Radiofrequency catheter ablation in a haemodynamically compromised premature neonate with hydrops fetalis.

A preterm infant was born at 35 weeks gestation after failed antenatal antiarrhythmic therapy. The infant had an incessant supraventricular tachycardia, impaired ventricular function and hypotension and failed to respond to adenosine, cardioversion and intravenous amiodarone. After resuscitation from cardiovascular collapse, a successful radiofrequency catheter ablation (RFA) of a left free wall atrioventricular pathway was performed at 24 h of age without extracorporeal support. The infant is normal on follow up at 12 months of age. Whilst most fetal and neonatal supraventricular tachyarrhythmias respond to antiarrhythmic medications and RFA is not required, this is the earliest RFA to be performed on a premature infant when antiarrhythmics have failed.

Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease.

AIM: To compare the efficacy of sotalol versus amiodarone for long-term treatment of ventricular tachyarrhythmias. METHODS: Patients (n=75) with spontaneous, sustained ventricular tachyarrhythmias secondary to remote myocardial infarction were studied. After intravenous electrophysiological testing, both sotalol and amiodarone were predicted to be ineffective in 50 (67%) patients. Five patients were excluded. Forty-five patients were randomized to receive sotalol (n=22) or amiodarone (n=23) for maintenance therapy. The primary outcome variable was the time to first recurrence of sustained ventricular tachyarrhythmia. RESULTS: At 36 months. 75% of those allocated sotalol remained free of ventricular tachyarrhythmia compared with 38% of those allocated amiodarone (P=0.05). On multivariate analysis the risk of recurrence of ventricular tachyarrhythmia for patients on amiodarone was 5.9 times higher (P=0.008) than that for patients on sotalol. CONCLUSION: Sotalol is superior to amiodarone for long-term treatment of ventricular tachyarrhythmia secondary to coronary artery disease when both drugs have been predicted to be ineffective at intravenous electrophysiological testing. Randomized trials in larger numbers of patients with ventricular tachyarrhythmia need to be performed comparing the two agents directly.

Comparison of the long-term efficacy of implantable defibrillators and sotalol for documented spontaneous sustained ventricular tachyarrhythmias secondary to coronary artery disease.

BACKGROUND: The relative efficacy of antitachycardia pacing implantable cardioverter defibrillators (ATPICD) and sotalol in the treatment of ventricular tachyarrhythmias is controversial. AIM: To compare the mortality in patients treated with ATPICD and sotalol for documented spontaneous sustained ventricular tachyarrhythmias occurring late after previous myocardial infarction. METHODS: In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol. RESULTS: The two groups were well-matched for age, type of presenting arrhythmia, severity of coronary artery disease and ventricular function. At 36 months Kaplan-Meier estimates of mortality from ventricular tachyarrhythmia were 0% with ATPICD and 15% with sotalol (p=0.03). Kaplan-Meier estimates of total mortality at 36 months were 12% with ATPICD and 25% with sotalol (p=0.09). Multivariate analysis showed hazard ratio of 7.9 (p=0.06) for death from ventricular tachyarrhythmia in patients treated with sotalol compared to ATPICD. CONCLUSIONS: While no difference in total mortality was demonstrated, treatment with ATPICD is probably superior to sotalol for preventing deaths due to ventricular tachyarrhythmia.

Risk to patients from radiation associated with radiofrequency ablation for supraventricular tachycardia.

BACKGROUND: Radiofrequency ablation may be associated with prolonged fluoroscopy times. Previous studies have calculated radiation risks by measuring the radiation dose at a limited number (6) of body sites. This is an inherently inaccurate measure. Our study aimed to quantify more precisely patient-related radiation risks associated with radiofrequency ablation for supraventricular tachycardia. METHODS AND RESULTS: Nine female patients having radiofrequency ablation for supraventricular tachycardia were studied. The radiation dose was determined at 41 body sites in each patient with the use of thermoluminescent dosimeters and was correlated with that measured simultaneously with a Diamentor dose-area product meter. The estimated mean organ doses (mGy) per 60 minutes of fluoroscopy were: lungs 30.8; bone marrow 4.3; left breast 5.1; right breast 3. 5; and thyroid 2.4. From the average organ doses, the estimated mean total lifetime excess risk of a fatal malignancy was 294 per million cases (0.03%) per 60 minutes of fluoroscopy. The risk calculation from the Diamentor dose-area product and thermoluminescent dosimeters were similar, suggesting that radiation dose was measured accurately. The estimated risk of radiation-induced malignancy increased with increasing body mass index (P=0.03). CONCLUSIONS: Prolonged fluoroscopy during radiofrequency ablation may potentially cause a small increase in the lifetime risk of fatal malignancy, with lung malignancy being most likely. This risk is small only with the use of techniques and x-ray equipment optimized to keep radiation as low as possible. The risk is increased in obese patients.

