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W M Jackman

Publications and source records attributed to W M Jackman.

At least 37 records · Page 2Linked to original sources
PubMed1998

Evidence for multiple atrio-AV nodal inputs in the normal dog heart.

INTRODUCTION: Complete AV block after combined fast pathway (FP) and slow pathway (SP) ablation is uncommon. The purpose of this study was to interrupt activation of these and additional inputs by placing a radiofrequency lesion across the interatrial septum between the FP and SP ablation sites. METHODS AND RESULTS: In eight anesthetized open chest dogs, FP ablation induced significant A-H prolongation (deltaA-H: 51 +/- 14 msec; P < 0.001) and a shift of earliest retrograde atrial activation from the anterior septum to the region of the coronary sinus (CS) os. Subsequently, ablation of the interatrial septum across the fossa ovalis was successful in 5 of 8 dogs, changing the sequence of atrial activation (A) so that A at the His-bundle electrogram, which initially preceded A at the CS os (18 +/- 4 msec vs 46 +/- 7 msec, P < 0.01), now followed CS os A (81 +/- 31 msec vs 59 +/- 20 msec, P < 0.05). Additional ablation of the SP caused a type II Mobitz AV block or complete AV block in 5 of 8 dogs. The four dogs with complete AV block showed a stable, high junctional escape rhythm at a rate of 64 +/- 16 beats/min. Pacing between the ablation lesions and the AV node in one dog showed 1:1 AV conduction and Wenckebach-type AV block indicating preserved AV nodal function. Histology showed necrotic changes in the FP and SP transitional cell zones and in the atrial tissue of the interatrial septum. However, the compact AV node, His bundle, and adjacent atria and transitional cells were undamaged. CONCLUSION: There are additional AV nodal inputs in the interatrial septum in addition to the anterior FP and posterior SP inputs. Ablation of all of these may be required, if the aim is production of complete AV block proximal to the AV node with a high junctional escape rhythm.

Animals↗
PubMed1997

Electrophysiology of the right anterior approach to the atrioventricular node: studies in vivo and in the isolated perfused dog heart.

INTRODUCTION: Previous reports have described electrophysiologic properties and rate-dependent responses in the transitional cell zone of the posterior AV nodal input (slow pathway). The purpose of this study was to investigate the electrophysiology of the anterior transitional cell zone (fast pathway) in vivo and in a Langendorff preparation perfused with a nonblood solution containing butanedionemonoxime to inhibit contraction. METHODS AND RESULTS: In five anesthetized dogs, the His-bundle electrogram recorded from the aortic root included atrial activity in close proximity to the anterior limbus of the fossa ovalis. During decremental atrial pacing, the atrial potential exhibited amplitude alternans at a pacing cycle length (CL) of 135 +/- 14 msec. In ten isolated perfused canine hearts, a bipolar electrode catheter was positioned with its tip against the right anterior interatrial septum just superior to the tendon of Todaro. The AV Wenckebach CL (WCL) averaged 262 +/- 21 msec. During further decreases in pacing CL, the bipolar atrial potential developed a 2:1 amplitude alternans (9/10 dogs) at CL = 168 +/- 15 msec and then split into two components with subsequent 2:1 block between these components (10/10 dogs) at CL = 152 +/- 19 msec. Radiofrequency ablation at this site in six dogs prolonged the stimulus to HB interval from 113 +/- 19 to 151 +/- 30 msec (P < 0.01) without changing the WCL, consistent with ablation of the fast AV nodal pathway. In six other isolated perfused canine hearts, an octapolar catheter (2-mm spacing) was positioned along the anterior limbus of the fossa ovalis with the tip electrode located over the anterior portion (apex) of the triangle of Koch. The aforementioned 2:1 amplitude alternans occurred at a longer CL in the distal electrodes located at the tendon of Todaro than in the proximal electrodes at farther distances from the tendon of Todaro (185 +/- 25 vs 171 +/- 20 msec, P < 0.05), as did the 2:1 block between the two components (161 +/- 18 vs 150 +/- 18 msec, P < 0.05). Microelectrode recordings obtained adjacent to the catheter demonstrated 2:1 alternans and block patterns in the action potentials of transitional cells but not in atrial cells, which exhibited 1:1 conduction at all CL. CONCLUSIONS: The transitional cell zone in the anterior interatrial septum exhibits a specific rate-dependent, spatial gradient of conduction block, which can be recorded in bipolar electrograms as well as microelectrode recordings. Electrophysiologic changes induced by radiofrequency ablation of this anterior atrial/transitional cell zone (corroborated by histology) provide strong presumptive evidence that this area constitutes all or a major part of the fast AV nodal pathway.

