Bursts Of Rapid Ventricular Pacing Research Articles

Rapid pacing using the 0.035-in. Retrograde left ventricular support wire in 208 cases of transcatheter aortic valve implantation and balloon aortic valvuloplasty.

Transcatheter aortic valve implantation (TAVI) and balloon aortic valvuloplasty (BAV) are now well established percutaneous procedures. These procedures almost always require bursts of rapid ventricular pacing to temporarily reduce cardiac output to facilitate the procedure, usually done via a temporary pacing wire inserted into the right ventricle. We describe a case series of 132 cases of TAVI and 76 BAV done using ventricular pacing via the left ventricular lead by simply connecting one electrode to the patient's skin and one electrode through the left ventricular (LV) wire. All of the 132 TAVI cases (a mixture of Edwards Sapien, Medtronic CoreValve and Boston Scientific Lotus) and 76 BAV were successfully performed using pacing through the LV wire. No BAV patients required temporary pacing wire (TPW) or permanent pacemaker (PPM) insertion. Of the TAVI patients, 6 (4.5%) required TPW during the procedure due to complete heart block to facilitate removal of the LV wire. 1 patient (0.8%) required a PPM urgently due to complete heart block and haemodynamic instability. Twenty eight Patients (21.2%) required PPM following TAVI, 9 of which were within the first 24 hr. Average time to pacemaker implantation was 3.7 days. Rapid ventricular pacing via the LV wire is a simple, safe and effective strategy for percutaneous aortic valve intervention and balloon aortic valvuloplasty. It eliminates the need for a temporary pacing wire with its attendant risks in the vast majority of cases. Furthermore, most pacemakers following TAVI are required late, after the first 24 hr period, by which time the TPW has already usually been removed. © 2016 Wiley Periodicals, Inc.

Sequential transvenous pacing and shock therapy for termination of sustained ventricular tachycardia

Rapid ventricular pacing and transvenous shocks are both effective in terminating sustained ventricular tachycardia (VT) only in selected patients. We prospectively examined efficacy and safety of an algorithm for VT termination combining rapid ventricular pacing with low and moderate energy transvenous shocks in patients with sustained VT. Sixty-three VT episodes in 23 patients, mean age 64 ± 12 years, were treated with the algorithm. Bursts of rapid ventricular pacing and transvenous shocks were delivered with a Medtronic 6880 catheter positioned in the right ventricular apex. VT episodes with cycle lengths >270 msec (group A) were treated with sequential therapy with rapid ventricular pacing (90%, 80%, and 70% of VT cycle length), low energy transvenous shocks (0.5 to 2.7 J), and moderate energy (2.7 to 10 J) transvenous shocks. Rapid VT episodes with cycle lengths <270 msec (group B) were treated with moderate energy transvenous shocks directly. Forty-one of 48 (85%) VT episodes in group A and 6 of 15 (40%) VT episodes in group B were successfully terminated by this algorithm. There was no difference in clinical or arrhythmia characteristics between responders and nonresponders in either group A or group B to the algorithm. VT acceleration was observed in 12% of episodes in group A and in 47% of episodes in group B. We conclude that an algorithm combining rapid ventricular pacing with low and moderate energy transvenous shocks is effective for VT termination in episodes with a cycle length >270 msec and can reduce the need for transthoracic cardioversion. Moderate energy transvenous shocks are inadequate to rellably convert rapid VT and frequently result in VT acceleration with the lead employed in this study Alternative electrode configurations need to be evaluated.

Mechanisms responsible for countershock-induced ventricular tachycardia in the intact canine heart

To determine the mechanism for postcountershock ventricular ectopy, internal and external shocks were delivered to 20 anesthetized dogs. Shock energies of 25 and 50 joules were employed internally while 100 and 200 joules were delivered externally. Experiments were performed in both the presence and absence of a nearly toxic dose of ouabain. All shocks resulted in the occurrence of nonsustained (<15 seconds) ventricular tachycardia. When bursts of rapid ventricular pacing were synchronized with a shock, the pacing stimuli invariably captured the ventricles and overdrove the shock-induced ventricular tachycardia. However, the burst pacing never appeared to break a tachycardia, since the termination of pacing was followed immediately by the resumption of the shock-induced ventricular tachycardia. The presence of ouabain did not alter the response of the ventricles to postshock burst pacing. Administration of verapamil (0.5 mg/kg) had no effect on the duration of shock-induced ventricular arrhythmia. Elevation of the serum potassium level to 8.5 ± 0.6 mEq/L drastically reduced the duration of postshock ventricular tachycardia in both the presence and absence of ouabain. The results suggest that postshock ventricular octopy results from an abnormality of impulse initiation rather than reentry.

Noninvasive cardiac pacing for termination of sustained, uniform ventricular tachycardia

Bursts of ventricular pacing are effective for terminating hemodynamically tolerated ventricular tachycardia (VT). 1 Endocardial stimulation using temporary transvenous pacemakers has been the preferred method for effecting VT termination. Zoll et al 2,3 developed a noninvasive, external cardiac pacemaker that has been effectively used for management of patients with bradyarrhythmic events. In this report we describe successful use of the noninvasive cardiac pacemaker to terminate VT using bursts of rapid ventricular pacing.