Efficacy and safety of a new protocol for continuous infusion of midazolam and fentanyl and its effects on patient distress during electrophysiological studies.

Electrophysiological studies are often distressing for patients. We devised a regime of continuous infusion of midazolam and fentanyl during electrophysiological studies without the presence of a specialist anaesthetist. The effects on key hemodynamic and respiratory variables and level of sedation were evaluated in detail in the first 775 patients. The safety of this practice was evaluated in 1,344 consecutive patients. Doses were calculated according to patients' weight and age. A mean total dose of 26 mg of midazolam and 115 mcg of fentanyl were infused. Satisfactory sedation was achieved in 97% of patients. The mean duration of procedure was 188 +/- 90 minutes. Complete amnesia of the procedure was obtained in 87% of patients. Sedation caused clinically insignificant changes in respiratory rate, oxygen saturation, end-tidal CO2 and blood pressure. There were no major complications related to sedation. Upper airway obstruction, usually minor, occurred in 42% and some restlessness in 20% of sedated patients. The assistance of a specialist anesthetist was required in 0.3% of sedated patients for management of restlessness, hypoventilation, or obstructive sleep apnea. The amount of distress experienced by sedated patients (n = 775) was significantly less compared to a previous series of nonsedated patients (n = 775) undergoing electrophysiological studies (P < 0.001). The degree of distress experienced by patients during electrophysiological studies can be reduced significantly by sedation with intravenous midazolam and fentanyl. Continuous infusion is an efficient, safe, and effective way of administering midazolam and fentanyl.

Behavior of late potentials on the body surface during programmed ventricular stimulation.

OBJECTIVES: This study sought to evaluate the behavior of late potentials on the body surface by signal averaging during programmed stimulation and to correlate the findings with the cycle length of induced ventricular tachycardia. BACKGROUND: Clinically relevant late potentials may be concealed within the QRS complex and may be missed by the conventional signal-averaged electrocardiogram (SAECG). In contrast, some late potentials may arise from dead-end pathways or pathways not capable of supporting sustained ventricular tachycardia (VT). It has been shown that durations of late potentials in sinus rhythm correlate poorly with VT cycle length. METHODS: Signal-averaged electrocardiography during sinus rhythm, right ventricular pacing (S1) and introduction of a right ventricular extrastimulus (S2) was performed in 95 patients: 11 patients with a structurally normal heart and no inducible VT (Group I); 44 with a previous myocardial infarction (MI) and no inducible monomorphic VT (Group II); and 40 with a previous MI and inducible monomorphic VT (Group III). RESULTS: The best subset of SAECG variables and the best cut points for each variable to differentiate between patients with and without VT were first established for each rhythm studied. Total duration of the filtered QRS complex (QRSD) was found to be the only independent predictor of inducibility of VT. When late potentials were defined for these criteria (QRSD > OR = 113, > or = 178 and > or = 168 ms for the SAECG during sinus rhythm, S1 and S2, respectively), there was no difference in the incidence of false positive (16% vs. 18%) or false negative (30% vs. 26%) late potentials between sinus rhythm and S1. During S2, there were significantly fewer false positive late potentials (11% vs. 16%) and fewer false negative late potentials (17% vs. 30%) than with sinus rhythm. Compared with sinus rhythm, 31% of the false positive late potentials detected during sinus rhythm were lost, whereas 43% of the false negative late potentials became detectable after S2, resulting in improved sensitivity (83% vs. 70%), specificity (89% vs. 84%) and predictive accuracy (86% vs. 77%, p < 0.05). Among the patients with VT, QRSD during S2 achieved the best correlation with VT cycle length (r = 0.74) and was the only independent predictor of VT cycle length when all SAECG variables were considered. CONCLUSIONS: Late potentials revealed by ventricular extrastimuli but concealed during sinus rhythm may be clinically relevant and may explain some of the false negative late potentials and reduced sensitivity of the conventional SAECG in predicting VT. In contrast, those late potentials that are detected during sinus rhythm but lost after ventricular extrastimuli are often clinically irrelevant and may account for the false positive late potentials and reduced specificity of the conventional SAECG.

