Effects of enhanced parasympathetic tone on atrioventricular nodal conduction during atrioventricular nodal reentrant tachycardia

The effects of various physiologic and pharmacologic stimuli on the anterograde slow pathway in patients with atrioventricular nodal reentrant tachycardia are well characterized. We sought to further characterize the nature of anterograde and retrograde conduction during tachycardia and to define the differential input of the parasympathetic nervous system to these pathways. A custom-made neck suction collar was placed to stimulate the carotid body baroreceptors during supraventricular tachycardia. Neck suction at -60 mm Hg was applied and changes in tachycardia cycle length, AH, and ventriculoatrial intervals were measured in 20 patients. These measurements were repeated after intravenous administration of 10 mg of edrophonium to enhance vagal tone. We observed a 15 +/- 6 ms increase in tachycardia cycle length from baseline (p <0.0001) and a 14 +/- 6 ms increase in AH interval (p <0.0001), but no change in the VA interval with neck suction alone. The tachycardia cycle length prolonged 26 +/- 55 ms (p <0.0001) with edrophonium and an additional 12 +/- 43 ms (p <0.001) with neck suction after edrophonium. There was no change in the VA interval before or after edrophonium during neck suction. There were 10 tachycardia terminations in 8 patients during anterograde slow pathway block during neck suction, with tachycardia cycle length prolongation and mean AH prolongation before termination of 45 +/- 37 ms (vs 15 +/- 7 ms increase in AH interval without tachycardia termination, p = 0.10). There were 12 tachycardia terminations in 4 patients with retrograde block during neck suction, only after edrophonium, without any preceding change in tachycardia cycle length during 11 episodes. We conclude that anterograde slow pathway demonstrates gradual conduction slowing with parasympathetic enhancement, whereas retrograde fast pathway responds with abrupt block.     

Catheter ablation for the common type of atrioventricular nodal reentrant tachycardia

Radiofrequency (RF) catheter ablation of the slow AV nodal pathway was attempted in 34 patients with common type of AV nodal reentrant tachycardia (AVNRT). Radiofrequency energy of 18-32 watts was applied for 30-60 seconds at sites exhibiting atrial-slow pathway potentials or slow potentials. These potentials were recorded at the mid or posterior septum, anterior to the coronary sinus ostium. A mean of two radiofrequency applications successfully eliminated AVNRT in all patients. The incidence of junctional ectopy was significantly higher during 34 effective applications of radiofrequency energy than during 36 ineffective applications (100% versus 17%). Thus, the recording of atrial-slow pathway potentials or slow potentials, and the development of junctional ectopy can be used as a marker for successful ablation. Slow AV nodal conduction was eliminated in 22 patients and persisted without inducible AVNRT in 12. None of the patients had recurrences of AVNRT over a mean follow-up interval of 12 months, and all had preserved AV conduction. Long-term follow-up studies with an electrophysiological method confirmed that the ablation was effective. Transient AV block was observed in only 1 patient, and no major complications were noted. Thus, radiofrequency catheter ablation of the slow AV nodal pathway is highly effective and safe, with a low rate of complication, for the treatment of common type of AVNRT.     

Adenosine-sensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area

INTRODUCTION: Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 +/- 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unaffected after successful ablation. CONCLUSION: There may be an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can be ablated without disturbing AV nodal conduction from the right atrial septum.     

Absence of junctional rhythm during successful slow-pathway ablation in patients with atrioventricular nodal reentrant tachycardia

