Exercise-induced double (atrial and ventricular) tachycardia: a report of three cases.

Exercise-induced double tachycardia, i.e., the simultaneous occurrence of atrial and ventricular tachycardia, is described in three patients: one patient had coronary artery disease; the other two were young and had no apparent heart disease. One of the latter patients later died suddenly. Double tachycardia could not be initiated by programmed atrial or ventricular stimulation. In two patients atrial tachycardia always preceded ventricular tachycardia and, in one patient, ventricular tachycardia was terminated by the administration of adenosine triphosphate. Reentry does not seem to be the underlying mechanism for these arrhythmias; abnormal automaticity or triggered activity may be the mechanism.

Recovery of retrograde fast pathway excitability in the atrioventricular node reentrant circuit after concealed anterograde impulse penetration.

The recovery of the retrograde fast pathway excitability in atrioventricular (AV) node reentry has been difficult to assess with ventricular extrastimulation because of difficulty in achieving sufficiently short intranodal coupling intervals and the potential interposition of "lower common pathway" nodal tissue. To circumvent these methodologic obstacles in 10 patients with inducible AV node reentrant tachycardia, a fixed atrial extrastimulus (A2) coupled to a basic atrial drive (A1) at a cycle length of 500 ms was utilized to reproducibly initiate AV node reentrant echoes. A ventricular extrastimulus (V3) was then introduced after A2 at progressively shorter coupling intervals (A2V3) in an attempt to pre-excite the retrograde fast pathway after concealed anterograde penetration by A2. In six patients, retrograde fast pathway pre-excitation was achieved at critical A2V3 intervals, as evidenced by the appearance of A3 by up to 28 +/- 6 ms in advance of the expected first AV node reentrant echo. In five of the six cases, the V3A3 interval was virtually unaltered (less than or equal to 5 ms decrease) when A2 was omitted. In seven patients, at a critically short A2V3 coupling interval (195 +/- 27 ms ), V3 abruptly failed to elicit A3 and concomitantly abolished all AV node echoes; yet when A2 was omitted, an A3 response returned, with V3A3 identical to previous values.(ABSTRACT TRUNCATED AT 250 WORDS)

Sudden death in implantable cardioverter-defibrillator recipients: clinical context, arrhythmic events and device responses.

OBJECTIVES: We sought to investigate the nature of terminal events and potential contributory clinical and nonclinical (e.g., device-related) factors associated with sudden death (SD) in recipients of an implantable cardioverter-defibrillator (ICD). BACKGROUND: The ICD is very effective in terminating ventricular tachycardia (VT) or ventricular fibrillation (VF), but protection against SD is not absolute. Little is known about the nature and potential causes of SD in patients with ICDs. METHODS: We analyzed 25 cases of out-of-hospital SD among patients enrolled in the clinical investigation of the Cadence Tiered-Therapy Defibrillator System. RESULTS: All patients (24 men and 1 woman, mean age 62+/-10 years) received epicardial lead systems. The majority (92%) had coronary artery disease and a previous myocardial infarction (MI), with a mean left ventricular ejection fraction 0.25+/-0.07. At device implantation, the mean defibrillation threshold was 13+/-5 J. Sudden death occurred 13+/-11 months later. Twenty patients (80%) had received appropriate ICD therapies before death, and 18 (72%) were receiving > or = 1 antiarrhythmic drugs at the time of death. Sudden death was tachyarrhythmia-associated in 16 patients (64%), non-tachyarrhythmia-associated in 7 (28%) and indeterminate in 2 (8%). In the 16 patients with tachyarrhythmia-associated SD, the overall first therapy success rate in tachycardia and fibrillation zones was 60% and 67%, respectively. However, despite protracted therapies (> or = 2 shocks) in 7 (66%) of 12 patients who received fibrillation therapies, the final tachyarrhythmic episode was ultimately terminated by the ICD in 15 (94%) of the 16 patients, whereas 1 patient died after multiple (initially successful) internal and external shocks for intractable VT/VF during exercise. In 10 patients (40%) one or more, primarily clinical, factors potentially contributory to SD were identified: heart failure (n=8), angina (n=2), hypokalemia (n=1), adverse antiarrhythmic drug treatment (n=1) and acute MI (n=1). An additional 10 patients (40%) had experienced an increase in frequency of ICD shocks within 3 months of SD. Appropriate battery voltages and normal circuitry function were found in all devices interrogated and analyzed after death. CONCLUSIONS: In this select group of patients receiving a third-generation ICD, SD was associated with VT or VF events in nearly two-thirds of patients, and death occurred despite ultimately successful, although often protracted, device therapies. These observations, along with evidence of recent worsening clinical status, suggest acute cardiac mechanical dysfunction as a frequent terminal factor. In recipients with ICDs, SD directly attributable to device failure seems to be rare.