Does sotalol have reverse-use dependence during tachyarrhythmias?

This study assessed the effect of intravenous sotalol on right ventricular effective refractory period at right ventricular pacing rates of 600 and 300 ms cycle length at 3, 6, 9, and approximately 30 minutes after the dose of sotalol. Similar percent increases occurred in the ventricular effective period at the 2 heart rates at all tested times (p >0.2 in each case), and it was concluded that there is no evidence for reverse-use dependence of intravenous sotalol in its effects on right ventricular refractoriness over this range of heart rates.

Radiation exposure to patient and operator during radiofrequency ablation for supraventricular tachycardia.

BACKGROUND: Radiofrequency (RF) ablation has become the primary method of treatment for supraventricular tachycardia and often requires prolonged fluoroscopy times. AIM: To quantitate radiation exposure to patient and operator during RF ablation for supraventricular tachycardia. METHODS: Thermoluminescent dosemeters were used to monitor radiation at seven sites. Positions were: patient's thyroid, left scapula, T9 vertebra, right scapula and L4-L5 vertebra and the operator's thyroid and left hand. Monitoring was performed during 22 procedures. Of the patients studied 10 (45%) had atrioventricular junctional re-entry tachycardia (AVJRT) and 12 (55%) had accessory pathway tachycardia. RESULTS: The median fluoroscopy times (minutes) and inter-quartile ranges were 46 (39-65) for AVJRT, 55 (52-60) for left free wall accessory pathway (LFW), 107 (89-140) for septal and 166 (128-176) for RFW pathways. The mean radiation doses (mGy) to the chest wall were 50 for AVJRT, 47 for LFW, 87 for septal and 151 for RFW pathways. The mean radiation to the chest wall of the patient per case was found to be 3.9 times that reported for diagnostic cardiac catheterisation and 1.5 times that reported for angioplasty. CONCLUSIONS: Radiofrequency ablation is associated with significant irradiation of the patient and operator. All precautions should be taken to decrease this exposure. If eye irradiation is assumed to be equal to that to the thyroid, more than 45 procedures per month by a single operator (using ceiling-suspended lead glass shielding) may result in exceeding the recommended dose limit to the eye.

Localisation of ventricular tachycardia substrates by analysis of the surface QRS recorded during ventricular tachycardia.

BACKGROUND: Analysis of the surface ECG can predict the locations of pacing foci but is of limited value for locating arrhythmogenic substrates causing ventricular tachycardia because of the effects of myocardial infarction, ischaemia, and bundle branch block on ventricular activation. AIM: To determine whether analysis of the initial 60 ms segment of the surface QRS improves the accuracy of the ECG for predicting ventricular tachycardia origin we correlated the locations of 37 arrhythmogenic areas present in 20 patients with the 3D vectors of the ventricular tachycardias generated by each respective area. METHODS: The 3D vector of each ventricular tachycardia morphology was calculated from the integrals of the initial 60 ms of the surface vectorcardiogram and from the entire QRS recorded in each lead of the Frank orthogonal lead vectorcardiogram. Sixty eight-morphologies of ventricular tachycardia were mapped using simultaneous recordings from 60 catheter electrodes. RESULTS: Ventricular tachycardias with 3D vectors directed inferiorly and posteriorly or superiorly and anteriorly were more likely to originate from the septum, P = 0.04, whereas tachycardias directed superiorly and to the right were more likely to originate from the inferior wall and the cardiac apex, P = 0.001. However, the same arrhythmogenic area could generate multiple ventricular tachycardias with different 3D vectors. In addition, ventricular tachycardias with similar 3D vectors were generated by arrhythmogenic areas in the septal, apical and inferior walls. The variances of the mean 3D vectors of ventricular tachycardias originating from each of 12 different cardiac regions were no different when based on the initial 60 ms of the surface QRS than on the entire surface QRS. CONCLUSION: Analysis of the surface ECG provides only an approximate guide to the locations of arrhythmogenic areas generating ventricular tachycardia even when analysis is restricted to the initial forces in the surface QRS. Therefore, detailed mapping is needed to accurately determine the number and location of arrhythmogenic areas.

