Multicenter cohort study on duration of antiarrhythmic medication for supraventricular tachycardia in infants.

Antiarrhythmic medication (AM) is commonly used to prevent supraventricular tachycardia (SVT) recurrence in infants. Our aim was to determine whether a shorter duration of AM is sufficient to prevent atrioventricular reentrant tachycardia (AVRT) recurrence and evaluate risk factors for recurrence of SVT after discontinued AM.This multicenter cohort study included all infants diagnosed with SVT in the five university hospitals in Finland between 2005 and 2017. Those diagnosed between 2005 and 2012 received AM for 12 months (group 1), and those diagnosed between 2013 and 2017 received AM for 6 months (group 2). A total of 278 infants presented with AVRT (group 1, n = 181; group 2, n = 97), and the median AM duration was 12.0 months (interquartile range [IQR] 11.4-13.4) and 7.0 months (IQR 6.0-10.2), respectively. Propranolol was the most frequently used first-line AM (92% and 95%). Recurrence-free survival rates were over 88% until 12 months after AM prophylaxis in both groups, without any statistically significant difference between them. Independent risk factors for recurrence of SVT after discontinuation of AM were need of combination AM (HR 2.2, 95% CI 1.14-4.20), Wolff-Parkinson-White (WPW) syndrome (HR 2.4, 95% CI 1.25-4.59), and age over 1 month at admission (HR 2.2, 95% CI 1.12-4.48).    Conclusion: Shortening AM duration in infants from 12 to 6 months does not seem to lead to more frequent SVT recurrence. The risk factors for recurrence of SVT were WPW syndrome, need of combination AM, and age over 1 month.

Adenosine-induced tachycardia acceleration: an unusual proarrhythmia.

Adenosine is an effective agent for termination of most re-entrant supraventricular arrhythmias involving the atrioventricular node and often also used as a diagnostic agent for wide QRS tachycardias. Adenosine terminates 90-99% of re-entrant supraventricular tachycardias but it may rarely accelerate tachycardias. Adenosine-induced tachycardia acceleration is a rare phenomenon, as only a handful of cases have been described in the literature. We present a case of a 36-year-old man with a narrow complex, short RP tachycardia at a rate of 165 bpm and an initial blood pressure of 110/78 mm Hg. A bolus of 12 mg of adenosine resulted in slowing of the tachycardia to 150 bpm for 2-3 s, followed by acceleration of the tachycardia to 185 bpm that lasted for approximately 20 s and returned to baseline at 165 bpm. The main mechanism of adenosine-induced acceleration may be the secondary sympathetic stimulation, which may be preceded by transient bradycardia and/or hypotension.

A new method for induction of atrioventricular nodal reentrant tachycardia in non-inducible cases.

AIM: In some patients with clinical paroxysmal supraventricular tachycardia (PSVT), who are candidates for radiofrequency (RF) catheter ablation, attempts for the induction of arrhythmia during the electrophysiological study (EPS) fail despite different stimulation protocols even during the isoproterenol infusion and atropine injection. The presence of an atrial-His interval (AH) jump during decremental pre-mature atrial stimulation is the only clue for slow pathway ablation in these patients; in occasional patients, however, the AH jump is an accidental finding and the real arrhythmia is not atrioventricularnodal reentrant tachycardia (AVNRT). We aimed to introduce a new method for the induction of AVNRT in these patients. METHODS AND RESULTS: Ten patients (50% male, mean age=44.40 ± 12.80 years) with clinical PSVT who were referred to our department for the EPS and RF catheter ablation were selected. These patients had documented clinical PSVT with non-inducible arrhythmia during the EPS with different stimulation protocols even during the isoproterenol infusion and atropine injection but they only showed an AH jump. To induce AVNRT, low-watt (15-20), low-temperature (40-45°C) RF currents were delivered into the slow pathway area for a maximum of 40 s. Atrioventricularnodal reentrant tachycardia was inducible in five cases (50%, three male, mean age=45.80 ± 9.65 years). Induction of AVNRT occurred either during the RF current application after the occurrence of junctional ectopic beats or after another stimulation protocol. CONCLUSION: A low-watt, low-temperature RF current application into the slow pathway area can be a provocative method for the induction of AVNRT probably by AV-junction warming and conduction-velocity augmentation.

Atrial tachycardia with 1:1 atrioventricular conduction precipitated by propafenone.