Systematic characterization of the reentrant circuit during atrioventricular nodal reentrant tachycardia.

This study was conducted to systematically characterize the excitable gap and conduction properties of the reentrant circuit during atrioventricular nodal reentrant tachycardia (AVNRT). Previous studies have attempted to analyze these properties by introducing single ventricular extrastimuli during tachycardia. These studies have been limited, however, by the inability of single extrastimuli to engage the circuit in the majority of patients studied. Thus, in most cases, the nature of the excitable gap and the conduction properties of the anterograde and retrograde limbs of the circuit during tachycardia remain undefined. In this series, 11 patients with typical AVNRT were studied. During tachycardia, both single and double ventricular extrastimuli (the first extrastimulus acting as a conditioning stimulus) were used to scan diastole. The resetting response of the reentrant circuit, as well as the conduction properties of the retrograde fast and anterograde slow pathways, was recorded and analyzed. Whereas atrial preexcitation and resetting of the reentrant circuit could be demonstrated in only 1 patient with single ventricular extrastimuli, resetting was achieved in all 11 patients with closely coupled double ventricular extrastimuli. Over the full range of coupling intervals used, no retrograde delay in fast pathway conduction could be demonstrated before tachycardia termination or ventricular refractoriness. Penetration of the reentrant circuit resulted in a progressive increasing delay in the anterograde portion of the subsequent return cycle and an increasing resetting response pattern in all cases. Thus, the reentrant circuit during AVNRT demonstrates heterogeneous excitability. While the fast pathway remains fully excitable during tachycardia, the slow pathway uniformly demonstrates decremental conduction, resulting in an increasing resetting response pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Reemployment following implantation of the automatic cardioverter defibrillator.

One hundred one patients who received an implantable automatic cardioverter defibrillator (ACD) were evaluated to determine the reemployment rate and factors associated with return to work. Forty-seven were employed before ACD implantation. Their mean (+/- standard deviation) age was 53 +/- 11 years, 83% were men, 75% had coronary artery disease, 76% presented with cardiac arrest and 28% had concomitant cardiac surgery. The mean ejection fraction of these patients was 0.41 +/- 0.15. At follow-up, 29 patients (62%) had resumed work at 11 +/- 9 weeks after implantation. Those who returned to work were better educated (15 vs 11 years, p less than 0.001) and less likely to have a history of prior myocardial infarction (p less than 0.05). There were no significant differences between patients who returned to work and those who did not in terms of age, sex, race, functional class, ejection fraction, extent of coronary artery disease, reason for ACD, or concomitant surgery. Multivariate analysis revealed that level of education was the single best predictor of reemployment status. The only other factors found to add significant predictive power in a stepwise analysis were extent of coronary artery disease and marital status. The model using these 3 variables had a sensitivity of 83% and a specificity of 72%. It was concluded that (1) most patients employed before ACD implantation are able to return to work after the procedure, and (2) nonmedical factors play an important role in the resumption of work-related activities. These findings have important quality-of-life and cost-effectiveness implications for ACD implantees.

Does subclinical hypothyroidism explain the increased susceptibility of women to torsades de pointes?

Among 20 consecutive patients (65% women) with drug-associated torsades de pointes, chemical evidence for hypothyroidism was found in only 10% of both women and men. Subclinical hypothyroidism is therefore unlikely to account for the consistently observed sex difference in the propensity to torsades de pointes.

Clinical management of patients with atrioventricular nodal reentrant tachycardia.

