Distribution of contact force during impact to the hip

The aim of the present study was to investigate the effects of almokalant on sustained reentrant supraventricular tachycardias. Reentrant tachycardias were induced, using transesophageal atrial stimulation, in 82 patients with atrioventricular reentrant tachycardia (n = 54) or AV nodal reentrant tachycardia (n = 28). After a baseline procedure during which the tachycardia was induced and overdrive terminated, the tachycardia was reinduced and studied during 12 minutes of infusion of either placebo or almokalant, aiming at plasma concentrations of 20, 50, 100, and 150 nmol/l. Each patient was studied at two dose levels during the same procedure. There was an increase in the RR interval during tachycardia of 6% at 100 nmol/l (p = 0.001 vs. baseline tachycardia). The QT interval during tachycardia increased by 5% (p = 0.001) at 50 nmol/l and by 10% (p = 0.001) at 100 nmol/l. Bundle branch block during tachycardia developed in 13% during almokalant infusion, aiming at 20 nmol/l, in 25% at 50 nmol/l, in 50% at 100 nmol/l, and in 33% at 150 nmol/l. Rapid baseline tachycardia, increasing almokalant dose, and an increasing number of induced tachycardias correlated with the appearance of bundle branch block. In six patients with AV nodal reentrant tachycardia, 2:1 AV block occurred, in all cases preceded by bundle branch block. The QT prolongation during sustained tachycardia was larger in patients who were noninducible at the same plasma concentration level than in the inducible patients. Almokalant caused bundle branch block and 2:1 AV block during sustained supraventricular tachycardia. These findings emphasize the importance of studying drug effects at rates in the range of clinical tachycardias that expose the conduction system to the limits of its refractoriness.     

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.     

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.     

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.     

A gradient inverse planning algorithm with dose-volume constraints

There are still some AV nodal reentrant tachycardias with unusual AV nodal properties that need further study to understand these complexities. Accordingly, the two-dimensional model with alpha and beta pathways in the AV nodal reentrant tachycardia circuit certainly is an oversimplification and does not explain adequately the anatomic and physiologic complexity of the AV junctional area. The modern concept suggests that this arrhythmia takes place in a highly complex three-dimensional model with nonuniform anisotropy and discontinuous conduction property in the AV junctional area. Application of radiofrequency energy within the AV junctional area should always be performed carefully to achieve a successful ablation procedure and to minimize possible injury of AV nodal conduction.     

Different modes of cell death induced by 5-fluoro-2''-deoxyuridine in two clones of the mouse mammary tumor FM3A cell line

OBJECTIVES: To clarify the prevalence and mechanism of supraventricular tachycardia in patients with right atrial isomerism. BACKGROUND: Paired SA and dual atrioventricular (AV) nodes have been described in patients with right atrial isomerism. However, the clinical significance remains unclear. METHODS: From 1987 to 1996, a total of 101 patients (61 male, 40 female) and four fetuses were identified with right atrial isomerism. The diagnosis of supraventricular tachycardia exclude the tachycardia with prolonged QRS duration or AV dissociation, and primary atrial tachycardia. RESULTS: The median follow-up duration was 38 months (range 0.2-270 months). Supraventricular tachycardia was documented in 25 patients (24.8%) and one fetus (25%) (onset age ranged from prenatal to 14 years old; median 4 years old). Actuarial Kaplan-Meier analysis revealed that the probability of being free from tachycardia was 67% and 50% at 6 and 10 years of age, respectively. These tachycardias could be converted by vagal maneuvers in one, verapamil in seven, propranolol in four, digoxin in two, procainamide in one, and rapid pacing in five. Spontaneous conversion was noted in six (including the fetus). Seven cases had received electrophysiological studies. Reciprocating AV tachycardia could be induced in five and echo beats in one. The tachycardia in three patients was documented as incorporating a posterior AV node (antegrade) and an anterior or a lateral AV node (retrograde). Two of them received radiofrequency ablation. Successful ablation in both was obtained by delivering energy during tachycardia, aimed at the earliest retrograde atrial activity and accompanied by junctional ectopic rhythm. The patient with echo beats developed tachycardia soon after operation. CONCLUSIONS: Supraventricular tachycardia is common in patients with right atrial isomerism and can occur during the prenatal stage. Drugs to slow conduction through the AV node may help to terminate the tachycardia. Radiofrequency ablation is a safe and effective treatment alternative to eliminate tachycardia.     