BACKGROUND: The presence of junctional rhythm has been considered to be a sensitive marker of successful slow-pathway ablation. However, in rare cases, junctional rhythm was absent despite multiple radiofrequency applications delivered over a large area in the Koch's triangle, and successful ablation was achieved in the absence of a junctional rhythm. METHODS AND RESULTS: This study included 353 patients with AV nodal reentrant tachycardia (143 men and 210 women; mean age, 50+/-17 years) who underwent catheter ablation of the slow pathway. Combined anatomic and electrogram approaches were used to guide ablation. Inducibility of AV nodal reentrant tachycardia was assessed after each application of radiofrequency energy. Successful sites were located in the posterior area in 18 (90%) of 20 patients without junctional rhythm during slow-pathway ablation compared with 200 (60%) of 333 patients with junctional rhythm (P<0.001). The fast-slow form of tachycardia was more common in patients without than in those with junctional rhythm (30% versus 3%; P=0.001). At the successful ablation sites, patients with junctional rhythm had a higher incidence of a multicomponent or slow-pathway potential (51% versus 10%; P<0.001), a longer duration of the atrial electrogram (64+/-8 versus 50+/-9 ms; P=0.04), and a smaller atrial/ventricular electrogram amplitude ratio (0.29+/-0.18 versus 0.65+/-0.27; P<0. 001) than those without junctional rhythm. Mean temperatures at successful sites (56+/-6 degreesC versus 58+/-9 degreesC; P=0.57) and incidence of transient AV block (2% versus 0%; P=0.86) were similar between patients with and without junctional rhythms. By multivariate analysis, location of ablation sites, atrial/ventricular electrogram amplitude ratio, absence of a multicomponent or slow-pathway potential, and occurrence of the fast-slow form of tachycardia were independent predictors of the absence of a junctional rhythm during successful slow-pathway ablation. CONCLUSIONS: In some rare cases, successful slow-pathway ablation is possible in the absence of a junctional rhythm.     

Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves

BACKGROUND: Although typical atrioventricular nodal reentrant tachycardia (AVNRT) with discontinuous AV node function curves has been well studied, there has been a lack of any significant information about AVNRT without evidence of dual AV nodal pathway physiology during atrial extrastimulus testing or atrial pacing. METHODS AND RESULTS: Group 1 included 9 patients with continuous curves during atrial extrastimulus testing but without a jump (> or = 50 ms) of the atrial-His bundle (AH) interval during incremental atrial pacing. The maximal AH interval during atrial pacing (266 +/- 61 versus 168 +/- 27 ms, P = .007) or extrastimulus testing (290 +/- 60 versus 176 +/- 18 ms, P = .005) shortened significantly after ablation. Antegrade and retrograde AV node properties were similar before and after ablation. Group 2 included 14 patients with continuous curves and a jump of the AH interval during incremental atrial pacing. The atrial pacing cycle length with 1:1 AV conduction and effective refractory period (ERP) of the antegrade AV node increased significantly, whereas the maximal AH interval during atrial pacing (358 +/- 70 versus 203 +/- 28 ms, P = .001) or extrastimulus testing (338 +/- 75 versus 196 +/- 34 ms, P = .002) shortened significantly after ablation. Group 3 included 24 patients with discontinuous curves. The maximal AH interval during atrial pacing or extrastimulus testing and the ERP of the antegrade fast AV node shortened, whereas the ERP of the antegrade AV node increased significantly after ablation. The maximal AH interval before ablation, extent of decrease in maximal AH interval after ablation, ERP of the retrograde AV node before ablation, and tachycardia cycle length were significantly shorter in group 1 than groups 2 and 3. CONCLUSIONS: In AVNRT with continuous AV node function curves, dual AV nodal pathway physiology may or may not be demonstrated during atrial pacing. Significant shortening of the maximal AH interval during atrial pacing after radiofrequency ablation suggests successful elimination of AVNRT.     

Difficulties with pharmacologic treatment of a patient with atrioventricular nodal reentrant tachycardia

A case history of a 38 year old teacher with AVNRT is described. She had been treated for 11 years with 11 antiarrhythmic drugs in various combinations. No treatment prevented recurrence of arrhythmia. During long term treatment with class IA, IC, II, III and IV antiarrhythmic drugs, various side effects occurred. There was also suspicion of proarrhythmic effect, especially of prajmaline. Some of the drugs terminated tachycardia while administered intravenously. But often deep hypotonia, heart automatism disturbances and even asystole occurred, MAS syndrome occurred 5 times. The patient was referred to our laboratory to perform percutaneous radiofrequency ablation of the slow pathway. The procedure was performed without any complications. Efficacy of the ablation was proved by electrophysiologic study before and after intravenous atropine administration. During the 11 months follow-up the patient had no tachycardia. She is on no antiarrhythmic medication and continues her normal activity.     

