1. Prolongation of the QT interval is associated with a risk of life-threatening cardiac arrhythmias. In the present study, we examined whether reversible blockade of preganglionic sympathetic fibres of the heart, achieved by thoracic epidural anaesthesia, affects cardiac repolarization and thus confers an anti-arrhythmic effect. 2. Fifty-two men, aged between 28 and 65 years, were included in the study: 28 were patients scheduled for thoracic epidural anaesthesia (Group T) and 24 were patients scheduled for lumbar epidural anaesthesia (Group L). Epidural blockade was achieved with 0.5% isobaric bupivacaine solution. Measurements were taken from electrocardiogram fragments obtained before epidural anaesthesia and after detection of blockade (T1 or T8 segment sensory block in Groups T and L, respectively). Correction of the QT interval was calculated using Bazett's formula (QTcb), Fridericia's correction (QTcf) and the Framingham formula (QTcF). Transmural dispersion of repolarization (TDR) was determined using the Tpeak--Tend time, where Tpeak is the peak of the T wave and Tend is the end of the T wave. 3. Significant shortening of the QTcb interval and TDR was detected after blockade in Group T. However, there were no changes in the ECG parameters in Group L. 4. In conclusion, reversible blockade of preganglionic sympathetic fibres to the heart, achieved by thoracic epidural anaesthesia, results in a reduction in QTcb, as well as the TDR. These changes may explain the anti-arrhythmic action seen with central blockade.

W e present a case of a 23-year-old woman with no major cardiovascular risk factors, who presented with recurrent complete loss of consciousness during her drivinglicense examination. The patient was transferred to the emergency room, where she had the next episode of syncope with ventricular fibrillation (VF). Her ECG before VF revealed ST-segment elevation in leads II, III, aVF, and V3-V6 (Figure 1), although the patient did not mention any chest pain. On admission, her echocardiogram showed no abnormalities, her left ventricular ejection fraction (LVEF) was 70%, and myocardial necrosis markers were negative. Several days later, the patient was referred for coronary angiography, which was free of coronary artery stenosis; however, the second contrast pass and catheter positioning revealed long-lasting diffused spasm of left main, proximal part of left descending and circumflex arteries, which persisted despite intracoronary infusion of nitroglycerin. An ECG taken at this time demonstrated ST-segment elevation in the V2-V6 leads, which was followed by the occurrence of VF an hour later and recovered in 2 hours. Serially obtained blood samples showed a significant increase in cardiac troponin I (maximum, 101.6 ng/mL). On the next day, ECG showed hypokinesis of apical segments of anterior and interventricular wall, and LVEF was 40%. Those abnormalities resolved 2 weeks later, and a subsequent echocardiogram demonstrated LVEF of 60% and no wall motion abnormalities. Thereafter, an implantable cardioverter-defibrillator (Lexos DR, Biotronik) was implanted, and combination therapy with metoprolol (50 mg/d) and verapamil (60 mg/d) was initiated. At discharge, her ECG showed QT prolongation up to 480 ms (QTc, 570 ms), with negative T waves in the I, aVL, and V3-V5 leads. An ECG taken at 10-month follow-up showed positive T wave with a QT of 440 ms (QTc, 550 ms; Figure 2). At any time, the patient did not receive any drugs prolonging the QT interval.The patient's family history was positive for sudden cardiac death and sudden infant death syndrome. We performed genetic testing, and we found the R591H mutation in the KCNQ1 gene in the patient, her mother, and siblings. The clinical evaluation, particularly QTc prolongation during exercise tests, confirmed clinical diagnosis of long QT syndrome (LQTS) in all genetically affected family members. DiscussionTo our knowledge, this is the first report on spontaneous ST-segment elevation preceding an episode of VF in LQTS. Generally, cardiac events in LQTS occur either during exercise and emotional stress (LQT1 and LQT2 types) or at rest (LQT3), 1 whereas ST-segment elevation may precede episodes of VF in patients with vasospastic angina or stressinduced cardiomyopathy (so-called Takotsubo syndrome [TTS]). Some clinical features of our patient may resemble TTS. First, the syncopal event was triggered by emotional stress. Second, ECG at admission showed ST elevation and negative T waves with QT prolongation, and coronary angiography showed no organic stenosis. Finally, wall mot...

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