Coexistence of atrioventricular nodal reentrant tachycardia and idiopathic left ventricular outflow-tract tachycardia

Double tachycardia is a relatively rare condition. We describe a 21 year old woman with history of frequent palpitations. In one of these episodes, she had wide complex tachycardia with right bundle branch and inferior axis morphology. A typical atrioventricular nodal tachycardia was induced during electrophysiologic study, aimed at induction of clinically documented tachycardia. Initially no ventricular tachycardia was inducible. After successful ablation of slow pathway, a wide complex tachycardia was induced by programmed stimulation from right ventricular outflow tract. Mapping localized the focus of tachycardia in left ventricular outflow tract and successfully ablated via retrograde aortic approach. During 7 month's follow-up, she has been symptom free with no recurrence. This work describes successful ablation of rare combination of typical atrioventricular nodal tachycardia and left ventricular outflow tract tachycardia in the same patient during one session.     

Emergency epicardial dissection of the accessory pathway in a patient with atrioventricular nodal reentrant tachycardia]

Diagnostic and therapeutic problems in 14 year old patient with concealed WPW syndrome were presented. Paroxysms of atrio-ventricular reentrant tachycardia 180-220/min were frequently recurring, usually with normal QRS pattern. Tachycardias often had to be terminated by intravenous administration of antiarrhythmic drugs. Long term treatment with various antiarrhythmic agents did not prevent recurrence of tachycardias but they became sustained and were recurring more often. Their other side effects manifested with sinus node disfunction and depression of the heart muscle. The electrophysiologic study revealed right anterior septal accessory pathway. Epicardial dissection of the accessory pathway was urgently performed. The control electrophysiologic study revealed no evidence of conduction through the accessory pathway. The patient did not require antiarrhythmic treatment. During the 12 months follow up no tachycardia occurred.     

AH jump duration is associated with elimination of slow pathway during ablation of atrioventricular nodal reentrant tachycardia

IntroductionAblating the slow pathway (SP) is the superior treatment for atrioventricular nodal reentrant tachycardia (AVNRT) with a low complication rate. However, the ablation of the SP could result in either complete elimination or modification of the SP. We aimed to investigate whether the duration of AH jump pre-ablation associated with the outcome of elimination of SP.MethodsWe included 56 patients with typical AVNRT (slow-fast), 20 males and 36 females, aged 44.2 ± 15.1 years. Slow pathway ablation was performed using classical approach. Univariate and multivariate analysis was performed for potential predictors of SP elimination.ResultsTypical AVNRT was inducible in all patients. Post-ablation, non-inducibility of AVNRT was obtained in all 56 (100%) patients, with SP elimination in 33 (61%) patients and SP modification in 23 (39%) patients. Patients with SP elimination had significantly longer AH jump than patients with SP modification. Cox regression analysis showed that AH jump duration was the independent predictor of SP elimination, in which every 20 ms increase in AH jump duration was associated with 1.30 higher rate of SP elimination. Furthermore, ROC curve analysis indicated that the AH jump duration of ≥100 ms had 6.14 times higher probability for complete elimination of the SP with a sensitivity of 79%, specificity of 70%, PPV of 79% and NPV of 70%.ConclusionsAH jump duration pre-ablation is associated with complete elimination of slow pathway during AVNRT ablation.     

The HAV pattern in pediatric patients with atrioventricular node reentrant tachycardia

ObjectivesThe purpose of this study is to assess the prevalence of a His-Atrial-Ventricular (HAV) pattern, i.e. the atrial electrogram following the His bundle -HB- electrogram and preceding the ventricular one, on the catheter placed in the His position in pediatric patients during typical atrioventricular node reentry (AVNRT).Materials and methodsThe pediatric electrophysiology databases of two separate institutions were queried for patients with a diagnosis of AVNRT. Demographic, clinical data and the electrophysiology study (EPS) information were assessed.ResultsThirty-nine consecutive patients were included. Twenty-five were female. The average age at the time of the EPS was 12 ± 3.7 years. Induction was achieved with atrial pacing in 23, with a single atrial extra stimulus in 8 and with dual atrial extra stimuli in 8. Isoproterenol was needed to induce tachycardia in 21. Tachycardia cycle length averaged 320 ± 50 ms. An HAV pattern was present in 35 (74%) of the patients, and in 100% of the patients younger than 8.ConclusionsAn HAV pattern on the catheter placed in the His position, is common in pediatric patients with AVNRT, occurring in up to 74% of the patients in this population, being more common in younger patients.     

Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia.

A woman with tachycardia associated with polyuria was investigated. Electrophysiological analysis showed that the tachycardia was an atrioventricular nodal re-entrant tachycardia. Programmed stimulation was then used to provoke and sustain the tachycardia for 40 minutes. Polyuria, with an appreciable increase in free water clearance, was observed. This was associated with reduction in plasma and urinary arginine vasopressin concentrations. Appreciable natriuresis also developed. These results support the hypothesis that the polyuria with increased free water clearance and the natriuresis occurring during sustained tachycardia in man are due to inhibition of secretion of vasopressin and the release of natriuretic factor.     