Value of serial electropharmacological testing in managing patients resuscitated from cardiac arrest.

Electrophysiologic studies were performed in 11 patients (9 men, 2 women; mean age: 59.9 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose of the studies was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. Ten of the patients were suffering from chronic ischemic heart disease with one or more previous myocardial infarctions while one had no evidence of structural heart disease. A ventricular aneurysm was present in four of them. During control electrophysiologic study, a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths plus bursts of rapid ventricular pacing) in nine of the ten patients (90%) who were studied while not receiving antiarrhythmic drugs; a non-sustained VT was induced in one of them (10%). In three patients (30%) VT could be initiated only by right ventricular stimulation at a side different from the apex (outflow tract). No arrhythmia was observed in the only patient who was studied while taking amiodarone orally (400 mg/day for more than three months). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in seven of the ten patients (70%) who underwent this procedure and a partially effective drug regimen (a sustained VT was no longer inducible; it was easier to interrupt and it was considerably slower) was found in two patients (20%). None of the nine patients who received chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14 months (range: 3-28) and only one had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of follow-up. These results indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest.

Sensitivity of various extrastimulus techniques in patients with serious ventricular arrhythmias

One hundred seventeen consecutive patients with a history of sudden cardiac death (group I = 62 patients) or recurrent symptomatic ventricular tachycardia (group II = 55 patients) as well as 11 control subjects (group III) were studied with programmed electrical stimulation over the past year. Programmed right ventricular stimulation included premature stimulation during atrial pacing (A 1V 2 mode) and during ventricular pacing (V 1V 2 mode), double ventricular extrastimuli during ventricular pacing (V 1V 2V 3), and brief bursts of rapid ventricular pacing (V burst). Repetitive ventricular responses were defined as two or more ventricular premature beats produced by the final ventricular pacing stimulus occurring by intraventricular reentry. All but 13 patients were on antiarrhythmic therapy at the time of study. The incidence of repetitive ventricular responses induced by A 1V 2 pacing mode was 22% (22 of 104 patients) and that of sustained ventricular tachycardia was 1%. The sensitivity of inducing repetitive ventricular responses with V 1V 2 stimulation was 44% and that of sustained ventricular tachycardia was 7%; the sensitivity with V 1V 2V 3 pacing mode was significantly higher at 77% and 25%, respectively. When V 1V 2V 3 and V burst stimulation were directly compared, the incidence of induction of repetitive ventricular responses and sustained ventricular tachycardia were comparable. The incidence of induction of repetitive ventricular responses and sustained ventricular tachycardia in groups I and II was similar; no repetitive ventricular responses were induced in group III patients. There was no significant difference in the sensitivity of either repetitive ventricular response or sustained ventricular tachycardia induction in patients with coronary disease compared with those with the diagnosis of noncoronary disease. We conclude that, contrary to an earlier report from our group, the incidence of induction of repetitive ventricular responses to single ventricular extrastimuli during atrial pacing is low in patients with a history of sudden death or recurrent ventricular tachycardia. The incidence of induction of repetitive ventricular responses and sustained ventricular tachycardia is highest using the V 1V 2V 3 and V burst modes of stimulation.

Ventricular activation patterns of spontaneous and induced ventricular rhythms in canine one-day-old myocardial infarction. Evidence for focal and reentrant mechanisms.

We studied isochronal maps of ventricular activation during spontaneous multiform ventricular rhythms (rates 120-190/min) and pacing-induced ventricular tachyarrhythmias (rate 230-450/min) in dogs 1 day after myocardial infarction. Recordings were obtained from the entire epicardial surface and from selected endocardial and intramural sites utilizing a computerized multiplexing technique. Spontaneous ventricular rhythms had a focal origin from the surviving subendocardial Purkinje network underlying the infarction and showed frequent shift of the pacemaker site. On the other hand, fast ventricular tachyarrhythmias were consistently induced in the same dogs by bursts of rapid ventricular pacing or programmed premature stimulation and had a tendency to degenerate into ventricular fibrillation. Pacing-induced rhythms were due to reentrant activation that developed mainly in the surviving, electrophysiologically abnormal, epicardial layer overlying the infarction. The last stimulated heat that initiated reentry resulted in a continuous arc of functional conduction block and two slowly circulating activation fronts around both ends of the arc of block. The activation fronts rejoined on the distal side of the arc of block before breaking through the arc to reactivate an area proximal to the block. This resulted in splitting of the initial single arc of block into two separate arcs. Reentrant activation subsequently continued as two synchronous circuits which conducted in clockwise and counterclockwise directions, respectively. Reentry spontaneously terminated when the leading edge of both reentrant circuits encountered refractory tissue and failed to advance. The presence of two synchronous circuits was the hallmark of a stable reentrant activation. The development of three or more asynchronous circuits resulted in an activation pattern that was "prefibrillatory." This pattern was seen to develop during pleomorphic ventricular rhythms and ventricular tachycardias of the torsades de pointes type that degenerated into ventricular fibrillation. Ventricular fibrillation was maintained by continuously changing multiple asynchronous circuits. The transition from a stable reentrant activation pattern to that of ventricular fibrillation was probably related to nonhomogeneous shortening of refractoriness in different parts of the myocardium.

