabetic controls at baseline (52+/-13 ms vs. 41+/-12 ms, p<0.001 and 62+/-17 ms vs. 42+/-11 ms, p<0.001, respectively). Simvastatin therapy significantly decreased both QTd and QTcd at the end of first year compared to baseline (51+/-15 ms vs. 33+/-11 ms, p<0.001 and 60+/-18 ms vs. 38+/-12 ms, p<0.001, respectively). No significant change were found in QTd and QTcd in the non-diabetic (p=0.29 and p=0.87 by ANOVA, respectively) and in the diabetic controls (p=0.72 and p=0.57, by ANOVA, respectively). This study suggests for the first time that simvastatin treatment in diabetic patients with hyperlipidemia is associated with an improvement in the heterogeneity of cardiac repolarization. This may be one of the mechanisms for the reduction in clinical events reported in the survival studies with statins. Further prospective randomized studies are warranted to confirm our findings.

Background: Slow coronary flow (SCF) in a normal coronary angiogram is a well-recognized clinical entity, but its etiopathogenesis remains unclear. However, previous studies have suggested that microvascular abnormalities and endothelial dysfunction responsible for SCF. Accordingly, we hypothesized that SCF phenomenon may be a form, at least early phase, of atherosclerosis that involve both small vessels and epicardial coronary arteries, and therefore we investigated coronary flow reserve (CFR) reflecting coronary microvascular function in patients with SCF., Methods: Twenty subjects with SCF and 15 control subjects with normal coronary flow were studied. Coronary flow was quantified according to TIMI frame count (TFC). Coronary diastolic peak flow velocities were measured at baseline and after dipyridamole infusion. CFR was calculated as the ratio of hyperemic to baseline diastolic peak velocities., Results: Demographic features, coronary risk factors, echocardiographic measurements except diastolic function parameters, and biochemical measurements were similar between the groups. CFR values were significantly lower in subjects with SCF than in the control group (1.99+/-0.38 versus 2.99+/-0.47, P<0.0001). In addition, TIMI frame count independently correlated with CFR., Conclusion: These findings suggest that CFR, which reflects coronary microvascular function, is impaired in patients with SCF, and corrected TFC well correlates with CFR.

Heart rate recovery at 1min (HRR1) is a strong predictor of all-cause mortality. The effects of statins on the autonomic nervous system may account for their beneficial effects in survival. Our aim was to determine if statin therapy improves heart rate recovery in hypercholesterolemic patients with type 2 diabetes mellitus. Thirty type 2 diabetic patients without known coronary artery disease and low density lipoprotein cholesterol>100mg/dl and 30 age and sex matched non-diabetic controls were included in a prospective study. Patients with diabetes were treated with simvastatin 40mg/day for 1 year. No lipid-lowering therapy was administered to the control group. Exercise testing with 2min cool-down period was performed at baseline, 6, 12 weeks and at 1 year. The diabetics had significantly lower HRR1 compared with non-diabetics at baseline (19.2+/-5.4bpm versus 24.2+/-4bpm, p<0.0001). Simvastatin therapy significantly improved HRR1 after 12 weeks compared to baseline (19.2+/-5.4bpm versus 24+/-5bpm, p<0.0001) and this improvement remained significant at 1 year (26+/-4.4bpm, p<0.0001 compared to baseline). HRR1 did not change in the control group (p=0.39 by ANOVA). This study demonstrates that treatment with simvastatin might improve the attenuated heart rate recovery of diabetic subjects. In patients with diabetes, the mortality benefit provided by statins might involve their effects on the autonomic nervous system.

Background: Isolated myocardial bridging (MB) often is considered to be an unimportant angiographic finding; however, its association with cardiovascular event has been shown. In this study we aimed to assess exercise-induced electrocardiographic (ECG) changes and susceptibility to arrhythmia in patients with MB., Method: 21 consecutive patients who had angiographically proven MB (group I) and 25 subjects (group II) who had normal coronary arteries underwent exercise test using Bruce protocol. Before and after the exercise test the changes in QT interval duration and dispersion were compared., Results: Baseline characteristics of both groups were similar. Heart rate significantly increased after exercise test in both groups. In group I, after exercise mean QT(max) and QT(min) durations did not change significantly compared to baseline values, respectively. (QT(max): 411+/-20 vs. 421+/-18 ms, p>0.05 and QT(min): 380+/-12 vs. 378+/-10 ms, p>0.05). However, following exercise test QT dispersion (QT(d)) and corrected QT dispersion (QT(cd)) significantly increased when compared to baseline values, respectively. (34+/-13 vs. 66+/-14 ms, p<0.05 and 37+/-14 vs. 69+/-17 ms, p<0.05) On the other hand, in control group QT(max) and QT(min) durations, QT(c) and QT(cd) did not change significantly compared to baseline values, respectively. (QT(max): 408+/-18 vs. 412+/-17 ms, p>0.05 and QT(min): 390+/-11 vs. 387+/-10 ms, p>0.05; QT(d): 25+/-14 vs. 31+/-16 ms, p>0.05; QT(cd): 27+/-15 vs. 33+/-17 ms, p>0.05)., Conclusion: Treadmill exercise test significantly increased QT dispersion in patients with MB. This increase may result from exercise-induced ischemia at the area perfused by bridged artery.