Biomedical subjects
Publications and source records attributed to Y Iesaka.
A case is presented of a 73-year-old man with drug resistant ventricular tachycardia that originated from the right ventricular outflow tract. A right ventriculogram showed a diverticulum in the interventricular septum at the right ventricular outflow tract. Low energy radiofrequency catheter ablation within the diverticulum was performed successfully and safely.
We describe two patients with idiopathic left ventricular tachycardia that were cured by radiofrequency catheter ablation. Tachycardia was inducible by ventricular stimulation and was verapamil sensitive. Two distinct presystolic potentials (P1 and P2) were recorded during tachycardia in the mid-septal or inferoapical area, but only one potential (P2) was recorded during sinus rhythm. After catheter ablation at this site, the P1 potential was noted after the QRS complex during sinus rhythm, while the P2 was still observed before the QRS complex. The P1 potential showed a decremental property during atrial or ventricular pacing. These data suggest that Purkinje tissue with decremental properties was responsible for the tachycardia mechanism, and that the reentry circuit involving this tissue is likely to be of considerable size.
INTRODUCTION: Verapamil-sensitive left ventricular tachycardia (VT) with a right bundle branch block (RBBB) configuration and left-axis deviation has been demonstrated to arise from the left posterior fascicle, and can be cured by catheter ablation guided by Purkinje potentials. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation is rare, and may originate in the left anterior fascicle. METHODS AND RESULTS: Six patients (five men and one woman, mean age 54+/-15 years) with a history of sustained VT with an RBBB configuration and right-axis deviation underwent electrophysiologic study and radiofrequency (RF) ablation. VT was slowed and terminated by intravenous administration of verapamil in all six patients. Left ventricular endocardial mapping during VT identified the earliest ventricular activation in the anterolateral wall of the left ventricle in all patients. RF current delivered to this site suppressed the VT in three patients (ablation at the VT exit). The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 35, 30, and 20 msec, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. In the remaining three patients, RF catheter ablation at the site of the earliest ventricular activation was unsuccessful. In these three patients, Purkinje potential was recorded in the diastolic phase during VT at the mid-anterior left ventricular septum. The Purkinje potential preceded the QRS during VT by 66, 56, and 63 msec, and catheter ablation at these sites was successful (ablation at the zone of slow conduction). During 19 to 46 months of follow-up (mean 32+/-9 months), one patient in the group of ablation at the VT exit had sustained VT with a left bundle branch block configuration and an inferior axis, and one patient in the group of ablation at the zone of slow conduction experienced typical idiopathic VT with an RBBB configuration and left-axis deviation. CONCLUSION: Verapamil-sensitive VT with an RBBB configuration and right-axis deviation originates close to the anterior fascicle. RF catheter ablation can be performed successfully from the VT exit site or the zone of slow conduction where the Purkinje potential was recorded in the diastolic phase.
INTRODUCTION: The determinants of susceptibility to atrial fibrillation (AF) and the existence of accessory pathway conduction have remained unidentified in the Wolff-Parkinson-White (WPW) syndrome. We tested the hypothesis that excitation inputs into the atrium over a retrograde multiple or multifiber accessory pathway during AV reentrant tachycardia (AVRT) could precipitate initiation of AF. METHODS AND RESULTS: Two hundred fifty consecutive patients with WPW syndrome underwent electrophysiologic study and radiofrequency catheter ablation. The patients were classified into two groups according to the study results: 29 with retrograde multiple or multifiber accessory pathway (MP) and 221 with retrograde single accessory pathway (SP). Compared with the SP patients, the MP patients showed a significantly higher incidence of clinical AF (MP vs SP: 19/29 vs 51/221, P < 0.01), induced AF (12/29 vs 32/221, P < 0.01), and initiated AF during ventricular pacing and AVRT (10/12 vs 17/32, P < 0.05). There were no differences between the two groups in incidence of clinical and induced AVRT (24/29 vs 200/221 and 25/29 vs 206/221, respectively), mean cycle length of induced AVRT, or electrophysiologic parameters of the accessory pathway. AF inducibility during AVRT or ventricular pacing was eliminated by partial ablation in 7 of 10 patients with MP. After total ablation, the incidence of induced AF was similar between the two groups (MP vs SP: 1/29 vs 11/221). CONCLUSION: The existence of a retrograde multiple or multifiber accessory pathway in patients with WPW syndrome is associated with a higher incidence of clinical and induced AF. Successful ablation of the retrograde multiple or multifiber accessory pathway can eliminate the induction of both AVRT and AF.