Animals↗
PubMed1997

Electrophysiology of the atrio-AV nodal inputs and exits in the normal dog heart: radiofrequency ablation using an epicardial approach.

INTRODUCTION: We studied the effects of selective and combined ablation of the fast (FP) and slow pathway (SP) on AV and VA conduction in the normal dog heart using a novel epicardial ablation technique. METHODS AND RESULTS: For FP ablation, radiofrequency current (RFC) was applied to a catheter tip that was held epicardially against the base of the right atrial wall. SP ablation was performed epicardially at the crux the heart. Twenty-three dogs were assigned to two ablation protocols: FP/SP ablation group (n = 17) and SP/FP ablation group (n = 6). In 12 of 17 dogs, FP ablation prolonged the PR interval (97 +/- 10 to 149 +/- 22 msec, P < 0.005) with no significant change in anterograde Wenckebach cycle length (WBCL). Subsequent SP ablation performed in 8 dogs further prolonged the PR interval and the anterograde WBCL (117 +/- 22 to 193 +/- 27, P < 0.005). Complete AV block was seen in 1 of 8 dogs, whereas complete or high-grade VA block was seen in 6 of 8 dogs. In the SP/FP ablation group, SP ablation significantly increased WBCL with no PR changes. Combined SP/FP ablation in 6 dogs prolonged the PR interval significantly, but no instance of complete AV block was seen. VA block was found in 50% of these cases. Histologic studies revealed that RFC ablation affected the anterior and posterior atrium adjacent to the undamaged AV node and His bundle. CONCLUSION: Using an epicardial approach, combined ablation of the FP and SP AV nodal inputs can be achieved with an unexpectedly low incidence of complete AV block, although retrograde VA conduction was significantly compromised.

Animals↗
PubMed1997

Critical atrial site for ablation of pacing-induced atrial fibrillation in the normal dog heart.

INTRODUCTION: Radiofrequency catheter ablation (RFA) has been used recently to treat atrial fibrillation (AF). The purpose of this study was to investigate a new approach to preventing AF by RFA. METHODS AND RESULTS: In open chest, anesthetized dogs, AF (lasting > 30 sec) was induced after burst stimulation, and electrophysiologic parameters were recorded before and after RFA. In group 1 (9 dogs) we performed selective and combined slow and fast pathway RFA, whereas in group 2 (11 dogs) RFA was applied as a linear lesion at the mid-atrial septum between the inferior vena cava and the fossa ovalis. After ablation, the Wenckebach cycle length was significantly prolonged only in group 1 (194 +/- 23 vs 282 +/- 35 msec, P = 0.002), whereas the interval between the stimulus (S) artifact applied at the high right atrium to the His bundle (H) (SH interval) prolonged to the same extent in both groups (162 +/- 14 vs 146 +/- 45 msec, P = NS); group 1 due to an A-H prolongation whereas in group 2 it was due to an intra-atrial conduction delay. In group 1 AF still remained inducible, although with a longer mean R-R interval (215 +/- 16 vs 433 +/- 88 msec, P < 0.05). No instance of complete AV block developed. In group 2, sustained AF was noninducible in 10 dogs and its duration was markedly shorter in the remaining one (8 sec). Gross anatomy and histology did not reveal any damage inside of Koch's triangle, and particularly to the compact AV node. CONCLUSION: These findings suggest that RFA at the mid-atrial septum prevents AF in the normal dog heart. This approach might also be successful in those clinical settings in which the atrial septum plays a critical role in the maintenance of sustained AF.

Animals↗
PubMed1996

Para-Hisian pacing. A new method for differentiating retrograde conduction over an accessory AV pathway from conduction over the AV node.