Simultaneous mapping of the tricuspid and mitral valve annuli at electrophysiological study.

BACKGROUND: Mapping of the right free wall in patients with accessory pathways is difficult compared with that of the left free wall where the coronary sinus permits stable and accurate location of the electrodes used for endocardial mapping. Furthermore, the sequential roving catheter method is less satisfactory than multiple simultaneous electrode recordings spanning the circumference of the valve annulus. A new method for mapping the tricuspid annulus is described. METHODS: Mapping was performed in nine patients with a suspected right free wall accessory pathway or an atriofascicular connection. The tricuspid annulus was mapped using a specially shaped 1 cm interelectrode 10 pole catheter positioned in the right atrium immediately above the annulus. The coronary sinus was mapped with a 5 mm interelectrode 10 pole catheter and a 2 mm interelectrode 10 pole catheter recorded His bundle activity. Catheter positions were confirmed by multiplane fluoroscopy. Electrograms were digitised and recorded simultaneously using a custom computerised mapping system. The position of the multielectrode catheter around the tricuspid annulus relative to that of the coronary arteries was examined by coronary angiography in three patients. RESULTS: Seven right free wall and two posterior septal accessory pathways, and three atriofascicular connections were detected. Ventricular activation adjacent to both valve annuli was mapped in five patients with pre-excitation. The locations of eight of the nine accessory pathways and the three atriofascicular connections were confirmed at operative mapping. One right free wall accessory pathway in a patient with Ebstein's anomaly was not detected at operative mapping. No additional accessory pathways were found at operative mapping or routine 6 month postoperative electrophysiological study, or during a mean (SD) clinical follow up of 22 (7) months. The tricuspid annulus catheter was located during coronary angiography at a mean (SD) of about 2.5 (0.7) cm above and parallel to the right coronary artery in the right atrioventricular groove. CONCLUSIONS: This new catheter technique permits rapid detailed mapping of atrial and ventricular activation around the tricuspid annulus with a resolution of at least < or = % 1 cm, depending on the number and spacing of electrodes in each catheter. The technique was accurate as judged by mapping at surgery. This method is simple and safe compared with that of others for mapping the right free wall via the right coronary artery. It should facilitate detection and ablation of right free wall accessory pathways and atriofascicular connections.

Does the induction of ventricular flutter or fibrillation at electrophysiologic testing after myocardial infarction have any prognostic significance?

This study examines the significance of inducing sustained ventricular fibrillation (VF) or ventricular flutter by programmed stimulation after infarction. Programmed ventricular stimulation was performed for prognostic reasons from the right ventricular apex at twice diastolic threshold using a protocol containing 4 extrastimuli. Of 502 patients tested 11 +/- 4 days after acute infarction, VF was induced in 164 (33%), ventricular flutter in 134 (27%), ventricular tachycardia (VT) in 44 (9%), and no arrhythmia in 160 (32%). All groups were similar in age, sex distribution, and sites of index infarction. Those with inducible VT had a higher incidence of multiple infarctions and a lower mean left ventricular ejection fraction at the time of testing. Without antiarrhythmic drug therapy, 8 patients (18%) with inducible VT experienced spontaneous VT or died instantaneously during the first year of follow-up. By contrast, only 1 (0.6%) patient with inducible VF, 1 (0.7%) with ventricular flutter, and 1 (0.6%) without any inducible arrhythmias experienced similar events in the same period (p < 0.001). By relating the cycle length of the induced monomorphic arrhythmia to later spontaneous electrical events, induced arrhythmias with cycle length as low as 230 ms still identified patients at high risk for spontaneous arrhythmias. Only the induction of sustained monomorphic VT with a cycle length > 230 ms indicates patients with ventricular electrical instability after infarction. The induction of VF or ventricular flutter is a negative test result with no adverse long-term prognostic significance.