Two wide QRS tachycardias with identical morphology but different cycle lengths (CLs) developed in a 63-year-old man. Electrophysiological study demonstrated inducible atrioventricular reentrant tachycardia (AVRT) due to a concealed left posterior accessory pathway (AP), which was successfully ablated by radiofrequency application. Neither dual AV nodal pathways nor other APs were documented. Splitting of the His-bundle electrogram was shown, and programmed stimulation induced sudden prolongation of intra-hisian conduction time. These results suggest longitudinal dissociation in the His bundle may be responsible for two distinct CLs in AVRT without dual AV nodal physiology.
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.
A case is presented of a 63-year-old woman with a concealed accessory pathway that exhibited retrograde supernormal conduction after radiofrequency catheter ablation. Although ventricular pacing at a slow rate revealed no retrograde conduction over the accessory pathway following ablation, the tachycardia recurred 15 months later. During ventricular pacing there was retrograde 1:1 conduction over the accessory pathway at a fast rate while there was intermittent VA dissociation with rare retrograde conduction at the slower rate. Ventricular extrastimulus testing demonstrated a supernormal conduction zone of the coupling interval. Thus, accessory pathways may exhibit supernormal conduction after catheter ablation. Pacing should be performed at both slow and fast rates to confirm the presence of conduction block following ablation.
The electrographic features of successful sites of radiofrequency catheter ablation were analyzed in 33 cases of posteroseptal accessory pathways and compared with those from 155 cases of free wall accessory pathways. The atrioventricular intervals in the posteroseptal cases were significantly longer than in the free wall cases (posteroseptal vs left and right free wall; 38 vs 33 and 26 msec, respectively; p < 0.05), and the incidences of continuous electrograms (42 vs 63 and 79%; p < 0.01) and PQS-pattern unipolar electrograms (50 vs 76 and 78%; p < 0.05) were significantly lower in the posteroseptal cases. The V-delta intervals in the posteroseptal cases were significantly longer than in the left free wall cases (17 vs 13 msec; p < 0.05), but shorter than in the right free wall cases (17 vs 23 msec; p < 0.05). No statistically significant difference in the incidence of Kent potentials among the 3 groups was observed. In radiofrequency ablation of posteroseptal pathways, the length of the atrioventricular interval and the incidences of continuous electrograms and PQS-pattern unipolar electrograms may be unsatisfactory even at the appropriate target site, but the V-delta interval and Kent potential are good indicators of suitable target sites.
UNLABELLED: The mechanism of cure in AV nodal reentrant tachycardia (AVNRT) by catheter ablation has not been fully clarified. We hypothesized that disruption of a shortcut link between the fast and slow pathways is responsible for the elimination of tachycardia. RESULTS: AVNRT was eliminated in 20 patients by catheter ablation. In five patients (25%; group I) slow pathway conduction disappeared 1 week after ablation. In six patients (30%; group II), the effective refractory period of the slow pathway was prolonged by more than 50 ms (212 +/- 81 ms vs 340 +/- 81 ms; P < 0.05). In the remaining nine patients (45%; group III), there was no change in the refractory period (270 +/- 65 ms vs 273 +/- 74 ms), although tachycardia was not inducible. A shortcut link between the fast and slow pathways was examined by comparing the A-H intervals over the slow pathway during the tachycardia and during atrial pacing at the tachycardia cycle length. Prior to ablation, a shortcut link was assumed in 1 of group I patients, 2 of group II patients, and 8 of group III patients. Of the 9 patients in whom the slow pathway was not impaired after ablation (group III), 8 patients were found to have a shortcut link, while 8 of 11 patients with impairment of the slow pathway after ablation (groups I and II) had no shortcut link between the fast and slow pathways (P < 0.05). CONCLUSION: In patients with a shortcut link between the fast and slow pathways, slow pathway conduction itself does not need to be impaired to eliminate the AVNRT, whereas in patients without this shortcut link, slow pathway conduction must be impaired.