BACKGROUND: Differentiation between ventriculoatrial (VA) conduction over an accessory AV pathway (AP) and the AV node (AVN) may be difficult, especially in patients with a septal AP. METHODS AND RESULTS: A new pacing method, para-Hisian pacing, was tested in 149 patients with AP and 53 patients without AP who had AV nodal reentrant tachycardia (AVNRT). Ventricular pacing was performed adjacent to the His bundle and proximal right bundle branch (HB-RB), initially at high output to capture both RV and HB-RB. The output was then decreased to lose HB-RB capture. The change in timing and sequence of retrograde atrial activation between HB-RB capture and noncapture was examined. Loss of HB-RB capture without change in stimulus-atrial (S-A) interval or atrial activation sequence indicated exclusive retrograde AP conduction. An increase in S-A interval without change in His bundle-atrial interval or atrial activation sequence indicated exclusive retrograde AVN conduction. A change in atrial activation sequence indicated the presence of both retrograde AP and AVN conduction. Para-Hisian pacing correctly identified retrograde AP conduction in 132 of 147 AP patients, including all septal and right free wall APs. Retrograde AVN conduction masked AP conduction in 9 of 34 patients with a left free wall AP and 6 of 9 patients with the permanent form of junctional reciprocating tachycardia. Para-Hisian pacing correctly excluded AP conduction in all 53 patients with AVNRT. CONCLUSIONS: Para-Hisian pacing reliably identifies retrograde conduction over septal and right free wall APs, but AVN conduction may mask APs located far from the pacing site or with a long retrograde conduction time.

Adolescent↗
PubMed1996

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success.

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.

Adult↗
PubMed1996

Thermal latency in radiofrequency ablation.

BACKGROUND: Progression of unintentionally induced atrioventricular delay is occasionally observed directly after termination of radiofrequency delivery in the vicinity of the atrioventricular node. We postulated that the application of a radiofrequency pulse may result in a tissue temperature rise that continues after the pulse. METHODS AND RESULTS: Using the thigh muscle preparation, 5-, 10-, 20-, and 30-second pulses were applied as 30 to 40 W via a standard 4-mm tip electrode with 10-g contact pressure. Forty-one undisturbed pulses were delivered while recording intramural temperatures at 2-, 4-, and 7-mm depth. Maximal "thermal latency" was observed with the shortest pulse duration and at greatest depth. With 5-second applications, tissue temperature at 7-mm depth peaked 11.6 seconds after termination of radiofrequency delivery and stayed above end-of-pulse value as long as 34.5 seconds after the pulse. The additional rise in tissue temperature was 2.9 degrees C. If only recording within the lesion border zone were considered, the duration of latency was maximal with 10-second pulses: an additional gain in tissue temperature of 3.4 degrees C was observed 6.4 seconds after the pulse while tissue temperature stayed above end-of-pulse value during 18.3 seconds. CONCLUSIONS: With relatively short applications, tissue temperature continues to rise after termination of radiofrequency delivery. This "thermal latency" may result in lesion growth after the pulse and may so explain the incidentally observed progression of conduction block after short pulses in the vicinity of the atrioventricular node. It also may explain the apparent discrepancy between lesion growth rate and intramural temperature rise studies.

Animals↗
PubMed1996

Anatomic substrate for idiopathic left ventricular tachycardia.

BACKGROUND: Idiopathic left ventricular tachycardia (ILVT) characterized by QRS complexes with right bundle-branch block (RBBB) morphology and left axis deviation is a distinct clinical syndrome that also demonstrates a characteristic response to verapamil and inducibility from the atrium in patients without structural heart disease. A false tendon has been described in the left ventricle in a patient with ILVT in whom surgical resection of the false tendon resulted in cure. We hypothesized that the false tendon is responsible for the genesis of similar ventricular tachycardia (VT) in others. METHODS AND RESULTS: We performed transthoracic (TTE) and/or transesophageal (TEE) two-dimensional echocardiograms in 15 patients undergoing catheter ablation for ILVT. There were 12 men and 3 women (mean age, 31 +/- 12 years, with average symptom duration of 11 +/- 9 years). The mean VT cycle length was 360 +/- 70 ms, and all had RBBB morphology with left axis deviation. Cardiac chamber sizes, left ventricular wall thickness, and wall motion were normal in all ILVT patients. TTE and/or TEE demonstrated a false tendon extending from the posteroinferior left ventricular free wall to the left ventricular septum in all ILVT patients. The false tendons were thick (> or = 2 mm maximal thickness) in 5 patients and thin (< 2 mm maximal thickness) in 10 patients. We compared ILVT patients with a control group of 671 consecutive patients referred for echocardiography for other reasons. The mean age for the control group was 42 years. A false tendon was seen in the left ventricle in 34 of 671 (5%). In the control group patients with a false tendon, 2 patients had a history of VT (left bundle-branch block morphology) and 1 had ventricular fibrillation. The false tendons in the control patients were also oriented transversely across the ventricular cavity but were somewhat thinner (< 2 mm maximal thickness in 32 of 34 patients). Catheter ablation with the use of radiofrequency and/or direct current applied to the posteroapical septum resulted in cure in 14 of 15 patients. CONCLUSIONS: A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT and probably is responsible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje fiber network on the interventricular septum.

