RECURRENT VT: MECHANISMS/Josephson et al.of coronary artery bypass grafting on resting and exercise hemodynamics in patients with stable angina pectoris: A prospective randomized study. Am J Cardiol 37: 823, 1976 The present study was undertaken to investigate the mechanism of chronic sustained ventricular tachycardia and the role of the bundle branches and ventricular myocardium in its initiation and maintenance.

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Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

Recurrent, medically refractory ventricular tachycardia is usually associated with ventricular aneurysms after myocardial infarction, but aneurysmectomy alone has not been consistently effective in abolishing this dangerous arrhythmia. Therefore, we have used endocardial and epicardial mapping during induced ventricular tachycardia in 30 consecutive patients to identify the probable site where arrhythmia originated in the endocardial tissue. Complete resection of the site was possible in 27 patients, and partial resection in three. In addition aneurysmectomy was performed in 27 patients, and coronary-bypass grafting in 21. There were two operative and three late nonarrhythmic deaths. None of the 25 surviving patients have had ventricular tachycardia during follow-up of four to 28 months; three patients, who had incomplete resections, have required antiarrhythmic drugs. We conclude that surgical therapy of recurrent ventricular tachycardia can be improved through identification of the endocardial origin of the arrhythmia followed by appropriately guided resection.

The phrase paroxysmal supraventricular tachycardia describes a group of arrhythmias with similar electrocardiographic features but different mechanisms that have been clarified in recent years with specialized intracardiac recording and pacing techniques. Reentry accounts for most cases and has been localized to the A-V node and less frequently to the sinus node, the atria themselves, and A-V nodal bypass tracts (Wolff-Parkinson-White syndrome). These forms of supraventricular tachycardia are initiated by premature beats that dissociate conduction between two pathways and permit the establishment of circulating electrical activity that spreads to atrial and ventricular myocardium. Paroxysms cease when the conducting properties of the reentrant circuits are disturbed by changes in autonomic tone or the application of certain drugs, pacing, or cardioversion. Supraventricular tachycardia may also result from abnormal automaticity in atrial tissues. Such automatic atrial tachycardias are often associated with A-V block ("paroxysmal atrial tachycardia with block") and may be due to digitalis intoxication. This arrhythmia is treated by withdrawal of digitalis or administration of antiarrhythmic drugs that decrease automaticity.

SUMMARYElectrophysiologic characteristics of five patients with Ebstein's anomaly of the tricuspid valve were defined with studies using luminal intracardiac electrode catheters. The diagnosis was made in each case from clinical data and confirmed at.cardiac catheterization by the presence of an atrialized right ventricular chamber with atrial mechanical activity and ventricular electrical activity. In three cases intra-right atrial conduction was prolonged (P-A intervals of 50, 50,

The effective refractory period of the right ventricle (ERP-V) was measured in 27 patients during atrial or ventricular pacing using the ventricular extra stimulus method. Pacing was conducted with impulses of 1.5-2 times diastolic threshold. The ERP-V was directly related to the basic cycle length (BCL) although the ERP-V was always greater for atrial pacing than for ventricular pacing at a given BCL. The ratio ERP-V/BCL was greater at shorter cycle lengths indicating that a larger fraction of the cycle was refractory at faster heart rates. The ratio ERP-V/QT interval did not change over a range of BCLs, but the ratio was larger for atrial pacing (.77 +/- .05 SD) than for ventricular pacing (.60 +/- .05). Atropine (1 mg i.v.) was given to six patients. The drug did not affect the ERP-V in six of eleven determinations, prolonged ERP-V twice and shortened it slightly three times. Measurements were reproducible over an hour but varied at a given BCL when measured on separate days. Asymptomatic repetitive beating occurred in seven of 27 patients when the premature stimulus was within 20 msec of the ERP-V. The effective refractory period of the right ventricle in man can be determined reproducibly and with safety. Changes induced by various perturbations parallel results from in vitro single cell and myocardial studies.