To determine whether time- and frequency-domain analyses differ in their ability to predict sustained ventricular tachycardia (VT) induced by programmed ventricular stimulation, 60 consecutive patients with myocardial infarction and 30 healthy control subjects were evaluated. Programmed ventricular stimulation using three extrastimuli and signal-averaged ECG recordings were performed in patients with myocardial infarction. Of the 60 patients, sustained monomorphic VT (SMVT) with cycle length (CL) > or = 250 ms (slow SMVT) was inducible in 9, and SMVT with CL < 250 ms (fast SMVT) was inducible in 9. The durations of the filtered QRS (f-QRS) at each high-pass filter (25, 40, and 80 Hz) and the low amplitude signal (LAS) at 25-Hz high-pass filtering were significantly longer in the slow SMVT group than in the fast SMVT, no VT, or normal control group. The root-mean-square voltages at 25-Hz and 80-Hz high-pass filters in the slow SMVT group were significantly lower than in the fast SMVT, no VT, or normal control group. There was no significant difference in time-domain variables among fast SMVT, no VT, and normal control groups. The CL of the induced sustained VT was significantly correlated with the durations of f-QRS and LAS. Concerning frequency-domain variables (area ratio and factor of normality), there was no significant difference between slow and fast SMVT groups. Both the slow and fast SMVT groups had a significantly higher area ratio and a significantly lower factor of normality than the group with no VT or the normal control subjects. In conclusion, there were significant correlations between time-domain variables and CL of SMVT, while there was no correlation when using frequency-domain parameters.
The utility of selective radiofrequency catheter ablation of the slow pathway for the treatment of common and uncommon atrioventricular nodal reentrant tachycardia (AVNRT) was studied in 110 consecutive patients, 94 with slow-fast form common AVNRT, and 11 and 5, respectively, with the fast-slow and slow-slow forms of uncommon AVNRT. Ablation sites were determined by mapping a late and spiky "slow pathway potential" in the posterior right atrial septum in common AVNRT, and also the earliest retrograde atrial activation over the retrograde slow pathway in uncommon AVNRT. AVNRT was successfully eliminated in all patients with a mean number of radiofrequency pulses of 2.9 +/- 3.0 and a mean total energy applied of 3536 +/- 2996 joules. There were no early or late complications, except for transient AV block for 15 sec immediately after energy application in one common AVNRT patient, and no recurrence of AVNRT in a mean follow-up period of 24 +/- 13 months. There were no significant differences between common and uncommon AVNRT in success rate, mean application number and total energy applied. However, the AVN physiology post-ablation was different. Slow pathway conduction was eliminated in only 32% of the patients post-ablation in common AVNRT, while it was elininated in 100% in uncommon AVNRT. Selective radiofrequency catheter ablation of the slow pathway can cure common and uncommon AVNRT effectively and safely. Common AVNRT can be eliminated irrespective of the persistence of slow pathway conduction, while uncommon AVNRT can be eliminated by the eradication of slow pathway conduction.