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.     

Impact of severity of coronary artery stenosis and the collateral circulation on the functional outcome of dyssynergic myocardium after revascularization in patients with healed myocardial infarction and chronic left ventricular dysfunction

The inferoposterior region of the triangle of Koch is hypothesized to be the location of the atrial insertion of the slow atrioventricular (AV) nodal pathway. However, the actual site of conduction slowing in the slow AV nodal pathway is unknown. Entrainment mapping during AV nodal reentry can localize the reentrant pathway as follows: the AH interval measured from the mapping catheter = A'H (where A' is the exit site of the reentrant circuit) minus A'A (the conduction time from A' to the site of mapping); the SH interval during entrainment = SA' (the conduction time from stimulus into the reentry circuit) plus A'H. Thus, in all cases, the SH interval should be greater than or equal to the AH interval, and the deltaAH-SH should increase as distance and conduction time (SA' and A'A) from the reentry circuit increases. Fourteen patients with typical AV nodal reentry (cycle length 346 +/- 62 ms) and 1 with fast-slow (cycle length 430 ms) underwent activation and entrainment mapping from 8 to 12 sites in the triangle of Koch and coronary sinus. Pacing was performed at 2 to 3 mA above threshold, at a cycle length 10 ms shorter than tachycardia. A mapping site was defined as being in close proximity to the circuit if the deltaAH-SH was within 120% of the shortest 20th percentile deltaAH-SH value from all measured sites. In the 14 typical cases, 45 of 83 sites (54%) in the anatomic slow pathway region fulfilled criteria for close proximity to the reentry circuit compared with 13 of 50 sites (26%) outside of this region (p = 0.005). For these patients, the shortest SH interval measured from any entrainment site was 294 +/- 58 ms (89 +/- 10% of tachycardia cycle length, range 70% to 119%), indicating that the site of slow conduction in the slow pathway during AV nodal reentrant tachycardia was distal to all mapped sites. Thus, during typical AV nodal reentry, the "slow" pathway does not conduct slowly, and its insertion is located at or within the inferoposterior or midseptal regions in most cases.     

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.     

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.     

Malaise scores in adulthood of children and young people who have been in care

Junctional rhythm is commonly observed during radiofrequency catheter ablation of the fast or slow pathways of atrioventricular nodal reentrant tachycardia (AVNRT). However, the origin of these beats remains unclear. We analyzed the retrograde atrial activation sequence of 16 patients (mean +/- SD: 41.2 +/- 18.9 years old) undergoing catheter ablation for typical AVNRT with detailed catheter mapping of the triangle of Koch. The earliest atrial activations were concordant during tachycardia and junctional rhythm in only 5 of 16 patients. The findings suggest that junctional rhythm is unlikely to represent direct stimulation of the atrioventricular (AV) node via a discrete slow pathway but rather results from enhanced automaticity from > or =1 sites in the AV nodal transitional zone. The ensuing atrial activation pattern results from anisotropic spread from these sites. In addition, these data imply that the original concept of the AV node comprising 2 anatomically defined pathways may not be valid, and that a functionally defined pathway model may be a more accurate representation.     

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.     

Novel form of atrial tachycardia originating at the atrioventricular annulus

We report two patients with reentrant atrial tachycardia that originated at the AV annulus. Atrial tachycardia originated in the posterior portion of mitral annulus in one patient (case 1) and the posterolateral portion of tricuspid annulus in one patient (case 2). Tachycardia was successfully eliminated by RF catheter ablation in both patients, with the catheter placed underneath the mitral valve in case 1 and on the tricuspid annulus in case 2. Spiky potentials were recorded in the diastolic phase of the atrium during tachycardia at the sites of successful ablation. Spiky potentials were also recorded after atrial electrogram during sinus rhythm, and showed decremental properties during atrial pacing. An accelerated atrial rhythm was observed during RF application, and tachycardia could not be induced after ablation in either patient. Tachycardia in these patients seemed to be due to reentrant tachycardia originating in the accessory AV node (Mahaim fiber) without ventricular connection.     