L-type calcium current in right ventricular outflow tract myocytes of rabbit heart

The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this because of the technical difficulties associated with examining this theory. The L-type calcium current (I _Ca-L), an important inward current of the action potential (AP), plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular (RV) and RVOT cardiomyocytes, and differences in electrophysiological characteristics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and I _Ca-L were investigated using the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration (APD) than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolarization (EAD) and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a higher current density for I _Ca-L than RV myocytes (RVOT (13.16±0.87) pA pF⁻¹, RV (8.59±1.97) pA pF⁻¹; P<0.05). The I _Ca-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine (10 μmol L⁻¹), which blocks the I _Ca-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for I _Ca-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.     

Right bundle branch block pattern after uncomplicated right ventricular outflow tract pacing in a patient with a left sided superior vena cava and corrected tetralogy of Fallot

Usually an electrocardiogram after right ventricular (RV) pacing should yield left bundle branch block (LBBB) pattern. However, the presence of right bundle branch block (RBBB) pattern after pacemaker implantation should alert the physician to a malposition of lead. We report a case of 18-year-old female who underwent dual chamber pacemaker implantation and had RBBB pattern post implantation. Detailed evaluation revealed an uncomplicated right ventricular outflow tract pacing. The possible causes of this abnormal pattern after an uncomplicated RV pacing are also reviewed.     

Heterogeneous expression of connexin 43 in the myocardium of rabbit right ventricular outflow tract

The right ventricular outflow tract (RVOT) has been demonstrated as an important focus in idiopathic ventricular arrhythmias. However, the role of the gap junction in this region in arrhythmic events has not been fully investigated. The purpose of this study was to evaluate the expression and distribution of the gap junction protein connexin 43 (Cx43) in the myocardium of the RVOT area of normal adult rabbits. Tissue samples were obtained from 6 regions of normal rabbit heart, i.e. the left ventricle (LV) free wall, the LV papillary muscle, the RVOT free wall, and the RVOT septum which was subdivided into the RV side, the central layer, and the LV side. Immunohistochemical analysis was performed to investigate the characteristics of Cx43 distribution in the RVOT area. In the LV free wall and papillary muscle, Cx43 was abundantly, homogeneously, and approximately equally expressed in end-to-end- and side-to-side intercellular connections. In the free wall of the RVOT, Cx43 expression was poor compared to both these LV regions and side-to-side cell connections were predominant. Cx43 was as richly and homogeneously distributed in the central layer and LV side of the RVOT septum as in the two LV regions. However, in the RV side of the RVOT septum, its distribution was scant and an unstained area was noted. The heterogeneous expression of Cx43 in the RVOT area may serve as substrate for idiopathic ventricular arrhythmia.     

Correlation between the sudden jump-like increases of the atrio-Hisian interval induced during burst atrial pacing and during programmed atrial stimulation in patients with atrioventricular nodal reentrant tachycardia

Purpose

To study the correlation between the sudden prolongations of the atrio-Hisian (AH) interval with ≥50 ms during burst and programmed atrial stimulation, and to define whether the AH jump during burst atrial pacing is a reliable diagnostic criterion for dual AV nodal physiology.

Calcium dysregulation increases right ventricular outflow tract arrhythmogenesis in rabbit model of chronic kidney disease

Chronic kidney disease (CKD) increases the risk of arrhythmia. The right ventricular outflow tract (RVOT) is a crucial site of ventricular tachycardia (VT) origination. We hypothesize that CKD increases RVOT arrhythmogenesis through its effects on calcium dysregulation. We analysed measurements obtained using conventional microelectrodes, patch clamp, confocal microscopy, western blotting, immunohistochemical examination and lipid peroxidation for both control and CKD (induced by 150 mg/kg neomycin and 500 mg/kg cefazolin daily) rabbit RVOT tissues or cardiomyocytes. The RVOT of CKD rabbits exhibited a short action potential duration, high incidence of tachypacing (20 Hz)-induced sustained VT, and long duration of isoproterenol and tachypacing-induced sustained and non-sustained VT. Tachypacing-induced sustained and non-sustained VT in isoproterenol-treated CKD RVOT tissues were attenuated by KB-R7943 and partially inhibited by KN93 and H89. The CKD RVOT myocytes had high levels of phosphorylated CaMKII and PKA, and an increased expression of tyrosine hydroxylase-positive neural density. The CKD RVOT myocytes exhibited large levels of I_to, I_Kr, NCX and L-type calcium currents, calcium leak and malondialdehyde but low sodium current, SERCA2a activity and SR calcium content. The RVOT in CKD with oxidative stress and autonomic neuron hyperactivity exhibited calcium handling abnormalities, which contributed to the induction of VT.     

