The occurrence of ventricular premature depolarizations in survivors of myocardial infarction is a risk factor for subsequent sudden death, but whether antiarrhythmic therapy reduces the risk is not known. The Cardiac Arrhythmia Suppression Trial (CAST) is evaluating the effect of antiarrhythmic therapy (encainide, flecainide, or moricizine) in patients with asymptomatic or mildly symptomatic ventricular arrhythmia (six or more ventricular premature beats per hour) after myocardial infarction. As of March 30, 1989, 2309 patients had been recruited for the initial drug-titration phase of the study: 1727 (75 percent) had initial suppression of their arrhythmia (as assessed by Holter recording) through the use of one of the three study drugs and had been randomly assigned to receive active drug or placebo. During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5). They also accounted for the higher total mortality (56 of 730 [7.7 percent] and 22 of 725 [3.0 percent], respectively; relative risk, 2.5; 95 percent confidence interval, 1.6 to 4.5). Because of these results, the part of the trial involving encainide and flecainide has been discontinued. We conclude that neither encainide nor flecainide should be used in the treatment of patients with asymptomatic or minimally symptomatic ventricular arrhythmia after myocardial infarction, even though these drugs may be effective initially in suppressing ventricular arrhythmia. Whether these results apply to other patients who might be candidates for antiarrhythmic therapy is unknown.

SUMMARY To evaluate the mechanism of the abnormal motion of the interventricular septum (IVS) seen echocardiographically in some patients with relatively delayed ventricular activation, we simultaneously recorded high-fidelity left and right ventricular pressures and electrograms and echocardiograms of the IVS in nine open-chest dogs. During sinus rhythm and during left IVS pacing, the IVS was activated from left to right, preejection left ventricular pressure exceeded right ventricular pressure, and IVS motion was normal. During right ventricular pacing from the outflow tract, apex, free wall or right IVS, the IVS was activated from right to left, right ventricular pressure increased before left ventricular pressure and simultaneously there was an abrupt posterior IVS motion. Simultaneous pacing from the right IVS and left ventricular free wall activated the IVS from right to left and produced a normal transseptal preejection pressure gradient and normal IVS motion. Simultaneous pacing from the left IVS and right ventricular free wall activated the IVS from left to right, and produced abrupt preejection posterior IVS motion coincident with an altered transseptal pressure gradient. During right ventricular pacing, IVS motion after the abrupt preejection posterior movement was variable. Anterior motion was associated with a greater asynchrony of right and left ventricular contraction than was normal posterior motion.We conclude that abrupt preejection posterior IVS motion seen with delayed left ventricular activation from right ventricular pacing is due to passive IVS displacement from an altered transseptal pressure gradient, and subsequent IVS motion depends on the degree of asynchrony between right and left ventricular contraction.ABNORMAL interventricular septal motion is seen echocardiographically in some patients with relatively delayed left ventricular activation caused by left bundle branch block,'-" right ventricular pacing,9'"e' tion period and passively shifting the interventricular septum toward the left ventricle.36' , 8 This study was undertaken to investigate these potential mechanisms for abnormal interventricular septal motion in delayed left ventricular activation produced by pacing the right ventricle in dogs. MethodsNine dogs were anesthetized with pentobarbital, 30 mg/kg, and ventilated through a cuffed endotracheal tube. The heart was exposed by median sternotomy and the pericardium was incised. Pacing electrodes were sutured onto the epicardium over the right ventricular outflow tract, the right ventricular free wall, the right ventricular apex and the left ventricular lateral free wall. Equisensitive micromanometertipped catheters with fluid-filled lumens were placed in the right ventricle through the left internal jugular vein and left ventricle through the right carotid artery. The zero pressure level for the fluid-filled lumens was the midchest level. The micromanometer zeros were adjusted to superimpose the micromanometer and fluid-filled catheter pressure wave forms. The difference b...

SUMMARY We studied transient entrainment and interruption of atrioventricular (AV) bypass pathway-type paroxysmal atrial tachycardia in 15 patients during overdrive pacing from selected atrial sites. Overdrive atrial pacing at less than a critically rapid rate for interruption transiently entrained the tachycardia. Transient entrainment was due to repeated early entrance of the wave front from the pacing impulse into the reentry loop in both antidromic and orthodromic directions. The antidromic wave front of each pacing impulse was repeatedly blocked as it collided with the orthodromic wave front of the previous beat, in effect extinguishing the tachycardia. However, the early entrance of the orthodromic wave front of each pacing impulse repeatedly reset the tachycardia. The result was that during transient entrainment, the tachycardia rate increased to the pacing rate. Interruption of the tachycardia occurred when overdrive pacing produced block within the reentry loop of both the antidromic and orthodromic wave fronts of the same pacing impulse, the block occurring either at separate sites within the reentry loop or at the same site. Atrial fusion beats were demonstrated during transient entrainment in nine patients and resulted from intraatrial collision of the antidromic wave front from the pacing impulse with the orthodromic wave front of the previous beat. The presence offusion beats depended critically on the relationship of the pacing site to the reentry loop and the duration of conduction around the reentry loop, particularly through the area of slow conduction.The data from this study suggest that (1) if one can demonstrate constant fusion beats during transient entrainment of a tachyarrhythmia except for the last transiently entrained beat; or (2) if during transient entrainment of a tachyarrhythmia at two or more different pacing rates, one can demonstrate constant fusion at each of the different pacing rates, but different degrees of fusion at the different rates; or (3) if interruption of a tachyarrhythmia by overdrive pacing is associated with localized conduction block to a site followed by activation of that site by the next pacing impulse from a different direction and with a shorter conduction time, then the underlying mechanism of the arrhythmia can be best explained by reentry.PAROXYSMAL atrial tachycardia that involves antegrade conduction from the atria through the atrioventricular (AV) node-His-Purkinje system to the ventricles with retrograde conduction from the ventricles via an AV bypass pathway back to the atria is the best understood example of putative reentrant rhythms.1AThis arrhythmia is often found in patients with the Wolff-Parkinson-White syndrome and in patients with a so-called concealed AV bypass pathway, i.e., one that conducts only in the retrograde direction. The many types of treatment for this arrhythmia include its interruption by overdrive cardiac pacing.' We have found that overdrive pacing used to interrupt paroxysmal atrial tachycardia of this variety has much in ...

No abstract

Recent years have seen significant improvements in catheter technology and electroanatomic mapping (EAM) systems. Contact force (CF)-sensing catheters have improved procedural efficiency and efficacy [5] . Meanwhile, improvements to EAM systems now allow objective measurement of catheter stability and CF during radiofrequency (RF) energy delivery. As a consequence of these latest technological advances, operators are challenged with a paucity of data on how to better incorporate them into an effective, efficient, and safe workflow.The objective of this study was to describe a single center experience with a workflow developed to integrate and optimize the use of new CF catheter technology and compare it with prior technologies. Our goal was to provide a strategy to help minimize the learning curve required for full incorporation of the new technologies, such that procedural efficiency and effectiveness are optimized, and safety is uncompromised. MethodsThis study represents the experience of a real world paroxysmal atrial fibrillation (PAF) population presenting for an index catheter ablation at a single high volume EP practice between July 2013 and June 2016. All patients were treated according to standard clinical practice, and were ablated by an operator experienced in both RF and cryoballoon ablation (>100 cases with each technology). Baseline patient characteristics, procedural details, and acute outcomes were collected for all ablations during the study period. Effectiveness outcomes at 12 months were collected systematically beginning in July 2014.

No abstract

No abstract

No abstract