Inducible Sustained Tachycardia Research Articles

Outcome of ACHD patients with non-inducible versus inducible IART undergoing cavo-tricuspid isthmus ablation: the role of empiric ablation.

Catheter ablation for supraventricular tachycardia (SVT) in adults with congenital heart disease (ACHD) is an important therapeutic option. Cavo-tricuspid isthmus (CTI)-dependent intraatrial re-entrant tachycardia (IART) is common. However, induction of sustained tachycardia at the time of ablation is not always possible. We hypothesised that performing an empiric CTI line in case of non-inducibility leads to good outcomes. Long-term outcomes of empiric versus entrained CTI ablation in ACHD patients were examined. Retrospective, single-centre, case-control study over 7years. Arrhythmia-free survival after empiric versus entrained CTI ablation was compared. Eighty-seven CTI ablations were performed in 85 ACHD patients between 2010 and 2017. The mean age of the cohort was 43years and 48% were male. Underlying aetiology included ASD (31%), VSD (11.4%), AVSD (9.1%), AVR (4.8%), Fallot's (18.4%), Ebstein's (2.3%), Fontan's palliation (9.2%) and atrial switch (13.8%). CTI-dependent IART was entrained in 59 patients whereas it was non-inducible in 28. The latter had an empiric CTI ablation. Forty-three percent of procedures were performed under general anaesthesia. There were no reported procedural complications. There was no significant difference in the mean procedure or fluoroscopy times between the groups (empiric vs entrained CTI; 169.1 vs 183.3 and 28.1 vs 19.9min). Arrhythmia-free survival was 64.3% versus 72.8% (p value 0.44) in the empiric and entrained groups at 21months follow-up. Long-term outcomes after empiric and entrained CTI ablation for IART in ACHD patients are comparable. This is a safe and effective therapeutic option. In the case of non-inducibility of IART, an empiric CTI line should be considered in this cohort.

78 Empiric versus entrained cavotricuspid isthmus line ablation in congenital heart disease: a single centre experience

IntroductionCatheter ablation for supraventricular tachycardia (SVT) in patients with congenital heart disease (CHD) is an important therapeutic option. Complex atrial substrate in this cohort makes atrial flutter (AFl) a common...

Cryoablation of AVNRT When Sustained Tachycardia Cannot be Induced

Inducibility of sustained tachycardia is preferred prior to cryoablation for atrioventricular nodal reentrant tachycardia (AVNRT). The Pediatric Electrophysiology Database of a single institution was retrospectively reviewed for patients with clinical sustained (≥ 30 seconds of symptoms) AVNRT documented by noninvasive means who underwent cryoablation for AVNRT to determine if intermediate-term success with cryoablation for AVNRT can be achieved without inducibility of sustained AVNRT during electrophysiology study (EPS). There were no differences between patients with sustained (≥ 30 seconds of tachycardia) AVNRT (N = 67) and patients with nonsustained (ns, ≥ 3 beats and <30 seconds of tachycardia) AVNRT at EPS (N = 16). Acute success was achieved without PR prolongation in all patients. Although duration of follow-up was shorter for the sustained group than the nonsustained group (2.7 ± 1.6 years vs 3.8 ± 1.4 years, P = 0.008), recurrence rate was similar (6% vs 6.3%, P = 0.6). In patients with only nonsustained AVNRT at EPS, supportive findings for procedural effectiveness seen: (1) Dual atrioventricular node physiology (DAVNP) was eliminated in 14/14, (2) the fast pathway effective refractory period (FPERP) decreased after ablation in 10/11, (3) sustained slow pathway conduction was eliminated in 8/8 including both patients without discrete DAVNP prior to ablation, and (4) FPERP increased during lesion formation in 10/10. Intermediate-term success can be achieved with cryoablation of ns AVNRT. Attention should be paid to supportive indicators of damage to slow pathway.

Implantable defibrillators and sudden cardiac death.

Sudden cardiac death (SCD) is among the most common causes of death in developed countries throughout the world. It is estimated that more than 3 million people die yearly from SCD, with a survival rate of less than 1%. In the United States, the Center for Disease Control recently estimated an annual incidence of 450 000 sudden deaths,1 with a survival rate of approximately 5%, although this probably is an overestimation. Although there has been a reduction in total cardiac mortality from 728 115 in 1989 to 719 456 in 1999, the percentage of deaths that are sudden has actually increased from 38% to 47%. The increase was greatest in women older than 65 years of age, from 56.3% to 63.9%. This has resulted primarily from an increase in out-of-hospital sudden deaths. There is a comparable incidence of SCD and survival rate in Western Europe.2 The magnitude of this problem can be understood by noting that SCD accounts for more deaths each year than the total number of deaths from AIDS, breast cancer, lung cancer, and stroke (Figure 1). Unfortunately, it is the first presentation of cardiac disease in 33% to 50% of patients and is 3 times as common in men than in women. Figure 1. Magnitude of the problem of sudden cardiac arrest. Coronary artery disease, with or without myocardial infarction, is by far the most common underlying disease for SCD in the western world, being responsible for approximately 75% of all SCDs.3,4 Cardiomyopathies (dilated and hypertrophic) and primary electrical heart disease account for most of the remainder. The two most important risk factors for SCD (ie, those with highest predictive value) are left ventricular ejection fraction (LVEF) less than 40% and clinical congestive heart failure.3,4 These are followed by significant ventricular arrhythmias (particularly …

Adenosine-sensitive atrial tachycardia.