Electrophysiological mechanisms and determinants of vagal maneuvers for termination of paroxysmal supraventricular tachycardia

BACKGROUND: The vagal maneuvers used for termination of paroxysmal supraventricular reentrant tachycardia (PSVT) appear to involve more complex mechanisms than we have known, and further study should be done to explore the possible mechanisms. METHODS AND RESULTS: In this study, 133 patients with PSVT and 30 age- and sex-matched control subjects were included. We assessed the effects of different vagal maneuvers on termination of PSVT and compared baroreflex sensitivity and beta-adrenergic sensitivity between the patients with PSVT and control subjects. Out of 85 patients with atrioventricular reciprocating tachycardia (AVRT), vagal maneuvers terminated in 45 (53%). Of these, 28 (33%) terminated in the antegrade limb and 17 (20%) terminated in the retrograde limb. Out of 48 patients with atrioventricular nodal reentrant tachycardia (AVNRT), vagal maneuvers terminated the tachycardia in the antegrade slow pathway (14%) or in the retrograde fast pathway (19%). Baroreflex sensitivity was poorer but isoproterenol sensitivity test better in patients with AVNRT. Poorer antegrade atrioventricular node conduction properties and better vagal response determined successful antegrade termination of AVRT by vagal maneuvers. Poorer retrograde accessory pathway conduction property but better vagal response determined successful retrograde termination of AVRT. Better sympathetic and vagal response associated with poorer retrograde atrioventricular node conduction determined retrograde termination of AVNRT by the Valsalva maneuver. CONCLUSIONS: Both the vagal response and conduction properties of the reentrant circuit determine the tachycardia termination by vagal maneuvers. Improved understanding of the interaction of autonomic and electrophysiological mechanisms in maintaining or terminating PSVT may provide important insight into the pathophysiology of these two tachycardias.     

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.     

Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia

OBJECTIVES: This study sought to present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may participate in typical AV node reentry. BACKGROUND: Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the preferred therapeutic approach in patients with AV node reentrant tachycardia. Despite the success achieved with this approach, electrophysiologic changes consistent with fast pathway ablation are occasionally observed. One potential explanation is the presence of an aberrant posterior fast pathway. METHODS: The location of fast and slow AV node pathways was determined by atrial activation mapping along the tricuspid valve annulus during tachycardia and was further confirmed by the effect of radiofrequency catheter ablation. RESULTS: Seven patients with AV node reentrant tachycardia had evidence of a posterior fast pathway near the coronary sinus os. Abolition of anterograde and retrograde fast pathway conduction followed radiofrequency ablation in the posteroseptal region in six patients. Consistent with fast pathway ablation, the AH interval increased from 70 +/- 24 to 195 +/- 35 ms (mean +/- SD), and tachycardia was no longer inducible. Selective slow pathway ablation was performed in one other patient with a posterior fast pathway. CONCLUSIONS: Functionally fast AV node pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed. These data delineate the limitation of an anatomically guided slow pathway ablative approach and emphasize the importance of detailed mapping and localization of the retrograde fast pathway exit site before ablation. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV block, complicating posteroseptal ablation in patients with AV node reentry.     

