Changes in the QT and QTc intervals in 19 patients were studied at a ventricular paced rate difference of 50 beats/min. In all patients the measured QT interval shortened as the pacing rate was increased, from a mean value of 441 ms to 380 ms (p less than 0.001), but when corrected for heart rate the QTc lengthened from a mean value of 518 ms to 575 ms. In 11 patients the QT interval was measured at rest and immediately following exercise sufficient to increase the atrial rate by approximately 50 beats/min at identical ventricular paced rates. In all patients exercise-induced QT interval shortening from a mean value of 433 ms to 399 ms (p less than 0.001). These results show first that Bazett's formula is unsuitable for correction of QT interval induced by ventricular pacing, and second that heart rate and changes in sympathetic tone independently influence the duration of the QT interval. It is suggested that these results are relevant to the design of physiological pacemakers in which the duration of the QT interval influences the discharge frequency of the pacemaker and to the consideration of ventricular pacing for the treatment of abnormal repolarization syndromes.

To determine the effect of flecainide acetate, a Class IC antiarrhythmic drug, The medication was given to 28 patients with ventricular pacing electrodes. Eleven patients with temporary pacing electrodes (Group I) received intravenous flecainide (2 mg/kg over 10 minutes). Ten patients with chronic permanent electrodes (Group II) were given the same dose at the time of elective pulse generator change. Seven, with implanted multiprogrammable pacemakers capable of threshold analysis (Group III), were given intravenous flecainide and 5 of these were then given the drug orally for up to 3 weeks (100 mg/day increasing to 400 mg/day). In Group I the threshold measured at a pulse width of 0.5 ms rose from a control value of 0.66 to 1.44 volts after 10 minutes (p less than 0.01). In Group II the threshold rose from 1.73 to 2.13 volts (p less than 0.01) and 2 patients had total suppression of their ventricular escape rhythm for approximately one hour. In Group III patients, intravenous flecainide resulted in a rise escape rhythm for approximately one hour. In Group III patients, intravenous flecainide resulted in a rise of the pulse width threshold measured at 2.7 volts from 0.14 to 0.22 ms (p less than 0.02) and at 4.9 volts from 0.06 to 0.11 ms (p less than 0.05) after 10 minutes. After 3 weeks of oral therapy the threshold at 2.7 volts had risen to 0.11 ms /ms (p less than 0.05 after 10 minutes. After 3 weeks of oral therapy the threshold at 2.7 volts had risen from 0.09 to 0.28 ms (p less than 0.02) and at 4.9 volts from 0.06 to 0.16 ms (p less than 0.05) Flecainide significantly increased both acute and chronic thresholds and the most marked rise (greater than 200%) occurred during chronic oral therapy. Both intravenous and oral flecainide should be used with care in patients with either temporary or permanent pacing systems.

SUMMARY Changes in the QT and QTc intervals were studied in 16 patients by atrial pacing at rates of 100, 130, and 150 beats/minute. In all patients the measured QT shortened when the atrial paced rate was increased, but when corrected for heart rate the QTc lengthened. Intravenously administered propranolol produced a bradycardia and a lengthening ofthe QT interval in 15 ofthe 16 patients studied. When the QT interval was corrected for heart rate using Bazett's formula the QTc was shortened in 13 patients, unchanged in one, and lengthened in two. However, when the QT interval was measured atidentical atrial paced rates the QT of the 15 patients studied was lengthened in 10 and unchanged in five. In none was the QT interval shortened. These results show firstly that Bazett's formula is unsuitable for correction of QT interval changes induced by atrial pacing, and secondly that, though intravenously administered propranolol usually produces a shortening of the QTc, when its effect is assessed directly by using an identical atrial paced rate the QT interval usually lengthens, or may remain unchanged, but never shortens. It is suggested that the formal assessment of drug induced QT interval changes should be made at identical atrial paced rates.Prolongation of the QT interval may occur after the administration of drugs such as quinidine,' amiodarone,2 disopyramide,3 the tricyclics,4 and the phenothiazines.5 The effect of propranolol on the QT interval remains controversial. Previous studies suggest that though it lengthens the measured QT, correction for heart rate by Bazett's hyperbolic correction factor" shows that the QTc is usually shortened.7 8 As such drugs may also cause changes in the heart rate, when assessing their effect on the QT interval the use of a correction factor for heart rate becomes necessary. Of the many formulae available Bazett's hyperbolic correction factor which corrects to a rate of 60 beats/min has been most readily accepted for use because it is simple to apply. In order to overcome the necessity for rate correction a new method has been devised for the assessment of drug induced QT changes using atrial pacing at identical rates before and after the administration of propranolol. This allows a direct comparison of these changes to be made and precludes the need for a correction factor. The purpose of this study was twofold. Firstly, to test the validity of Bazett's hyperbolic correction factor for QT changes induced by atrial pacing, and, secondly, to assess the

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Summary:Twenty-eight patients with wide spectrum organ involvement of progressive systemic sclerosis but without signs or symptoms suggestive of cardiac involvement were studied by non-invasive cardiac techniques. The 12-lead electrocardiogram showed abnormalities in 6 patients: one had abnormal T waves and 5 had complete or incomplete right bundle branch block. Twenty four hour ambulatory electrocardiography demonstrated higher average heart rates than in similar aged controls (82 ± 9 vs 74 ± 9 beats/min, P <0.05). In one patient a short run ofventricular tachycardia was recorded. No other significant arrhythmia was documented. Echocardiographic measurements were within normal ranges but small pericardial effusions were observed in two patients (7%). Resting first pass radionuclide angiography, utilizing 12 mCi oftechnetium 99m were performed in 23 patients. Seven patients (30%) had abnonnal wall motion (diffuse hypokinesia), with a significant decrease in ejection fraction in comparison to those with normal wall motion (44 ± 6% vs 60 ± 6% P < 0.01). Those with abnormal wall motion had suffered the disease longer than those with normal wall motion (13 ± 4 vs 9.5 ± 7 y). In conclusion, the heart is involved in half of the patients in this series; non-invasive cardiac assessment is useful in disclosing the early cardiac involvement and may influence long-term management.