Effects of pharmacological autonomic blockade on dual atrioventricular nodal pathways physiology in patients with slow-fast atrioventricular nodal reentrant tachycardia

The purpose of this study was to investigate the atrioventricular AV nodal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 +/- 17 years) with clinical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71%) of 17 patients still demonstrated AV nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 +/- 105 ms vs 630 +/- 80 ms, P < 0.005) and AV blocking cycle length (365 +/- 64 ms vs 338 +/- 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and functional refractory period of the fast pathway (369 +/- 67 ms vs 305 +/- 73 ms, P < 0.005; 408 +/- 56 ms vs 350 +/- 62 ms, P < 0.005) and the slow pathway (271 +/- 30 ms vs 258 +/- 27 ms, P < 0.01; 344 +/- 60 ms vs 295 +/- 50 ms, P < 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 +/- 94 ms vs 326 +/- 89 ms, NS) and effective refractory period of retrograde fast pathway (228 +/- 38 ms vs 240 +/- 80 ms, NS) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the decreased inducibility of clinical AVNRT.     

Relation between impedance and electrode temperature during radiofrequency catheter ablation of accessory pathways and atrioventricular nodal reentrant tachycardia

OBJECTIVES: To evaluate and compare the clinical efficacy, impact on hemodynamics, safety profiles, and cost of combined administration of propofol and midazolam (synergistic sedation) vs. midazolam and propofol administered as sole agents, for sedation of mechanically ventilated patients after coronary artery bypass grafting. DESIGN: Prospective, controlled, randomized, double-blind clinical trial. SETTING: Intensive care unit of SCIAS-Hospital de Barcelona. PATIENTS: Seventy-five mechanically ventilated patients who underwent coronary artery bypass graft surgery under low-dose opioid anesthesia. INTERVENTIONS: According to the double-blind method, patients were randomly assigned to receive propofol (n = 25), midazolam (n = 25), or propofol combined with midazolam (n = 25). Infusion rates were adjusted to stay between 8 and 11 points on Glasgow Coma Score modified by Cook and Palma. MEASUREMENTS AND MAIN RESULTS: Mean +/- SD duration of sedation was 14.4 +/- 1.5 hrs, 14.1 +/- 1.1 hrs, and 14.7 +/- 1.9 hrs for the propofol, midazolam, and synergistic groups, respectively. The induction dose was 0.55 +/- 0.05 mg/kg for propofol as sole agent, 0.05 +/- 0.01 mg/kg for midazolam as sole agent, and 0.22 +/- 0.03 mg/kg for propofol administered in combination with 0.02 +/- 0.00 mg/kg of midazolam (p = .001). The maintenance dose was 1.20 +/- 0.03 mg/kg/hr for propofol as sole agent, 0.08 +/- 0.01 mg/kg/hr for midazolam as sole agent, and 0.50 +/- 0.09 mg/kg/hr for propofol administered in combination with 0.03 +/- 0.01 mg/kg/hr of midazolam (p < .001). All sedative regimens achieved similar efficacy in percentage of hours of adequate sedation (93% for propofol, 88% for midazolam, and 90% for the synergistic group, respectively). After induction, both propofol and midazolam groups had significant decreases in systolic blood pressure, diastolic blood pressure, left atrial pressure, and heart rate. Patients in the synergistic group had significant bradycardia throughout the study, without impairment in other hemodynamic parameters. Patients sedated with propofol or synergistic regimen awoke sooner and could be extubated before those patients sedated with midazolam (0.9 +/- 0.3 hrs and 1.2 +/- 0.6 hrs vs. 2.3 +/- 0.8 hrs, respectively, p = .01). Synergistic sedation produced cost savings of 28% with respect to midazolam and 68% with respect to propofol. CONCLUSIONS: In the study conditions, the new synergistic treatment with propofol and midazolam administered together is an effective and safe alternative for sedation, with some advantages over the conventional regimen with propofol or midazolam administered as sole agents, such as absence of hemodynamic impairment, >68% reduction in maintenance dose, and lower pharmaceutical cost.     