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6-12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 +/- 20 years (range 18-82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 +/- 80 msecs (range 260-580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on beta-adrenergic stimulation are most likely to be terminated by adenosine.

Late clinical and electrophysiologic outcome of radiofrequency ablation therapy by the inferior approach in atrioventricular node reentry tachycardia

A late electrophysiologic study was conducted in 182 of 289 patients with slow-fast atrioventricular node reentry tachycardia 81 ± 36 days after radiofrequency ablation therapy by the inferior approach. Of these 182 patients, electrophysiologic study immediately after ablation revealed a selective modification of the slow pathway in 159, a modification of both the slow and fast pathways in 15, a modification of the fast pathway alone in 3, and failure of ablation in 5. One hundred two patients had no induction of echoes; 75 had induction of fewer than four echoes; and 5 had induction of sustained tachycardia with or without isoproterenol infusion. The late electrophysiologic study in these 182 patients revealed a persistent effect without changes in conduction properties in 161 (88%) patients. A change in conduction properties was noted in 21 patients, including 5 with resumption of slow- or fast-pathway conduction with induction of sustained tachycardia, 8 with improved fast- or slow-pathway conduction, and 8 with an additional depression of fast- or slow-pathway conduction. Of the 102 patients with no induction of echoes and the 75 patients with induction of fewer than four echoes during the immediate postablation electrophysiologic study, 5 (3 and 2, respectively) patients had induction of tachycardia. Of the 5 patients with induction of sustained tachycardia in the immediate postablation electrophysiologic study, 3 continued to have induction of sustained tachycardia; 1 had induction of echoes only; and 1 had no induction of echoes. The predictability of late success by using a combination of induction of no and fewer than four echoes in the immediate postablation electrophysiologic study had a sensitivity of 99%, a specificity of 38%, a positive predictive value of 97%, a negative predictive value of 60%, and a total predictive accuracy of 96%. Thus the effects of radiofrequency ablation persist in the majority of patients during follow-up, and elimination of all echoes is unnecessary for achieving a late success.

A simple technique for selective radiofrequency ablation of the slow pathway in atrioventricular node reentrant tachycardia

Objectives. A simple technique was designed for radiofrequency ablation therapy of atrioventricular (AV) node reentrant tachycardia.Background. This technique was based on the hypothesis that slow pathway conduction reflects conduction through the compact node and its posterior atrial input.Methods. A total of 100 consecutive patients were studied; there were 37 men and 63 women, with a mean age of 48 ± 15 years. All 100 patients had induction of sustained tachycardia with (51 patients) or without (49 patients) administration of isoproterenol or atropine, or both. The ablation catheter was initially manipulated to record the largest His bundle deflection from the apex of Koch's triangle. It was then curved downward and clockwise to the area of the compact node when His deflection was no longer visible and the ratio of atrial to ventricular electrogram was < 1. The radiofrequency current was delivered from the 4-mm tip electrode a mean of 5 ± 7 times at a power of 25 ± 4 W for a duration of 21 ± 4 s. The total fluoroscopic time was 19 ± 11 min.Results. Selective ablation (56 patients) or modification (26 patients) of the slow pathway without affecting anterograde and retrograde fast pathway conduction was achieved in 82 patients. Ablation or modification of both the retrograde fast pathway and the slow pathway but with preservation of anterograde fast pathway conduction was noted in 12 patients. Ablation or modification of the retrograde fast pathway alone or both anterograde and retrograde fast pathway conduction was noted in three patients. Complete AV node block occurred in three patients. Seventy-three patients had no induction of echo beats or tachycardia and 24 patients had induction of a single echo beat after ablation. Follow-up study was performed in 62 patients 76 ± 18 days after ablation. Thirty-nine patients had no induction of echo beats or tachycardia, 22 had induction of echo beats alone and 1 patient had induction of sustained tachycardia.Conclusion. Selective ablation of the slow AV node pathway can be achieved by a simple procedure with a high success rate and few complications.

Effect of isoproterenol on serum potassium and magnesium.

