T wave concordance in the normal human electrocardiogram (ECG) generally is explained by assuming opposite directions of ventricular depolarization and repolarization; however, direct experimental evidence for this hypothesis is lacking. We used a contact electrode catheter to record monophasic action potentials (MAPs) from 54 left ventricular endocardial sites during cardiac catheterization (seven patients) and a new contact electrode probe to record MAPs from 23 epicardial sites during cardiac surgery (three patients). All patients had normal left ventricular funtion and ECGs with concordant T waves. MAP recordings during constant sinus rhythm or right atrial pacing were analyzed for (1) activation time (AT) = earliest QRS deflection to MAP upstroke, (2) action potential duration (APD) = MAP upstroke to 90% repolarization, and (3) repolarization time (RT) = AT plus APD. AT and APD varied by 32 and 64 msec, respectively, over the left ventricular endocardium and by 55 and 73 msec, respectively, over the left ventricular epicardium. On a regional basis, the diaphragmatic and apicoseptal endocardium had the shortest AT and the longest APD, and the anteroapical and posterolateral endocardium had the longest AT and the shortest APD (p < .05 to < .0001). RT was less heterogeneous than APD, and no significant transventricular gradients of RT were found. In percent of the simultaneously recorded QT interval,-epicardial RT ranged from 70.8 to 87.4 (mean 80.7 + 3.9) and endocardial RT ranged from 80 to 97.8 (mean 87.1 4.4) (p < .001). Plotting of APD as a function of AT, independent of the recording site, revealed a close inverse relationship, such that progressively later activation was associated with progressively earlier repolarization The linear regression slope of this relationship averaged from all 10 hearts was -1.32 + 0.45 (r = -.78 + . 10). These data suggest a transmural gradient of repolarization,with earlier repolarization occurring at the epicardium. The negative correlation between AT and APD, which was found at both the endocardial and epicardial surface and had an average slope of greater than unity, may further contribute to a positive ventricular gradient and T wave concordance.

Patients with typical angina or anginalike chest pain and normal coronary angiograms have a good long-term prognosis despite persistence of pain for many years; coronary morbidity and mortality are similar to those of the overall population. An increased risk for the development of coronary events is present mainly in patients with elevated risk factors.

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The effect of intravenous tedisamil (0.3 mg.kg-1), a newly developed potassium-blocking agent, on ventricular repolarization was studied in 10 patients (three women, seven men; mean age 53 +/- 8 years) with coronary artery disease (stenoses < or = 60%). Left ventricular monophasic action potentials, effective refractory periods and surface electrocardiograms were recorded during sinus rhythm and during constant atrial pacing at cycle lengths of 600, 500 and 400 ms. Under tedisamil there was a 12% reduction of heart rate and in parallel a prolongation of QTc interval (+10%) and left ventricular monophasic action potential duration (+16% at 90% repolarization). QRS duration remained unchanged. Tedisamil increased the duration of monophasic action potentials during constant atrial pacing, indicating a direct prolongation effect on left ventricular repolarization independent of sinus node activity. By increasing the atrial pacing rate this prolonging effect diminished. Left ventricular effective refractory periods also increased in a frequency-dependent fashion with a greater prolongation effect at long cycle lengths as compared to short cycle lengths. The ratio between effective refractory period and monophasic action potential duration, however, remained constant, independent of heart rate. We conclude that tedisamil is bradycardiac at the dose tested and has a reverse use dependent prolongation effect on left ventricular repolarization and refractoriness. The electrophysiologic profile is consistent with a class III antiarrhythmic classification.

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