Dimension and related anatomical distance of Koch's triangle in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: The dimension of Koch's triangle in patients with AV nodal reentrant tachycardia has not been well described. Understanding the dimension and anatomical distance related to Koch's triangle might be useful in avoiding accidental AV block during ablation of the slow pathway. The purposes of this study were to define the dimension of Koch's triangle and its related anatomical distance and correlate these parameters with the successful ablation sites in patients with AV nodal reentrant tachycardia. METHODS AND RESULTS: We studied 218 patients with AV nodal reentrant tachycardia. The distance between the presumed proximal His-bundle area and the base of the coronary sinus orifice (DHis-OS) measured in the right anterior oblique view was used to define the dimension of Koch's triangle. The distance of the proximal His-bundle recording site from the successful ablation site (DHis-Ab) and the distance as a fraction of the entire length of Koch's triangle (DHis-Ab/DHis-Os) were determined. The mean DHis-Os and DHis-Ab were 25.9 +/- 7.9 and 13.4 +/- 3.8 mm, respectively. DHis-Os negatively correlated with patient age (r = -0.41, P < 0.0001) and body mass index (r = -0.18, P = 0.004). Among the patients with successful ablation sites in the medial area, DHis-Os was longer (27.2 +/- 6.6 vs 24.6 +/- 8.4 mm, P < 0.005), DHis-Ab was similar (12.9 +/- 3.1 vs 13.9 +/- 4.0, P > 0.05) and DHis-Ab/DHis-Os was smaller (0.48 +/- 0.04 vs 0.74 +/- 0.11, P < 0.05). Furthermore, the patients with successful ablation sites in the medial location needed more radiofrequency pulse numbers than those in the posterior location (6 +/- 4 vs 4 +/- 3, P < 0.05). CONCLUSION: The site of successful slow pathway ablation was consistently about 13 mm from the site recording the proximal His-bundle deflection in patients with AV nodal reentrant tachycardia despite marked variability in the dimensions of Koch's triangle; therefore, patients with large triangles required ablation in the medial region rather than the posterior region. Care should be taken when delivering radiofrequency energy to the posteroseptal area in patients with shorter DHis-Os to avoid injury to AV node.     

Radiofrequency ablation in a patient with tachycardia incorporating triple free wall accessory pathways and atrioventricular nodal reentrant tachycardia

Bone marrow cells from 15 patients with normal deoxyuridine (dU) suppression test results, 3 healthy subjects, and 11 patients with megaloblastic anemia caused by vitamin B12 or folate deficiency were examined for misincorporation of uracil into DNA. Cells were incubated with [5-3H] uridine for 2 hours and their DNA extracted. The DNA was hydrolyzed to deoxyribonucleosides with DNase 1, phosphodiesterase and alkaline phosphatase, and any dU present was separated from other deoxyribonucleosides by Aminex A6 chromatography. The quantity of dU/mg DNA and the radioactivity in the dU peak/mg DNA were then calculated. The results clearly showed that there was markedly increased uracil misincorporation into the DNA of vitamin B12- or folate-deficient marrow cells. Misincorporation of uracil into DNA may be an important biochemical lesion underlying both the megaloblastic change and the ineffectiveness of hematopoiesis in vitamin B12 and folate deficiency.     

A randomized comparison of fixed power and temperature monitoring during slow pathway ablation in patients with atrioventricular nodal reentrant tachycardia

In the present study, using sodium dodecyl sulphate-polyacrylamide gel electrophoresis and Western blot techniques, the patterns of proteins extracted from C. neoformans yeast cells were analysed. A major 105 kilodalton (kDa) antigen that binds to Concanavalin A and cross-reacts with anti-mannan antibodies was identified. The 105 kDa mannoprotein, highly expressed in the acapsular mutant of C. neoformans with respect to the encapsulated strain, is involved in the lymphoproliferative response of T lymphocytes to Cryptococcus-sensitized monocytes.     