Some ventricular arrhythmias can be related to a decrease in the level of potassium (K) and/or magnesium (Mg). Because adrenergic stimulation decreases serum K+ and Mg++, we decided to investigate the effects of a beta-receptor agonist, isoproterenol, on serum K+ and Mg++, and their consequences on the induction of tachycardia. Programmed atrial and ventricular stimulation was performed in 95 patients before and during infusion of 1.6 micrograms.ml-1 of isoproterenol. During isoproterenol infusion, 61 patients had no inducible tachycardias (group I) and 34 had inducible sustained tachycardias (group II): 16 of them (group IIA) had inducible sustained supraventricular tachyarrhythmias and 18 (group IIB) had inducible sustained ventricular tachycardia. Serum K+ and Mg++ were measured at the end of stimulation in the control state and during isoproterenol infusion. The basal values in groups I and II did not differ (3.8 +/- 0.38 vs 3.86 +/- 0.39 mEq.l-1 for K+, and 20.18 +/- 2.68 vs 19.83 +/- 1.63 mg.l-1 for Mg++). Isoproterenol infusion induced a significant (P < 0.001) hypokalaemia in all groups and a decrease in serum Mg in group II: there was a significant decrease in serum Mg++ (P < 0.05) in group IIA (19.55 +/- 1.7 vs 20.4 +/- 4.6). The decrease in serum Mg++ in group IIB (18.9 +/- 1.55 vs 19.32 +/- 1.63) was not significant. However the serum Mg++ level during isoproterenol infusion was significantly lower in group IIB than in group I. In conclusion, the infusion of isoproterenol was responsible for a significant hypokalaemia, which did not explain the induction of tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: Evidence for distinct mechanisms

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infuse ot a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia.The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 ± 4 vs. 7.4 ± 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 ± 78 vs. 450 ± 81 ms, p = NS) and QRS duration (184 ± 38 vs. 185 ± 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.In summary, infusion of procsinamide with use of the described dosing regimen terminated 93% of sustained, nemodynamically tolerated ventricular tachycardia episodes without causing hypotension. The ability to terminate ventricular tachycardia with an infusion of procainamide did not reliably predict subsequent success in preventing inducible ventricular tachycardia. Finally, the reinitiation of ventricular tachycardia with an identical configuration and similar cycle length and at constant serum procainamide concentrations suggests that, at least in some patients (7 of 13; 54%), the electrophysiologic mechanism of drug-induced ventricular tachycardia termination is different from that of arrhythmia prevention.

Serial Electrophysiologic Studies of the Effects of Oral Diltiazem on Paroxysmal Supraventricular Tachycardia*

In 16 patients with paroxysmal supraventricular tachycardia, electrophysiologic studies were done before and serially at hourly intervals for eight hours after the third oral dose of 90 mg diltiazem given every eight hours. Diltiazem increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conducting system at all measurements. Before diltiazem, all 16 patients had induction of sustained tachycardia. After diltiazem, sustained tachycardia could not be induced in ten patients at any measurements; in these patients, either echo or nonsustained tachycardia was induced. In the remaining six patients, sustained tachycardia was induced, particularly after six hours. Follow-up observations in 12 patients receiving the same dosage of oral diltiazem for 6 +/- 2 months (mean +/- SD), showed that of the eight patients in whom electrophysiologic testing induced either echo or nonsustained tachycardia, six were asymptomatic and two experienced transient palpitation. Of the other four patients with induction of sustained tachycardia, three had transient palpitation and one had occasional attacks of sustained tachycardia requiring modification of therapy. Thus, oral diltiazem increases atrioventricular nodal refractoriness, with an effect lasting up to eight hours. It is an effective agent for the prophylaxis of paroxysmal supraventricular tachycardia.

A model of chronic ischemic arrhythmias: The relation between electrically inducible ventricular tachycardia, ventricular fibrillation threshold and myocardial infarct size

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a “clinical” stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction. Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean ± standard deviation 29 ± 11 to 10 ± 5 mA, p < 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct. It is concluded that: (1) Inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.

Digoxin, propranolol, and atrioventricular reentrant tachycardia in the Wolff-Parkinson-White syndrome.

In 22 patients with atrioventricular reentrant tachycardia incorporating a retrogradely conducting accessory pathway, electrophysiologic studies were done before and after oral digoxin, 1.25 mg, and propranolol, 160 to 240 mg, each given in 4 divided doses at 6-hour intervals. Before digoxin and propranolol, all 22 patients had induction of sustained tachycardia. After the medication six patients lost the ability to induce atrial echo and one lost the ability to sustain tachycardia due to an increased retrograde accessory pathway or atrial refractoriness or both. Six patients lost the ability to induce or sustain tachycardia due to increased atrioventricular nodal refractoriness. In the remaining nine patients with inducible sustained tachycardia, cycle lengths of tachycardia were prolonged. These findings suggest that combined use of oral digoxin and propranolol is useful in selected patients with atrioventricular reentrant tachycardia.