Adult↗
PubMed1995

Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation.

BACKGROUND: It is thought that only a thin layer of tissue adjacent to the electrode is heated directly by electrical current (resistive heating) during radiofrequency ablation. Most of the thermal injury is thought to result from conduction of heat from the surface layer. The purpose of this study was to determine whether lesion depth could be increased by producing direct resistive heating deeper in the tissue with higher radiofrequency power, allowed by cooling the ablation electrode with saline irrigation to prevent the rise in impedance that occurs when the electrode-tissue interface temperature reaches 100 degrees C. METHODS AND RESULTS: In 11 anesthetized dogs, the thigh muscle was exposed and bathed with heparinized canine blood (36 degrees C to 37 degrees C). A 7F catheter, with a central lumen, a 5-mm tip electrode with six irrigation holes, and an internal thermistor, was positioned perpendicular to the thigh muscle and held at a constant contact weight of 10 g. Radiofrequency current was delivered to 145 sites (1) at high constant voltage (66 V) without irrigation (CV group, n = 31), (2) at variable voltage (20 to 66 V) to maintain tip-electrode temperature at 80 degrees C to 90 degrees C without irrigation (temperature-control group, n = 39), and (3) at high CV (66 V) with saline irrigation through the catheter lumen and ablation electrode at 20 mL/min (CV irrigation group, n = 75). Radiofrequency current was applied for 60 seconds but was terminated immediately in the event of an impedance rise > or = 10 omega. Tip-electrode temperature and tissue temperature at depths of 3.5 and 7.0 mm were measured in all three groups (n = 145). In 33 CV irrigation group applications, temperature was also measured with a separate probe at the center (n = 18) or edge (n = 15) of the electrode-tissue interface. In all 31 CV group applications, radiofrequency energy delivery was terminated prematurely (at 11.6 +/- 4.8 seconds) owing to an impedance rise associated with an electrode temperature of 98.8 +/- 2.1 degrees C. All 39 temperature-control applications were delivered for 60 seconds without an impedance rise, but voltage had to be reduced to 38.4 +/- 6.1 V to avoid temperatures > 90 degrees C (mean tip-electrode temperature, 84.5 +/- 1.4 degrees C). In CV irrigation applications, the tip-electrode temperature was not > 48 degrees C (mean, 38.4 +/- 5.1 degrees C) and the electrode-tissue interface temperature was not > 80 degrees C (mean, 69.4 +/- 5.7 degrees C). An abrupt impedance rise with an audible pop and without coagulum occurred in 6 of 75 CV irrigation group applications at 30 to 51 seconds, probably owing to release of steam from below the surface. In the CV and temperature-control group applications, the temperatures at depths of 3.5 (62.1 +/- 15.1 degrees C and 67.9 +/- 7.5 degrees C) and 7.0 mm (40.3 +/- 5.3 degrees C and 48.3 +/- 4.8 degrees C) were always lower than the electrode temperature. Conversely, in CV irrigation group applications, electrode and electrode-tissue interface temperatures were consistently exceeded by the tissue temperature at depths of 3.5 mm (94.7 +/- 9.1 degrees C) and occasionally 7.0 mm (65.1 +/- 9.7 degrees C). Lesion dimensions were smallest in CV group applications (depth, 4.7 +/- 0.6 mm; maximal diameter, 9.8 +/- 0.8 mm; volume, 135 +/- 33 mm3), intermediate in temperature-control group applications (depth, 6.1 +/- 0.5 mm; maximal diameter, 11.3 +/- 0.9 mm; volume, 275 +/- 55 mm3), and largest in CV irrigation group applications (depth, 9.9 +/- 1.1 mm; maximal diameter, 14.3 +/- 1.5 mm; volume, 700 +/- 217 mm3; P < .01, respectively). CONCLUSIONS: Saline irrigation maintains a low electrode-tissue interface temperature during radiofrequency application at high power, which prevents an impedance rise and produces deeper and larger lesions. A higher temperature in the tissue (3.5 mm deep) than at the electrode-tissue interface indicates that direct resistive heating occurred deeper

Animals↗
PubMed1995

Atrial inputs as determinants of atrioventricular nodal conduction: re-evaluation and new concepts.