A broad array of therapeutic options is currently available for the management of patients with AV nodal reentrant tachycardia. While acute termination of tachycardias is readily achieved, either by vagal maneuvers or intravenous medication, the decision to embark on a long-term therapeutic plan to prevent recurrences must be clinically individualized. When a chronic pharmacologic approach is desired, electrophysiologic testing is invaluable for confirming the diagnosis and selecting appropriate medication. However, the growing awareness of potential proarrhythmic effects and the inconvenience and expense of lifelong drug therapy, coupled with other advances in the field, have made nonpharmacologic approaches more attractive. This is especially so for symptomatic younger patients. The definitive cure rates achievable with surgery are now being approached by transcatheter AV nodal modification procedures that ablate AV nodal reentrant tachycardia while preserving anterograde AV nodal conduction. Over the next decade, it is likely that the latter technique will become widely used for the long-term management of symptomatic AV nodal reentrant tachycardia.

The excitable gap in atrioventricular nodal reentrant tachycardia. Characterization with ventricular extrastimuli and pharmacologic intervention.

Our purpose was to characterize the excitable gap during atrioventricular nodal reentrant tachycardia (AVNRT) to elucidate the electrophysiologic substrate of this clinically familiar microreentrant arrhythmia. Accordingly, in 11 patients with classic slow-fast AVNRT (mean cycle length, 342 +/- 41 msec), a single ventricular extrastimulus (V2) was periodically delivered after a spontaneous tachycardia beat (V1) until ventricular refractoriness was reached. With this technique, an excitable gap was considered present when atrial preexcitation of at least 20 msec could be achieved along with tachycardia resetting (noncompensatory pause after V2). The range of V1V2 intervals that resulted in atrial preexcitation constituted the preexcitation zone. Five patients (45%) showed evidence of an excitable gap at baseline, with a maximal atrial preexcitation achievable of 33 +/- 6 msec, representing 9 +/- 1% of the tachycardia cycle length. Verapamil was then administered to all 11 patients with the purpose of slowing the anterograde tachycardia wavefront before arrival of V2. This resulted in widening of the preexcitation zone in three patients by a mean of 50 +/- 37 msec, with a corresponding increase in maximal atrial preexcitation to 70 +/- 32 msec, or 16 +/- 4% of AVNRT cycle length, and the appearance of atrial preexcitation in two patients who lacked it during baseline. In the remaining six patients, AVNRT was not sustained after verapamil or was too unstable for evaluation. During baseline, V2A2 conduction time increased by only 5 +/- 3 msec throughout the preexcitation zone, with values at the outer border unchanged after verapamil, implying a fully excitable gap in the retrograde limb. In all patients with a preexcitation zone, AVNRT was consistently reset by V2, both at baseline and after verapamil, with a "flat" but mainly "increasing" response pattern as V1V2 was shortened. Hence, a significant number of patients with AVNRT have evidence of an excitable gap whose demonstrability can be facilitated by pharmacologic intervention; documentation of an increasing resetting response pattern, most apparent after verapamil, provides new evidence for a reentrant mechanism in AVNRT; and while not definitively proven, the presence of a fully excitable gap during AVNRT is most consistent with a microreentry circuit that incorporates an anatomic obstacle.

Atrial sensing to augment ventricular tachycardia detection by the automatic implantable cardioverter defibrillator: a utility study.

The triggering of automatic implantable cardioverter defibrillator (AICD) discharges by supraventricular tachycardias, despite the presence of a probability density function algorithm, remains a limitation of an otherwise highly effective device. We systematically investigated the diagnostic utility which theroretically could derive form the addition of atrial sensing capability to the AICD in 25 patients with 30 inducible sustained monomorphic ventricular tachycardias (VTs) at clinically relevant rates (greater than or equal to 150 beats/min). Patients were included only if they were not taking medication capable of depressing ventriculoatrial (VA) conduction for at least 5 half-lives prior to electrophysiological testing. We tested the simple criterion for VT that ventricular cycle length (CL) be shorter than the atrial CL (not met in sinus or most other supraventricular tachycardias). Mean VT CL was 283 +/- 47 ms (range 210 to 370). In 25 (83%) VTs, the VT criterion was consistently satisfied. Of the five cases in which the criterion was not met, 1:1 VA conduction during VT was present in four, three of which initially manifested 2:1 VA conduction lasting from 14 to 28 s and therefore would have transiently fulfilled the VT criterion. The remaining patient who failed to satisfy the VT criterion had ongoing atrial flutter during a relatively slower sustained VT, but this circumstance could be recognized because of the varying AV interval. The absence of 1:1 VA conduction at CLS less than or equal to 400 ms during ventricular pacing accurately predicted the absence of 1:1 VA conduction during VT in 95% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Invasive electrophysiologic evaluation in octogenarians: is age a limiting factor?