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. METHODS AND RESULTS: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). CONCLUSION: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.     

Case report: radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia in a patient with heart transplantation

We have assessed hepatocellular integrity in patients anaesthetized with desflurane or isoflurane using glutathione transferase Alpha (GSTA) as a sensitive indicator. Volatile anaesthetic was administered to 72 women at 0.7 MAC for 25 min and thereafter at 1.0 MAC. GSTA was measured with a time-resolved immunofluorometric assay in serum samples. Mild or moderate increases in GSTA were found in approximately 40% of patients immediately after anaesthesia. In the desflurane group (n = 30) the increase in GSTA concentration was from a baseline value of the geometric mean of 1.3 microgram litre-1 (95% confidence interval 0.9-1.9 microgram litre-1) to a peak of 2.6 (1.8-3.8) micrograms litre-1. The corresponding increase in the isoflurane group (n = 31) was from 1.3 (0.9-1.9) microgram litre-1 to 3.0 (2.2-4.2) micrograms litre-1. The change in GSTA concentration was significant in both groups but not between groups. No predictive factors for the increase in GSTA concentrations were found. Increased GSTA concentrations were not accompanied by increases in amino-transferases. We conclude that desflurane and isoflurane anaesthesia were associated with a mild subclinical disturbance of hepatocellular integrity.     

Successful slow pathway ablation in a patient with atrioventricular nodal reentrant tachycardia having a proximal common pathway

Radiofrequency catheter ablation was attempted in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). AVNRT was easily inducible but an intermittent loss of the atrial activation was observed during AVNRT suggesting the presence of a proximal common pathway. During sinus rhythm, a relatively delayed activation that was compatible with a slow potential, was recorded anterior to the ostium of coronary sinus, and radiofrequency catheter ablation application (20 watts) to the site induced junction tachycardia. After an additional radiofrequency catheter ablation application to close the site, AVNRT became noninducible without deterioration of atrioventricular conduction through a fast pathway. This is the first case in which radiofrequency catheter ablation application to the slow potential recording site has been successful, even in AVNRT having a proximal common pathway.     

Radiofrequency catheter ablation of atrioventricular junctional ("AV nodal") reentrant tachycardia in patients with implantable cardioverter defibrillators

Catheter ablation of tachycardias has been undertaken successfully in patients with ICDs without damage to the ICD or lead. Ablation of the slow AV nodal pathway, however, is technically challenging because the lead of the ICD lies close to the ablation site. We report successful ablation of AV junctional reentrant tachycardia (AVJRT) in three patients with ICDs. In all cases, the ablation site was within a few millimeters of the ICD lead. The ablation was successful in all cases and did not cause damage to the ICD or lead. The patients have remained free of recurrence of AVJRT during a mean follow-up of 12 months.     

Atrioventricular nodal reentrant tachycardia in patients with ventriculo-atrial conduction block

OBJECTIVE: To demonstrate the reversibility of retrograde ventriculo-atrial block by isoproterenol in patients with atrioventricular nodal reentrant tachycardia (AVNRT). DESIGN: Three case reports and their electrophysiological features. PATIENTS: Three patients with documented or suspected paroxysmal supraventricular tachycardia. INTERVENTIONS: At routine electrophysiology study, no supraventricular tachycardia was inducible in the baseline state. Infusion of isoproterenol (1 to 5 micrograms/min) was given and stimulation procedures were repeated. RESULTS: At baseline, all three patients had discontinuous antegrade atrioventricular (AV) nodal conduction, but very poor (two patients) or absent (one patient) ventriculo atrial conduction prevented induction of AVNRT. During infusion of isoproterenol, retrograde conduction was enhanced so that 1:1 retrograde occurred to cycle lengths of 300, 340 and 260 ms. AVNRT was then inducible in all patients, reproducing their clinical symptoms. CONCLUSION: Absent or poor ventriculo-atrial conduction in patients with suspected AV node reentry does not preclude the development of tachycardia with sympathomimetic enhancement. Isoproterenol should be given to attempt reversal of retrograde block in these patients.