A 58-year-old man presented to the emergency department with sudden onset rapid palpitations and significant presyncope while walking on the flat. The previous day he had undergone DC cardioversion for atrial fibrillation (AF) which had been initially successful. However, 6 h after cardioversion he was aware of intermittently raised but regular heart rates. On arrival at the emergency department (ED) he was well with no haemodynamic compromise. The ECG showed an atrial tachycardia instead of AF. Medications consisted of propafenone 300 mg twice daily, bisoprolol 5 mg at night and warfarin. Bisoprolol was increased to 5 mg twice daily and he was discharged with a plan for outpatient ablation. He collapsed in the hospital car park with rapid palpitations, chest tightness and vagal symptoms. On return to the ED he was hypotensive with a heart rate of 200 bpm. The ECG showed 1:1 atrioventricular conduction (AV) of the atrial tachycardia which promptly improved after administering intravenous atenolol. Class 1c antiarrhythmic agents such as propafenone can precipitate 1:1 AV conduction of atrial tachycardias resulting in dangerous exacerbations of ventricular rate or even malignant tachyarrhythmias. It is therefore essential that concomitant AV blocking agents are used both prophylactically or acutely in suspected cases.

Frequency gradients during two different forms of fibrillation in the canine atria.

BACKGROUND: Atrial fibrillation (AF) is thought to be sustained by multiple reentrant wavelets or firing foci. OBJECTIVE: The aim of this study was to compare the spectral domain characteristics in the left atrium (LA) and right atrium (RA) in two different models of AF. METHODS: Rectangular 8 x 14 electrode arrays were placed on the LA and RA of 14 anesthetized dogs. AF episodes were induced with burst pacing and aconitine in each dog. For each model, AF was induced from the RA in six dogs and from the LA in six dogs. Dominant frequencies (DFs) were obtained using the fast Fourier transform of the unipolar recordings obtained from each electrode of the array. Standard deviation (SD) was used to compute the frequency dispersion within an atrium. Regularity of the signal was quantified using an organization index (OI). RESULTS: DFs were largest in the atrium where aconitine was applied. Aconitine AF had larger gradients than burst-pacing AF (5.0 +/- 4.5 vs. 0.9 +/- 1.0 Hz: P <.006). Aconitine AF when compared with burst-pacing AF had greater absolute LA-RA differences in the SD of DFs (2.3 +/- 1.9 vs. 0.2 +/- 0.2 Hz; P <.001) and in OI (0.11 +/- 0.07 vs. 0.06 +/- 0.07; P <.07). CONCLUSIONS: Differences in frequency gradients and organization were observed during AF induced by burst pacing and aconitine. This suggests that different mechanisms of AF are possible and may be identified with frequency domain analysis.

Reproducible induction of atrioventricular nodal reentrant tachycardia with adenosine triphosphate.

A 29-year-old woman was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation of a 8-year duration. The 12-lead ECG during palpitations showed narrow QRS tachycardia at a rate of 160 beats/min. Dual AVN physiology according to electrophysiological criteria was not shown by single atrial extrastimulation and the tachycardia could not be induced. Slow/fast atrioventricular nodal reentrant tachycardia (AVNRT) was induced once by double atrial extrastimuli, but it was not reproducible. However, intravenous bolus injection of adenosine triphosphate (12.5 mg) during sinus rhythm led to reproducible initiation of slow/fast AVNRT.

Irregular atrial activation during atrioventricular nodal reentrant tachycardia: evidence of an upper common pathway.

Controversy continues regarding the precise nature of the reentrant circuit of AV nodal reentrant tachycardia, especially the existence of an upper common pathway. In this case report, we show that marked variation and irregularity in atrial activation (maximum AA interval variation of 80 msec) can exist with fixed and constant activation of the His bundle and ventricles during AV nodal reentrant tachycardia in a 45-year-old female patient. We propose that irregular atrial activation is due to variable and inconsistent conduction from the AV node to the atria through the perinodal transitional cell envelope extrinsic to the reentrant circuit. Our observations support the concept of an upper common pathway, at least in some patients with AV nodal reentrant tachycardia.

Definition of the reentry circuit with demonstration of a low frequency diastolic potential in a patient with verapamil-sensitive idiopathic left ventricular tachycardia.

A low frequency slow potential preceding the Purkinje spike was recorded at the midseptum during tachycardia in a 69-year-old man with verapamil-sensitive left ventricular tachycardia. This potential was characteristically absent during sinus rhythm before radiofrequency ablation, but became evident following the QRS complex after successful ablation at the tachycardia exit site. Induction of tachycardia with programmed stimulation was dependent on emergence of this slow potential. Decremental conduction was noted between the QRS complex and the slow potential. Further energy application at a site proximal to where the slow potential was initially recorded totally eliminated the slow potential.

Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: response of control patients to incremental doses of adenosine.

BACKGROUND: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electrophysiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology. HYPOTHESIS: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT. METHODS: Thirty-seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred. RESULTS: The mean (+/- standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 +/- 3.9 and 7.4 +/- 4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0-8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine. CONCLUSION: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.