Rapid intravenous infusion of d-1 sotalol: time to onset of effects on ventricular refractoriness, and safety.

d-1 sotalol is one of the most effective antiarrhythmic agents currently available for ventricular tachyarrhythmias, but the recommended infusion rate of 10-20 min is too slow for rapid pharmacological termination of sustained ventricular tachycardia (VT) or for use during cardiac arrest. The safety of the drug and time lag from its rapid administration to onset of significant effects on ventricular refractoriness is unknown. One hundred and nine patients with a history of spontaneous and inducible sustained ventricular tachyarrhythmias were studied. d-1 sotalol (1.5 mg.kg-1) was infused over 5 min in the first 57 patients (mean age 61 +/- 13 years, mean ejection fraction 37 +/- 15%, range 15-70%). d-1 sotalol was then given over 1 min in the next 52 patients (mean age 61 +/- 12 years, mean ejection fraction 35 +/- 11%, range 18-58%). The time course of change in right ventricular effective refractory period (RVERP) was measured in 15 consecutive patients following the 5 min infusion and in all 52 patients following the bolus injection. Following the 5 min infusion, RVERP increased rapidly from a baseline of 231 +/- 17 ms, reaching a plateau of 268 +/- 23 ms at 10 min. Following the 1 min injection, RVERP increased virtually immediately from a baseline of 237 +/- 25 ms to reach a plateau of 271 +/- 31 ms at 5 min. Two patients (one in each group) developed symptomatic hypotension; both responded to volume replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Simultaneous 60-electrode mapping of ventricular tachycardia using percutaneous catheters.

OBJECTIVES: We developed a new approach for mapping ventricular tachycardia at electrophysiologic study using simultaneous recordings from up to 60 catheter electrodes. BACKGROUND: Good results for surgical or catheter ablation of ventricular tachycardia are limited by the ability to detect and completely map all of the underlying arrhythmogenic areas. Currently, catheter mapping of all configurations of ventricular tachycardia is impossible or unsatisfactory in at least 60% of patients because of poorly tolerated rapid rates, nonsustained ventricular tachycardia or multiple configurations. METHODS: Twenty-four patients with recurrent ventricular tachycardia refractory to antiarrhythmic drugs were studied using up to six percutaneous decapolar catheters introduced into the ventricles. Left ventricular maps of ventricular tachycardia were achieved by two to three transseptal catheters, two to three transaortic catheters, a coronary sinus catheter and right ventricular catheters. Simultaneous endocardial maps of either right or left ventricles were possible with a resolution of approximately 1 to 2 cm. Up to 60 electrograms were digitized and recorded simultaneously using a custom-computerized mapping system. RESULTS: Successful maps of 73 ventricular tachycardia configurations were obtained in 22 patients. The mapping procedure failed in two patients because of inability to catheterize the left ventricle in one and inability to induce monomorphic ventricular tachycardia in the other. The mean (+/- SD) ventricular tachycardia cycle length was 285 +/- 53 ms (range 215 to 470). A total of 39 separate arrhythmogenic areas (median 1, interquartile [25% to 75%] range 1 to 3/patient) were detected, of which 21 (54%) were in the left ventricular free wall, 17 (44%) were in the ventricular septum, and 1 (2%) was in the right ventricular outflow tract. Ten patients (45%) had at least two arrhythmogenic areas. Thirteen patients subsequently underwent operation. All but one of the arrhythmogenic areas found at surgical mapping had been identified at preoperative catheter mapping. Complications of the preoperative mapping procedure occurred in four patients, with complete resolution in three and minor long-term sequelae in the other. CONCLUSIONS: This technique permits detailed catheter mapping of all types of monomorphic ventricular tachycardias, including those leading to hemodynamic collapse, and should enable better choice and direction of surgical or catheter ablation.

Surgical procedure for the cure of atrioventricular junctional ("AV node") reentrant tachycardia: anatomic and electrophysiologic effects of dissection of the anterior atrionodal connections in a canine model.