Radiofrequency ablation was combined with standard recording and pacing procedures to determine the role of the perinodal fast pathway (FP) and slow pathway (SP) in atrioventricular (A-V) conduction in normal dog hearts. In 16 anesthetized, open-chest dogs, we recorded atrial (A) electrograms from the high right atrium (HRA), His bundle (Hb) region and coronary sinus (CS) ostium. In 8 dogs, during HRA pacing at a cycle length of 400 ms, FP ablation induced a significant change in A-H interval (61 +/- 12 to 107 +/- 9 ms, p < 0.001) but no change in Wenckebach cycle length (185 +/- 14 to 190 +/- 12 ms, NS). During ventricular pacing (400 ms cycle length) there was a shift in retrograde atrial activation so that Hb (A) delayed more than CS (A). Subsequent SP ablation in this same group of 8 dogs, produced a significant prolongation of antegrade Wenckebach cycle length (190 +/- 10 to 277 +/- 36 ms, p < 0.002) but only one instance of complete A-V block even though both FP and SP were ablated in accordance with clinical criteria. In another group of 8 dogs, a specially designed ablation electrode was inserted into the right atrium and positioned at the level of the fossa ovalis, 10-12 mm superior to the perinodal area. A radiofrequency linear lesion across the interatrial system induced a marked PR interval prolongation due to an intra-atrial rather than A-V nodal delay. The A-H interval was unchanged, and there was no change in antegrade or retrograde Wenckebach cycle length. In contrast, to the findings in both these groups direct damage to the A-V node showed immediate change in the A-H interval and at the same time progression to second degree and complete heart block. Taken together these results suggest that the perinodal FP and SP are composed of transitional cells which possess distinct electrophysiological properties not shared by adjacent atrial tissues or the compact A-V node itself. We conclude that the persistence of A-V conduction, albeit modified, after FP and SP ablation, suggests the existence of multiple atrio A-V nodal inputs whereas retrograde conduction relies mainly on dual exits from the A-V node to the atria.

Animals↗
PubMed1994

[Treatment of AV-nodal reentry tachycardia by transcatheter radiofrequency ablation].

A case history is presented of a patient in whom an AV-nodal reentrant tachycardia was cured by the selective transcatheter ablation of the extranodal slow pathway. Recent anatomical and electrophysiological findings connected with the mechanism of AV-nodal reentrant tachycardia are presented, which permitted development of the transcatheter radio frequency AV-nodal modification. The Hungarian introduction of this therapeutic modality is recommended.

Catheter Ablation↗
PubMed1994

Late potentials are unaffected by radiofrequency catheter ablation in patients with ventricular tachycardia.

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 +/- 50 msec; mean +/- SEM) 13-180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 +/- 4.0 msec postablation; 135.7 +/- 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 +/- 1.0 microV postablation; 5.9 +/- 0.4 microV preablation), or in the duration of the low amplitude signal (69.2 +/- 2.0 msec postablation; 62.7 +/- 3.4 msec preablation). At follow-up electrophysiology study performed 14 +/- 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study.

Action Potentials↗
PubMed1994

Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials.

BACKGROUND: Accessory pathways (APs) exhibiting "Mahaim fiber" physiology (antegrade conduction only, long conduction time, and decremental properties) often connect the lateral right atrium to the right bundle branch (right atriofascicular pathways). Potentials from these pathways have not been recorded previously. The purpose of this study was to determine whether AP activation potentials could be recorded from right atriofascicular APs and to determine whether these potentials could be used to localize a site for catheter ablation. METHODS AND RESULTS: Of 26 consecutive patients referred for catheter ablation of an AP producing a preexcited (antidromic) atrioventricular (AV) reentrant tachycardia having a left bundle branch block pattern with short ventriculoatrial and long AV intervals, 23 (88.5%) were found to have a right atriofascicular AP. During antidromic AV reentrant tachycardia, (1) right atrial extrastimuli (that did not penetrant tachycardia, (1) right atrial extrastimuli (that did not penetrate the AV node) advanced the timing of the next QRS complex, indicating that the AP was connected to the right atrium; (2) earliest antegrade ventricular activation was recorded at the apical right ventricular free wall, and (3) ventricular activation was preceded by activation of the distal right bundle branch, indicating a fascicular insertion or a ventricular insertion close to the terminus of the right bundle branch. A single, discrete, high-frequency AP potential was recorded at the lateral, anterolateral, or posterolateral tricuspid annulus in 22 of the 23 patients 63 +/- 12 milliseconds after the local atrial potential and 83 +/- 23 milliseconds before the local ventricular potential during sinus rhythm. The AP potential was also recorded at sites along the right ventricular free wall between the tricuspid annulus and the site of earliest ventricular activation at the apical region. Programmed atrial stimulation and adenosine each produced prolongation of AP conduction time because of an increase in the A-AP interval and Wenckebach block proximal to the AP potential. Radiofrequency current applied at a site recording the AP potential (tricuspid annulus in 19 patients and right ventricular free wall in 3 patients) eliminated AP conduction in all 22 patients. Tachycardia has not recurred in any patient during 18 +/- 13 months of follow-up. AP conduction was absent in all 9 patients who had a follow-up electrophysiological study 3.8 +/- 1.7 months after ablation. CONCLUSIONS: Right atriofascicular APs consist of two components. The proximal component is located at the lateral, anterolateral, or posterolateral tricuspid annulus, does not generate an AP potential recordable by catheter electrodes, and is responsible for the decremental conduction properties. The "distal" component extends from the tricuspid annulus to the distal right bundle branch at the apical right ventricular free wall and generates a large, high-frequency AP potential that accurately identifies a site for ablation.