Differential effects of atropine and isoproterenol on inducibility of atrioventricular nodal reentrant tachycardia.

BACKGROUND: Radiofrequency ablation of the "slow pathway" in atrioventricular nodal reentrant tachycardia (AVNRT) relies on tachycardia non-inducibility after ablation as success criterion. However, AVNRT is frequently non-inducible at baseline. Thus, autonomic enhancement using either atropine or isoproterenol is frequently used for arrhythmia induction before ablation. METHODS: 80 patients (57 women, 23 men, age 50+/-14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01 mg/kg atropine or 0.5-1.0 microg/kg/min isoproterenol before ablation after baseline assessment of AV conduction. The effects of either drug on ante- and retrograde conduction was assessed by measuring sinus cycle length, PR and AH interval, antegrade and retrograde Wenckebach cycle length (WBCL), antegrade effective refractory period (ERP) of slow and fast pathway and maximal stimulus-to-H interval during slow and fast pathway conduction. RESULTS: Inducibility of AVNRT at baseline was not different between patients randomized to atropine (73%) and isoproterenol (58%) but was reduced after atropine (45%) compared to isoproterenol (93%, P<0.001). Of the 28 patients non-inducible at baseline isoproterenol rendered AVNRT inducible in 21, atropine in 4 patients. Dual AV nodal pathway physiology was present in 88% before and 50% after atropine compared to 83% before and 73% after isoproterenol. Whereas both drugs exerted similar effects on ante- and retrograde fast pathway conduction maximal SH interval during slow pathway conduction was significantly shorter after isoproterenol (300+/-48 ms vs. 374+/-113 ms, P=0.012). CONCLUSION: Isoproterenol yields higher AVNRT inducibility than atropine in patients non-inducible at baseline. This may be caused by a more pronounced effect on antegrade slow pathway conduction.

Atrioventricular nodal re-entrant tachycardia associated with stimulant treatment.

A 13-year-old African-American female taking sertraline for obsessive compulsive disorder was diagnosed with her first episode of atrioventricular (AV) nodal re-entrant tachycardia five days after beginning Mixed Salts of a Single-Entity Amphetamine Product (Adderall) for treatment of attention-deficit hyperactivity disorder (ADHD). She received successful cardioversion with 6 mg of intravenous adenosine, but developed a second episode of possible AV nodal re-entrant tachycardia twelve days after Adderall was reinitiated at half the previous dose. The patient had clinically similar cardiac episodes five and six months after treatment was changed to slow-release methylphenidate. Stimulant medication may evoke onset of AV nodal tachyarrhythmias in patients who have the potential to develop them, possibly in combination with a selective serotonergic reuptake inhibitor (SSRI).

AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias.

An electrophysiological study was performed in a 61 year old man with Wolff- Parkinson-White (WPW) syndrome. At baseline, neither ventricular nor supraventricular tachycardias could be induced. During isoprenaline infusion, ventricular tachycardia originating from the right ventricular outflow tract (RVOT) with a cycle length of 280 ms was induced and subsequently atrioventricular reentrant tachycardia (AVRT) with a cycle length of 300 ms using an accessory pathway in the left free wall appeared. During these tachycardias, AVRT was entrained by ventricular tachycardia. The earliest ventricular activation site during the ventricular tachycardia was determined to be the RVOT site and a radiofrequency current at 30 W successfully ablated the ventricular tachycardia at this site. The left free wall accessory pathway was also successfully ablated during right ventricular pacing. The coexistence of WPW syndrome and cathecolamine sensitive ventricular tachycardia originating from the RVOT has rarely been reported. Furthermore, the tachycardias were triggered by previous tachycardias.

Induction of atrioventricular node reentrant tachycardia with adenosine: differential effect of adenosine on fast and slow atrioventricular node pathways.

OBJECTIVES: This study sought to evaluate the sensitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in patients with typical AV node reentrant tachycardia. BACKGROUND: Although adenosine is known to depress conduction through the AV node, the relative sensitivity to adenosine of the anterograde fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been studied. METHODS: Sixteen patients with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients were given incremental doses of adenosine during atrial pacing. RESULTS: In 14 of 16 patients with dual-AV node physiology, administration of small doses of adenosine during atrial pacing led consistently to transient block of impulse conduction in the fast pathway before block in the slow pathway, resulting in abrupt prolongation of the AH interval with continued 1:1 AV conduction. The mean (+/- SD) doses of adenosine required to cause conduction block in the fast and slow pathways were 2.7 +/- 3.0 and 7.2 +/- 4.7 mg, respectively (p = 0.004). In 9 of 16 patients, administration of low dose adenosine led to initiation of AV node reentrant tachycardia. The control patients showed no abrupt increases in AH interval with administration of adenosine during atrial pacing. CONCLUSIONS: In most patients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more sensitive than the slow pathway to the effects of adenosine.