OBJECTIVES: This study was undertaken to examine the electrophysiologic and anatomic effects of a surgical procedure that cures the anterior (common) type of atrioventricular (AV) junctional reentrant tachycardia. BACKGROUND: The procedure was designed to interrupt the reentrant circuit at the point of earliest atrial activation during AV junctional reentrant tachycardia, the anterior atrionodal connections. METHODS: Atrioventricular node function and the sequence of electrical excitation of Koch's triangle were examined in 18 dogs. Excitation of Koch's triangle was mapped using a 60-channel mapping system. Surgical dissection was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, AV node function and the atrial excitation pattern were reassessed. The AV junction was examined using light microscopy. RESULTS: Some degree of AV node damage was visible in all dogs in the dissection group, but it was minor in 40% of cases. The anterior part of the AV node was disconnected from the anterior atrionodal connections in all cases. Anterograde AV node function was mildly impaired. The median AH interval was increased (62 vs. 76 ms [interquartile ranges 48 to 72 and 64 to 104, respectively], p = 0.05), and the AV Wenckebach cycle length was increased (210 vs. 245 ms [interquartile ranges 200 to 230 and 210 to 260, respectively], p = 0.02). The degree of impairment of conduction was directly proportional to the length of dissection (p < 0.05) but not to the degree of damage to the AV node. Ventriculoatrial (VA) conduction was destroyed in 50% of dogs undergoing dissection but in none of those with a sham operation (p < 0.04). The AV node remained responsive to autonomic blocking drugs, and atrial mapping during ventricular pacing revealed that the site of exit from the AV node had been altered. CONCLUSIONS: The atrionodal connections closest to the His bundle are the preferred route of conduction through the AV node during normal AV or VA conduction. Destruction of these connections modifies AV node conduction. The surgical procedure selectively interrupts these connections, and this interruption is likely to be the mechanism of cure.

Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia.

The efficacy of antiarrhythmic drugs for terminating sustained ventricular tachycardia (VT) has been disappointing. Lignocaine is the traditional drug but it is not very effective. Sotalol, one of the most effective drugs in suppressing spontaneous or induced VT, should theoretically be useful in this setting. We have compared lignocaine with sotalol for the acute termination of spontaneous sustained VT not causing cardiac arrest in 33 patients (26 males, 7 females, aged 21-90) whose underlying heart disease was old myocardial infarction (28), acute myocardial infarction (2), dilated cardiomyopathy (1), or idiopathic cardiomyopathy (2). Left-ventricular ejection fraction was 35% (range 18-76%). Patients were randomly allocated in a double-blind fashion to lignocaine 100 mg (n = 17) or sotalol 100 mg (n = 16) given intravenously over 5 min. Those with persistent VT 15 min after onset of administration of the first drug were crossed over to the other drug. Sotalol was significantly more effective than lignocaine whether analysed on an intention-to-treat basis (69% vs 18%; 95% confidence interval for absolute difference of 51% 22-80%, p = 0.003) or by analysis limited to the 31 patients with subsequent electrophysiologically proven VT (69% vs 20%). 1 patient in each group required cardioversion after the first drug. Tachycardia persisted in 14 patients in the lignocaine group and 4 in the sotalol group after 15 min. Tachycardia ceased in 7 (50%) patients who crossed over to sotalol, and in 1 patient who crossed over to lignocaine. There was 1 death in each group after the first drug and 1 death after both drugs. We conclude that sotalol was superior to lignocaine for the acute termination of sustained VT. The incidence of adverse effects was similar for the two drugs.

Can the electrophysiologic study predict treatment outcome in patients with sustained ventricular tachyarrhythmias unrelated to coronary artery disease?