Action Potentials↗
PubMed1993

Radiofrequency ablation of a concealed accessory pathway as treatment for incessant supraventricular tachycardia in a dog.

A new technique for the treatment of certain types of cardiac arrhythmias was used in a 3-year-old dog that was evaluated for incessant supraventricular tachycardia (220 to 280 beats/min), which had been refractory to several treatment regimens. The mechanism of supraventricular tachycardia was atrioventricular (AV) reentry, using a dorsoseptal accessory pathway (AP) for retrograde ventriculoatrial conduction (concealed AP). With the dog under general anesthesia and with fluoroscopic monitoring, electrode catheters were introduced into the heart via peripheral vessels. Electrical recordings allowed localization of the accessory AV pathway. Programmed electrical stimulation was used to verify the function of the abnormal AV connection. At the atrial insertion site of the AP, 2 applications of radiofrequency current (45 V, 21.6 W) were delivered to the dorsoseptal right atrium (near the coronary sinus ostium), which eliminated AP conduction and AV reentrant tachycardia. The dog has remained free of tachycardia and has not required medication during more than 1 year of follow-up.

Anesthesia, General↗
PubMed1993

A functional approach to the preexcitation syndromes.

Electrophysiologic studies have been used to elicit the mechanisms of the preexcitation syndromes and have become a therapeutic tool over the past decade. A thorough understanding of the physiology and anatomy of accessory pathways that are responsible for preexcitation and the associated arrhythmias is necessary before considering the various forms of intervention. The approach to patients with preexcitation syndromes is discussed, with an emphasis on the functional properties of accessory pathways and the associated arrhythmias.

Electrocardiography↗
PubMed1992

Acute conversion of paroxysmal supraventricular tachycardia with intravenous diltiazem. IV Diltiazem Study Group.

Diltiazem has electrophysiologic effects similar to those of verapamil. Its efficacy and safety in 4 doses for treatment of induced supraventricular tachycardia (SVT) were examined and compared with those of placebo in 87 patients (25 with atrioventricular [AV] nodal reentry tachycardia, 60 with AV reentry associated with an accessory AV connection, and 2 with atrial tachycardia). Conversion to sinus rhythm occurred in 4 of 14 patients (29%) with 0.05 mg/kg of diltiazem, 16 of 19 (84%) with 0.15 mg/kg, 13 of 13 (100%) with 0.25 mg/kg, and 14 of 17 (82%) with 0.45 mg/kg compared with 6 of 24 (25%) treated with placebo. Conversion rates in groups receiving doses of 0.15 to 0.45 mg/kg of diltiazem were superior to that in the placebo group (p less than 0.001). Time to conversion was 3.0 +/- 2.6 minutes in responding diltiazem patients compared with 5.9 +/- 6.1 minutes in responding control patients. Diltiazem administration resulted in significant lengthening of SVT cycle length, AH interval, and AV nodal effective refractory period and block cycle length. The most frequent adverse response to diltiazem was hypotension (7 of 63 patients); however, only 4 patients had symptoms related to hypotension. Thus, intravenous diltiazem in doses of 0.15, 0.25 and 0.45 mg/kg is an effective and safe treatment for the acute management of SVT.

Cardiac Pacing, Artificial↗