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The AV nodal physiology before and 1 week after "slow pathway potential" guided catheter ablation was examined in 32 patients with AV nodal reentrant tachycardia. A mean of 4.9 applications of radiofrequency energy eliminated AV nodal reentrant tachycardia in all patients. There were no significant differences in sinus cycle length (815 +/- 159 msec vs 813 +/- 162 msec; P = NS) and fast pathway conduction properties before and 1 week after ablation. Slow pathway conduction was completely eliminated in 10 (31%) (group I) of 32 patients after ablation. In the remaining 22 patients residual slow pathway conduction associated with one AV node echo was observed. In 15 patients (47%) (group II), the effective refractory period of the slow pathway showed a change of < 30 msec (265 +/- 51 vs 266 +/- 51 msec; P = NS), and in 7 patients (22%) (group III), a prolongation of more than 80 msec (247 +/- 56 vs 340 +/- 42 msec; P = 0.0001) before and 1 week after ablation. Minimal and maximal A2-H2 interval over the slow pathway in group II was not significantly changed (Min A2-H2: 241 +/- 37 vs 247 +/- 40 msec; P = NS, Max A2-H2: 346 +/- 79 vs 350 +/- 60 msec; P = NS), while a significant prolongation was measured in group III (Min A2-H2: 261 +/- 53 vs 373 +/- 107 msec; P < 0.01, Max A2-H2: 359 +/- 41 vs 427 +/- 63 msec; P < 0.05) before and after ablation.(ABSTRACT TRUNCATED AT 250 WORDS)
Radiofrequency catheter ablation of atrioventricular accessory pathways was performed in 125 cases of the Wolff-Parkinson-White syndrome (type-A:54, type-B: 29, concealed: 42) complicated with drug-refractory and symptomatic atrioventricular reentrant tachycardia and/or paroxysmal atrial fibrillation. A total of 135 accessory pathways were identified: 50 left free-wall manifest, 34 left free-wall concealed, 21 right free-wall manifest, 2 right free-wall concealed, 15 posteroseptal manifest, 10 posteroseptal concealed, 2 right anteroseptal manifest and 1 right anteroseptal concealed. Accessory pathway conduction was successfully eliminated in 133 of these 135 accessory pathways (99%). Two right posteroseptal pathways were eventually ablated with direct current. Successful ablation required a mean 5.2 applications of radiofrequency current, a mean total energy of 2615 J and a mean fluoroscopic time of 52 min. The mean number of applications, applied energy and fluoroscopic time were greater in the right free-wall pathways than in the left free-wall pathways, and in the concealed pathways than in the manifest pathways. None of the procedures produced complications. During a mean follow-up period of 11.5 months, 1 right free-wall accessory pathway recurred and was ablated successfully in a repeat session. These results suggest that radiofrequency catheter ablation of accessory pathways is highly effective and safe irrespective of the accessory pathway location and properties, although these factors can affect the difficulty of this procedure. This technique may be an alternative to surgical therapy for Wolff-Parkinson-White syndrome with drug-refractory and symptomatic supraventricular tachyarrhythmias.
A 65-year-old male with Wolff-Parkinson-White syndrome presented with atrial fibrillation. The patient was found at the electrophysiological study to have two accessory pathways, a Kent fiber and an atrioventricular accessory pathway with decremental properties. The latter pathway conducted exclusively in the antegrade conduction and the ventricular insertion site was the tricuspid annulus. Both accessory pathways were successfully abolished by radiofrequency catheter ablations at the tricuspid annulus. We propose that an atrioventricular accessory pathway with decremental conduction may have various forms concerning not only sites of origin, but also sites of insertion.