UNLABELLED: Sustained ventricular tachyarrhythmias unrelated to coronary artery disease are uncommon. Currently there are no clear guidelines to aid selection of the most appropriate treatment strategy. Therefore, factors potentially predictive of arrhythmia recurrence and death and the ability of the electrophysiologic study to predict treatment outcome in patients with spontaneous sustained ventricular tachyarrhythmias unrelated to coronary artery disease were examined in 41 medically treated patients followed for a median of 25 (range 1-76) months. Examined factors were: syncope associated with the spontaneous arrhythmia, the morphology and cycle length of the presenting arrhythmia, underlying ventricular function, cardiac pathology, and the results of drug assessment at electrophysiologic study. Random variability in the ease of arrhythmia induction at electrophysiologic study was measured for the group as a whole and was allowed for in prediction of an effective drug response. The 95% confidence intervals for variability in the ease of repeat arrhythmia induction at the same study were < or = 1 extrastimulus and for variability in the ease of repeat arrhythmia inductions at different studies were < or = 2 extrastimuli. Poisson regression models were used for data analysis. Arrhythmia recurrence was most likely in: (1) patients on treatment not predicted to be anti-arrhythmic at electrophysiologic study; (2) patients whose treatment was not assessable at electrophysiologic study because the arrhythmia was not reliably inducible; (3) patients with impaired ventricular function; and (4) re-entered patients whose arrhythmia had recurred on previously allocated therapy. The risk of arrhythmia recurrence decreased with time from hospital assessment. All five deaths occurred in patients with impaired ventricular function. CONCLUSIONS: drug efficacy should be tested at electrophysiologic study in patients with reproducibly inducible clinical arrhythmias. Treatment not proven to be anti-arrhythmic at electrophysiologic study is usually ineffective. Patients with ventricular dysfunction are at highest risk of death from arrhythmia recurrence and should be considered for an implantable defibrillator, arrhythmia surgery, or heart transplantation if drug treatment is not predicted to be effective or is not assessable at electrophysiologic study.

Electrophysiologic and histologic effects of dissection of the connections between the atrium and posterior part of the atrioventricular node.

OBJECTIVES: This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node. BACKGROUND: Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node. METHODS: Atrioventricular node function and electrical excitation of Koch's triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy. RESULTS: The compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exists from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs. CONCLUSIONS: This procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.

Posterior ("atypical") atrioventricular junctional reentrant tachycardia.

The aim of this study was to characterize a relatively rare type of atrioventricular (AV) junctional reentrant tachycardia (AVJRT). Posterior AVJRT is a type of AV nodal tachycardia in which the site of earliest atrial activation is posterior to the AV node near the coronary sinus orifice. The mechanism of this tachycardia is not well understood. The characteristics of posterior AVJRT (n = 15) were compared with those of anterior ("common") AVJRT (n = 146) and supraventricular tachycardia using single posterior septal accessory pathways (n = 13). During posterior AVJRT, the AH interval was longer than the retrograde conduction time (His to earliest atrial activity) in 11 cases (73%), indicating that these tachycardias were not fast-slow types of AVJRT. The mean ventriculoatrial (VA) interval in posterior AVJRT (93 +/- 41 ms) was longer than in anterior AVJRT (11 +/- 20 ms; p < 0.005), but was similar to that in tachycardias using accessory pathways (106 +/- 16 ms; p = NS). The site of earliest atrial activation during posterior AVJRT was similar to that in tachycardias using accessory pathways. In all cases of accessory pathway-mediated tachycardia, atrial activation could be advanced by ventricular extrastimuli delivered coincident with the His deflection, but atrial activation was not advanced in any case of posterior AVJRT unless the extrastimulus was delivered > 80 ms before the His deflection. Anterograde conduction was similar in the posterior and anterior AVJRT groups.(ABSTRACT TRUNCATED AT 250 WORDS)

High resolution mapping of Koch's triangle using sixty electrodes in humans with atrioventricular junctional (AV nodal) reentrant tachycardia.