Role of implantable pacemakers in control of recurrent ventricular tachycardia

Implanted pacemakers can provide a viable alternative to pharmacologic therapy or surgical management of patients with recurrent ventricular tachycardia. An increasing variety of pacemaker techniques are proving useful for preventing, controlling the effective rate of or terminating ventricular tachycardia. To assess the role of permanent pacing in the treatment of ventricular tachycardia, a consecutive series of 160 patients undergoing electrophyslologic testing for recurrent ventricular tachycardia were analyzed. Thirty-nine patients received implantable pacemakers, of which 13 were intended for bursts of rapid ventricular pacing. No adverse responses were attributed to these burst pacemakers, but concern for possible acceleration of tachycardia and appropriate identification of the arrhythmia were among factors limiting more widespread use of antitachycardia pacing. Some of these limitations may be resolved with further advances in electrophysiologic understanding of arrhythmias combined with strides in medical electronics, which will permit the development of new generations of highly sophisticated antitachycardia pacemakers.

Repetitive responses to single ventricular extrastimuli in patients with serious ventricular arrhythmias: incidence and clinical significance.

Electrophysiologic studies were carried out in 85 patients with serious ventricular arrhythmias: 44 with recurrent sustained ventricular tachycardia (group A), 16 with recurrent nonsustained ventricular tachycardia (group B), and 25 with recent prehospital ventricular fibrillation not associated with acute myocardial infarction (group C). Programmed ventricular stimulation from the right ventricular apex included premature stimulation during normal sinus rhythm, atrial pacing, and ventricular pacing, as well as brief bursts of rapid ventricular pacing (RVP). A repetitive ventricular response (RVR) was defined as one or more non-stimulated premature ventricular depolarizations in response to a single paced premature ventricular depolarization during normal sinus rhythm or atrial pacing. RVRs were observed in seven of 44 (16%) group A patients, one of 16 (6%) group B patients, and three of 25 (12%) group C patients. In contrast, single and double premature ventricular stimuli during ventricular pacing and/or bursts of RVP resulted in the reproducible initiation of ventricular tachycardia in 40 of 44 (91%) group A patients, 10 of 16 (63%) group B patients, and 19 of 25 (76%) group C patients. We conclude that RVRs to single ventricular extrastimuli during normal sinus rhythm or atrial pacing are rare, and therefore are an insensitive index of susceptibility to serious ventricular arrhythmias in these patients.

Sustained ventricular tachycardia in recent canine myocardial infarction.

To study recurrent ventricular tachycardia in the late phase or myocardial infarction (MI), transmural anteroapical infarcts were created by ligation of the left anterior descending (LAD) coronary artery in 25 dogs. Twenty dogs survived LAD ligation and underwent an open-chest electrophysiologic study an average of 20 days after MI. Programmed electrical stimulation was carried out using the extrastimulus technique and short bursts of rapid ventricular pacing via bipolar electrodes positioned at multiple left ventricular endocardial sites. Sixteen dogs had electrically induced ventricular tachycardia, and in 11, sustained ventricular tachycardia was reproducibly initiated and terminated by programmed ventricular stimulation. Short bursts of rapid left ventricular pacing from areas in periinfarct zone was the most effective technique for initiating ventricular tachycardia. The electrophysiologic phenomena in this model of sustained ventricular tachycardia in 3-week-old MI included electrically induced changes in rate and morphology and biventricular capture without termination during tachycardia.

Intravenous disopyramide phosphate and ventricular overdrive pacing in the termination of paroxysmal ventricular tachycardia.

Both antiarrhythmic drugs and bursts of rapid ventricular pacing provide alternatives to DC cardioversion for the treatment of paroxysmal ventricular tachycardia. This report considers the individual and combined success of burst ventricular pacing and intravenous disopyramide phosphate in the tretment of 11 examples of paroxysmal ventricular tachycardia. Rapid ventricular pacing, at a rate of up to 50 beats/min faster than the tachycardia rate terminated 7 of the tachycardias. Intravenous disopyramide resulted in increased tachycardiac cycle length (342 +/- 34 ms-385 +/- 56 ms), increased QRS complex width (147 +/- 42 ms-180 +/- 41 ms) and termination of 8 the tachycardias. The remaining 3 tachycardias could be terminated by bursts of ventricular pacing following the infusion of disopyramide. Of these, 2 could not be terminated prior to disopyramide. The use of both techniques allowed the extinction of all 11 tachycardias and prevented the need to proceed to DC conversion.

Termination of ventricular tachycardia with bursts of rapid ventricular pacing

Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 512 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent ventricular tachycardia.