BACKGROUND: Time and frequency domain analyses of signal-averaged ECG (SAECG) have several individual limitations, and the results of the two methods sometimes vary considerably. The purpose of this study was to determine whether the combined use of time and frequency domain variables facilitates identification of patients who will have ventricular tachycardia (VT) induced during programmed ventricular stimulation (PVS). METHODS AND RESULTS: Nine myocardial infarction (MI) patients with clinically documented sustained monomorphic VT (SMVT), 40 MI patients without clinical VT, and 30 normal healthy control subjects were evaluated. PVS using three extrastimuli and SAECG recording were performed in the MI patients on day 36 +/- 4 after infarction. Of 40 MI patients, SMVT was inducible in 14, sustained polymorphic VT in three, nonsustained monomorphic VT in three, nonsustained polymorphic VT in two, and no inducible arrhythmia was obtained in 18. There were significant differences between MI patients with inducible SMVT and without inducible SMVT in the following SAECG variables: filtered QRS durations (high-pass filter setting, 25, 40, and 80 Hz); low-amplitude signal durations (LAS) under 10, 20, 30, and 40 microV (high-pass filter setting, 40 and 80 Hz); root-mean-square voltages (RMS) of the terminal 20, 30, 40, 50, and 60 msec (high-pass filter setting, 40 and 80 Hz); area ratio (area 20-50 Hz/area 0-20 Hz x 10(5)) of a 120-msec sampling interval starting 20 msec before QRS offset; factor of normality on lead X; and minimum value of the variables on lead X, Y, or Z. Stepwise logistic regression analysis selected only LAS under 30 microV (high-pass filter setting, 80 Hz) and area ratio as independent predictors of inducible SMVT. With these two variables, the predicted probability of inducible SMVT [p(VT)] was expressed as p(VT) = 1/[1+exp (6.2-0.11 LAS-0.01 area ratio)]. This function had 93% sensitivity, 81% specificity, 72% positive predictive value, 95% negative predictive value, and 85% predictive accuracy with greater than or equal to 0.3 as the criterion of a positive test. CONCLUSIONS: The combined use of time and frequency domain analysis of SAECG can enhance the accuracy of this technique as a screening test for results of PVS in MI patients without clinical VT.
A 65-year-old man with chronic type B dissecting aortic aneurysm, complicated by variant from of angina pectoris without any coronary artery obstructed disease on preoperative angiogram was operated upon through left posterolateral thoracotomy under the left heart bypass with Bio-pump system using preoperative Ca antagonists and intraoperative nitroglycerin infusion. Shortly before the end of operation the patient suddenly developed shock status definitely due to coronary artery spasm, associated with ST-elevation in II, III, aVF and bradycardia, then ventricular tachycardia, finally cardiac arrest. The patient was resuscitated by cardiac massage and administration of nifedipine and nitroglycerin. Such attacks repeated five times at ten or twenty minutes intervals. The coronary artery spasm could be successfully suppressed with the additive use of noradrenaline infusion. The patient had no attacks at all postoperatively and was discharged with good success. This case suggests that the prevention of intraoperative coronary artery spasm is essential, but if it occurs, additive use of noradrenaline infusion is effective for the cessation of coronary artery spasm.
To determine the influence of timing on the prognostic value of programmed ventricular stimulation after acute myocardial infarction (AMI), 32 patients were studied on day 19 (early study) and again on day 36 (late study) after AMI using up to 3 extrastimuli. At the early study, sustained monomorphic ventricular tachycardia (VT) was induced in 12 patients (38%), sustained polymorphic VT in 8 (25%), nonsustained monomorphic VT in 1 (3%), nonsustained polymorphic VT in 1 (3%) and no inducible arrhythmia in 10 (31%). At the late study, sustained monomorphic VT, nonsustained monomorphic VT and nonsustained polymorphic VT were induced in 8 patients (25%) each, and no inducible arrhythmia in 8 (25%). Of the 12 patients who had inducible sustained monomorphic VT at the early study, 7 had noninducibility of sustained monomorphic VT at the late study. Of the 20 patients who had noninducibility of sustained monomorphic VT at the early study, 3 had inducible sustained monomorphic VT at the late study. During the follow-up period (mean +/- standard deviation 21 +/- 8 months), there were 2 sudden cardiac deaths and 3 occurrences of sustained VT. Univariate analysis revealed both inducibilities of sustained monomorphic VT at the early study (p = 0.045) and at the late study (p less than 0.001) to be predictive of sudden cardiac death or clinical occurrence of sustained VT. However, inducibility of sustained monomorphic VT at the late study had a higher sensitivity (100%), specificity (89%), positive predictive value (63%) and negative predictive value (100%) than at the early study (80, 70, 33 and 95%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)