Cardiac anatomy and diastolic filling in professional road cyclists

The electrophysiologic effects of intravenous verapamil (0.15 mg/kg) and oral sustained-release verapamil (verapamil-SR) (240 mg once daily for 7 days) were studied in 17 patients with paroxysmal supraventricular tachycardia (SVT). Ten patients had atrioventricular (AV) nodal reentrant tachycardia and 7 had AV reciprocating tachycardia involving an accessory AV pathway. Both preparations significantly prolonged anterograde effective refractory period of the AV node and depressed the retrograde AV nodal conduction system. The sinus cycle length, and atrial and ventricular effective refractory periods were prolonged after oral verapamil-SR. Furthermore, oral verapamil-SR depressed retrograde accessory pathway conduction which was not interfered with by intravenous verapamil. Intravenous verapamil and oral verapamil-SR prevented induction of sustained SVT in 12 of 17 (71%) and 10 of 17 (59%) patients, respectively. Follow-up study with oral verapamil-SR 240 mg once daily in 15 patients for 19 +/- 6 months revealed that among the 8 patients without induction of sustained SVT, 7 have been free of symptomatic arrhythmia; only 1 patient had occasional SVT attacks. For the 7 patients with induction of sustained SVT, 3 patients failed to respond to oral verapamil-SR, 1 patient became symptom free, and the remaining 3 patients had less frequent SVT attacks. Thus, immediate intravenous verapamil testing predicts the electrophysiologic results of oral verapamil-SR therapy, and oral verapamil-SR once daily may be used for long-term prophylaxis of SVT with better patient compliance.     

Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia

OBJECTIVES: The purpose of this study was to prospectively compare in random fashion an anatomic and an electrogram mapping approach for ablation of the slow pathway of atrioventricular (AV) node reentrant tachycardia. BACKGROUND: Ablation of the slow pathway in patients with AV node reentrant tachycardia can be performed by using either an anatomic or an electrogram mapping approach to identify target sites for ablation. These two approaches have never been compared prospectively. METHODS: Fifty consecutive patients with typical AV node reentrant tachycardia were randomly assigned to undergo either an anatomic or an electrogram mapping approach for ablation of the slow AV node pathway. In 25 patients randomly assigned to the anatomic approach, sequential radiofrequency energy applications were delivered along the tricuspid annulus from the level of the coronary sinus ostium to the His bundle position. In 25 patients assigned to the electrogram mapping approach, target sites along the posteromedial tricuspid annulus near the coronary sinus ostium were sought where there was a multicomponent atrial electrogram or evidence of a possible slow pathway potential. If the initial approach was ineffective after 12 radiofrequency energy applications, the alternative approach was then used. RESULTS: The anatomic approach was effective in 21 (84%) of 25 patients, and the electrogram mapping approach was effective in all 25 patients (100%) randomly assigned to this technique (p = 0.1). The four patients with an ineffective anatomic approach had a successful outcome with the electrogram mapping approach. On the basis of intention to treat analysis, there were no significant differences between the electrogram mapping approach and the anatomic approach with respect to the time required for ablation (28 +/- 21 and 31 +/- 31 min, respectively, mean +/- SD, p = 0.7) duration of fluoroscopic exposure (27 +/- 20 and 27 +/- 18 min, respectively, p = 0.9) or mean number of radiofrequency applications delivered (6.3 +/- 3.9 vs. 7.2 +/- 8.0, p = 0.6). With both the anatomic and electrogram mapping approaches, the atrial electrogram duration and number of peaks in the atrial electrogram were significantly greater at successful target sites than at unsuccessful target sites. CONCLUSIONS: The anatomic and electrogram mapping approaches for ablation of the slow AV nodal pathway are comparable in efficacy and duration. If the anatomic approach is initially attempted and fails, the electrogram mapping approach may be successful at sites outside the areas targeted in the anatomic approach. With both the anatomic and electrogram mapping approaches, there are significant differences in the atrial electrogram configuration between successful and unsuccessful target sites.     

Paroxysmal atrial tachycardia with second-degree atrioventricular block

Paroxysmal atrial tachycardia with atrioventricular block usually indicates potentially dangerous overdigitalization, and serious heart disease is almost universally present. In this report, we describe a patient with a structurally normal heart who manifested spontaneously intra-atrial reentrant tachycardia with Wenckebach atrioventricular block in the absence of medications. In this patient, the longest atrial paced cycle length that induced atrioventricular nodal block was 390 ms, and the atrial cycle length during tachycardia ranged from 360 to 400 ms. The electrophysiologic study in our patient demonstrated that second-degree atrioventricular block during atrial tachycardia may occur in patients without structural heart diseases or taking any medication.     

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.