BACKGROUND: Recent evidence suggests that atrioventricular junctional reentrant tachycardia (AVJRT) uses a reentrant circuit that involves the atrioventricular (AV) node, the atrionodal connections, and perinodal atrial tissue. Electrogram morphology has been used to target the delivery of radiofrequency energy to the site of the "slow pathway," a component of this reentrant circuit. The aim of this study was to localize precisely the sites of atrionodal connections involved in AVJRT and to examine atrial electrogram morphologies and their spatial distribution over Koch's triangle. METHODS AND RESULTS: Electrical activation of Koch's triangle and the proximal coronary sinus was examined in 13 patients using a 60-point plaque electrode and computerized mapping system. Recordings were made during sinus rhythm (n = 12), left atrial pacing (n = 8), ventricular pacing (n = 12), and AVJRT (n = 12). During sinus rhythm electrical activation approached Koch's triangle and the AV node from the direction of the anterior limbus, activating the anterior part of the triangle before the posterior part. A zone of slow conduction during sinus rhythm was found within Koch's triangle in 64% of patients. The pattern of atrial activation in Koch's triangle during anterograde fast pathway conduction was similar to that seen during anterograde slow pathway conduction. Retrograde fast pathway conduction during ventricular pacing and during anterior (typical) AVJRT caused earliest atrial activation at the apex of Koch's triangle near the AV node-His bundle junction. In individual patients the site of earliest atrial activation was similar for both anterior AVJRT and retrograde fast pathway conduction during ventricular pacing. Retrograde slow pathway conduction during ventricular pacing and during posterior (uncommon or atypical) AVJRT caused earliest atrial activation posterior to the AV node near the orifice of the coronary sinus. This posterior or "slow pathway" exit site was 15 +/- 4 mm from the His bundle. In individual patients the site of earliest atrial activation was similar for both posterior AVJRT and retrograde slow pathway conduction during ventricular pacing. In one patient anterograde and retrograde conduction occurred via separate slow pathways during AVJRT: Complex atrial electrograms with two or more components were observed near the coronary sinus orifice and in the posterior part of Koch's triangle in all cases. These were categorized as either low or high frequency potentials according to the rapidity of the second component of the electrogram. Low frequency potentials were present at the site of earliest atrial excitation during retrograde slow pathway conduction in 5 of 5 cases (100%) and high frequency potentials in 4 of 5 cases (80%). However, both slow and high frequency potentials could be found at sites up to 16 mm from the site of earliest atrial excitation. CONCLUSIONS: At least two distinct groups of atrionodal connections exist. The site of earliest atrial activation during anterior AVJRT is similar to that of fast pathway conduction during ventricular pacing. This site is close to the His bundle-AV node junction. The site of earliest atrial activation during posterior AVJRT is similar to that of slow pathway conduction during ventricular pacing. This site is near the coronary sinus orifice, approximately 15 mm from the His bundle. The anterograde slow pathway appears to be different from the retrograde slow pathway in some patients. Double atrial electrograms are an imprecise guide to the site of earliest atrial excitation during retrograde slow pathway conduction.

Comparison of number of extrastimuli versus change in basic cycle length for induction of ventricular tachycardia by programmed ventricular stimulation.

OBJECTIVES: The purpose of this study was to examine the effects of varying basic cycle lengths in a programmed stimulation protocol if up to seven extrastimuli were available at each basic cycle length. BACKGROUND: There is no uniformly accepted protocol for induction of ventricular tachycardia. Most protocols limit the number of extrastimuli to two or three but use several basic cycle lengths. METHODS: Twenty-eight patients with coronary artery disease and documented spontaneous sustained ventricular tachycardia or ventricular fibrillation were studied. In the absence of antiarrhythmic drugs, each patient underwent three inductions of ventricular tachycardia/ventricular fibrillation using sinus rhythm or right ventricular pacing at 600 or 400 ms as the basic cycle length. Up to seven extrastimuli were allowed at each basic cycle length. RESULTS: The maximal yield of clinical tachycardia (96%) was identical for each basic cycle length and was achieved using a maximum of seven, five and four extrastimuli for sinus rhythm and 600 and 400 ms, respectively. A basic cycle length of 400 ms required fewer extrastimuli (2.4 +/- 0.7) to induce ventricular tachycardia/ventricular fibrillation than did 600 ms (2.7 +/- 1.1, p = 0.014) or sinus rhythm (3.4 +/- 1.2, p < 0.001). There was no significant difference in the cycle lengths of the induced ventricular tachycardia, incidence of induced ventricular fibrillation or requirement for direct current countershock. CONCLUSIONS: The use of an adequate number of extrastimuli obviates the need for multiple basic cycle lengths for induction of ventricular tachycardia and does not increase induction of unwanted ventricular fibrillation. If only one basic cycle length is used, the ease of inducibility can be quantified in terms of the number of extrastimuli required. Fewer extrastimuli were required for induction of ventricular tachycardia if a basic cycle length of 400 ms was used. These data favor the use of ventricular pacing at a basic cycle length of 400 ms with up to at least four extrastimuli as the standard stimulation protocol for induction of ventricular tachycardia.