Spatial and temporal heterogeneities are localized to the right ventricular outflow tract in a heterozygotic Scn5a mouse model

Ventricular tachycardia (VT) in Brugada Syndrome patients often originates in the right ventricular outflow tract (RVOT). We explore the physiological basis for this observation using murine whole heart preparations. Ventricular bipolar electrograms and monophasic action potentials were recorded from seven epicardial positions in Langendorff-perfused wild-type and Scn5a+/- hearts. VT first appeared in the RVOT, implicating it as an arrhythmogenic focus in Scn5a+/- hearts. RVOTs showed the greatest heterogeneity in refractory periods, response latencies, and action potential durations, and the most fractionated electrograms. However, incidences of concordant alternans in dynamic pacing protocol recordings were unaffected by the Scn5a+/- mutation or pharmacological intervention. Conversely, particularly at the RVOT, Scn5a+/- hearts showed earlier and more frequent transitions into discordant alternans. This was accentuated by flecainide, but reduced by quinidine, in parallel with their respective pro- and anti-arrhythmic effects. Discordant alternans preceded all episodes of VT. The RVOT of Scn5a+/- hearts also showed steeper restitution curves, with the diastolic interval at which the gradient equaled one strongly correlating with the diastolic interval at which discordant alternans commenced. We attribute the arrhythmic tendency within the RVOT to the greater spatial heterogeneities in baseline electrophysiological properties. These, in turn, give rise to a tendency to drive concordant alternans phenomena into an arrhythmogenic discordant alternans. Our findings may contribute to future work investigating possible pharmacological treatments for a disease in which the current mainstay of treatment is implantable cardioverter defibrillator implantation.     

An uncommon case of spontaneous conversion from AV re-entry tachycardia to AV nodal re-entry tachycardia in a patient with dual tachycardia

We report the case of a 46-year old patient in whom an electrophysiology study (EP) was performed due to paroxysmal supraventricular tachycardia documented in 12-lead ECG. During the EP study, supraventricular tachycardia was induced easily and it corresponded to orthodromic AV reentry tachycardia (AVRT) using a concealed left free wall accessory pathway. However, during the study AVRT spontaneously and repeatedly converted to the typical slow-fast AV node reentry tachycardia (AVNRT). Both accessory and AV nodal slow pathways were ablated, due to the finding that both AVRT and AVNRT were independently inducible during the EP study.     

Mapping of reentrant spontaneous polymorphic ventricular tachycardia in a Scn5a+/- mouse model

Two major mechanisms have been postulated for the arrhythmogenic tendency observed in Brugada Syndrome (BrS): delays in conduction or increased heterogeneities in repolarization. We use a contact mapping system to directly investigate the interacting roles of these two mechanisms in arrhythmogenesis using a genetic murine model for BrS for the first time. Electrograms were obtained from a multielectrode recording array placed against the left ventricle and right ventricle (RV) of spontaneously beating Langendorff-perfused wild type (WT) and Scn5a+/- mouse hearts. Scn5a+/- hearts showed activation waves arriving at the epicardial surface consistent with slowed conduction, which was exacerbated in the presence of flecainide. Lines of conduction block across the RV resulting from premature ventricular beats led to the formation of reentrant circuits and polymorphic ventricular tachycardia. WT hearts showed an inverse relationship between activation times and activation recovery intervals measured at the epicardial surface, which resulted in synchronicity of repolarization times. In contrast, Scn5a+/- hearts, despite having smaller mean activation recovery intervals, demonstrated a greater heterogeneity compared with WT. Isochronal maps showed that their normal activation recovery interval gradients at the epicardial surface were disrupted, leading to heterogeneity in repolarization times. We thus directly demonstrate the initiation of arrhythmia in the RV of Scn5a+/- hearts. This occurs as a result of the combination of repolarization heterogeneities leading to lines of conduction block and unidirectional conduction, with conduction slowing allowing the formation of reentrant circuits. The repolarization heterogeneities may also be responsible for the changing pattern of block, leading to the polymorphic character of the resulting ventricular tachycardia.     

Fate of the autologous tri-cusp-valved pericardial conduit in the right ventricular outflow tract of growing pigs.

No perfect valve or valved conduit is currently available to reconstruct the right ventricular outflow tract (RVOT) in pediatric patients. To investigate the fate of autologous pericardial valved conduit, twenty piglets weighing 12.2 +/- 1.4 kg were divided into two groups. In 10 of them, the pericardium was immersed in 0.6% glutaraldehyde for 5 minutes (Gr PG) and then washed with normal saline. In the other 10 pigs, the pericardium was immersed in normal saline only (Gr PN) after procurement. Afterwards the autologous pericardium was tailored as designed to build a tri-cusp-valve inside the pericardial conduit with reconstruction of the sinus of Valsalva. This conduit was connected to the pulmonary trunk (PT) distally and RVOT proximally without a pump. The PT was then doubly ligated just above the annulus. The pigs survived 114 +/- 92 days in Gr PG and 82 +/- 50 days in Gr PN. The body weight increased to 42 +/- 29 kg in Gr PG and 30 +/- 9 kg in Gr PN. No cusps adhered to the conduit wall in either group. In Gr PN, the valve became retracted; in 7 of them an aneurysm developed proximal to the stenotic pulmonary valve, while only one pig in Gr PG developed an aneurysm. In Gr PG, the leaflet and conduit showed evidence of growth. In contrast, no evidence of valve growth was found in Gr PN. Calcification was evident more in Gr PG than in Gr PN either on the leaflet (9/10 vs. 5/10) or in the wall of conduit (8/10 vs. 6/10), but the differences were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)