Iatrogenically induced intractable atrioventricular reentrant tachycardia after verapamil and catheter ablation in a patient with Wolff-Parkinson-White syndrome and idiopathic dilated cardiomyopathy.

In a patient with WPW syndrome and idiopathic dilated cardiomyopathy, intractable atrioventricular reentrant tachycardia (AVRT) was iatrogenically induced. QRS without preexcitation, caused by junctional escape beats after verapamil or unidirectional antegrade block of accessory pathway after catheter ablation, established frequent AVRT attack.

Theoretical study of cardiac transient conduction blocks on reentries induction. Applications to antiarrhythmic drugs.

Limitations of antiarrhythmic drugs on cardiac sudden death prevention appeared since the early 80's. The "Cardiac Arrhythmia Suppression Trial" (CAST) showed more recently that mortality was significantly higher in patients treated with some particular antiarrhythmic drugs than in non-treated patients. In this field, our group recently demonstrated that a bolus of a Class 1 B antiarrhythmic drug was able to trigger a ventricular fibrillation due to transient blocks induction. The aim of the present work was to systematically study, by use of the van Capelle and Durrer (VCD) model which allows to simulate ventricular activation wave propagation, the link between arrhythmogenic effects and the ability of transient blocks to possibly degenerate in severe arrhythmias. A fragment of the ventricular wall is represented by an array of 16384 elements electrically coupled. Effects of induction of one or several transient blocks, as the effects of their size and duration on possible induction of reentries have been studied. Results obtained show that various combinations between these different parameters may trigger reentries, ventricular tachycardia and/or more complex patterns assimilable to ventricular fibrillation. These results clearly evidence the fact that possible induction of transient blocks may directly be related to risk factor associated to arrhythmogenic effects of antiarrhythmic drugs.

The mechanisms responsible for lack of reproducible induction of atrioventricular nodal reentrant tachycardia.

INTRODUCTION: AV nodal reentrant tachycardia (AVNRT) is not always reproducibly inducible. The purpose of this study was to determine the mechanisms responsible for the lack of reproducible induction of AVNRT. METHODS AND RESULTS: The induction of AVNRT was assessed with atrial burst pacing, and with atrial and ventricular programmed stimulation, each with one and two extrastimuli, in 103 patients with AVNRT. The stimulation protocol was repeated 10 times in the baseline state, during isoproterenol infusion, and after atropine administration, or until AVNRT was induced in 7 of 10 attempts. The mechanisms responsible for < 7 of 10 inductions were classified as: (1) the inability to achieve critical AH prolongation; (2) fast pathway block; and (3) slow pathway block. The induction endpoint was achieved in 90 patients: 55 in the baseline state, 34 during isoproterenol infusion, and 1 after atropine. The mechanism of noninducibility in the baseline state (n = 48) was the inability to achieve a critical AH interval in 20%, fast pathway block in 49%, and slow pathway block in 31% (P = 0.02). During isoproterenol administration (n = 14) and after atropine administration (n = 13), the three mechanisms were equally responsible for nonreproducible induction of AVNRT. CONCLUSIONS: The induction of AVNRT is poorly reproducible in approximately 10% of patients. In the baseline state, the most common reason for the inability to reproducibly induce AVNRT is fast pathway block. In the presence of isoproterenol or atropine, each of the three mechanisms was equally responsible for noninducibility of AVNRT.

[Amiodarone-induced hyperthyroidism causing progression of arrhythmia]. / Amiodaron okozta hyperthyreosis által kiváltott arrhythmia-progresszió.

A case of a 38-year-old male with supraventricular paroxysmal tachycardia existing for more than a decade is reported. He has received amiodarone in a daily dose of 800 mg for three years and the tachycardia returned in 1992. New antiarrhythmic drugs were added but no beneficial effect has been achieved and moreover, a case of ventricular fibrillation occurred. The 12-lead ECG performed during tachycardia and the electrophysiological study showed orthodromic AV reentry tachycardia. Laboratory tests performed proved hyperthyreotic state. Attacks of paroxysmal tachycardia were returned and aggravated by the hyperthyreosis induced by amiodarone. Finally, antiarrhythmic drugs were discontinued and methimazol was introduced. Gradually, the patient become asymptomatic within two months. The most important conclusion of the case reported, that the amiodarone induced hyperthyreosis can be subclinical or obscure. Consequently, a regular control of serum thyreoid hormone levels at least twice a year on patients with long term amiodarone administration should be advised.