To assess the indications, diagnostic yield, and incidence of complications of electrophysiologic testing in the elderly we reviewed our experience with 60 procedures in 45 patients aged > or = 80 years (range 80 to 92 years, mean age 83) undergoing full electrophysiologic evaluation in our laboratory over the past 7 years. The yield of inducible ventricular tachycardia (31%), supraventricular tachycardia (4%), and previously unsuspected conduction abnormalities significant enough to warrant permanent pacemaker implantation (9%), together with the low incidence of complications (1 patient had a deep venous thrombosis and femoral artery pseudoaneurysm, representing an incidence of 2.2% of patients undergoing studies or 3.3% incidence of complications per procedure), suggest that invasive electrophysiologic procedures in the elderly can provide useful information at a complication rate comparable with that of younger patients.

Ventricular lead transection and atrial lead damage in a young softball player shortly after the insertion of a permanent pacemaker.

We report a case in which permanent pacemaker implantation using a conventional subclavian approach on the throwing side of an avid softball player resulted in complete transection of the ventricular lead and severe damage to the atrial lead. The site of the lead fracture suggested that both leads were crushed between the clavicle and the first rib as a result of the frequent and repetitive arm movement. This case illustrates the importance of the selection of the correct approach for permanent pacing lead insertion.

Wide QRS tachycardia in the conscious adult. Ventricular tachycardia is the most frequent cause.

Hemodynamic stability during wide QRS tachycardia is commonly, albeit erroneously, taken as evidence for a supraventricular mechanism. To determine the magnitude for potential misdiagnosis in applying this notion clinically, we analyzed 20 consecutive cases of regular wide QRS tachycardia in conscious adult patients (mean age, 64 years). The most common heart disease was atherosclerotic (75%), with an associated history of remote myocardial infarction in 73% of the cases. Tachycardia was sustained for a mean of 4.8 hours prior to medical evaluation, with a mean rate of 186 beats per minute and mean systolic blood pressure of 111 mm Hg. A diagnosis of ventricular tachycardia (VT) was established in 17 cases (85%). In the patients with VT, atrioventricular dissociation was recognized on the 12-lead electrocardiogram in 38%, with Wellens' morphological features favoring the diagnosis in 73%. Following conversion to sinus rhythm, electrophysiological testing in 17 patients reproduced the clinical arrhythmia in 94% (with a replication rate of 100% in 15 patients with VT), with at least one additional unsuspected VT morphology induced in 53% of patients with VT. Thus, VT should be considered the most likely cause of regular wide QRS tachycardia in the conscious adult patient, especially with a history of remote myocardial infarction. Recognition of this simple principle and careful examination of the 12-lead electrocardiogram may help to prevent the misapplication of pharmacotherapy in the vast majority of these patients.

Coincident idiopathic left ventricular tachycardia and atrioventricular nodal reentrant tachycardia: control by radiofrequency catheter ablation of the slow atrioventricular nodal pathway.

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.

Sinus node and atrioventricular nodal function in 220 patients recovering from acute myocardial infarction.

Sinus node and atriventricular (A-V) nodal functions were evaluated by right atrial pacing in 220 consecutive patients recovering from acute myocardial infarction (AMI), 10-28 days after the infarct (mean = 14 days). In the 188 patients in whom a pacing rate of 120 beats/min could be achieved, sinus node recovery time, corrected sinus node recovery time (CSNRT) and total recovery time were correlated to infarct site and the presence or absence of myocardial ischemia. Sinus node recovery time and total recovery time were significantly longer in patients with inferior (1,153 + 28 and 3,129 + 179 ms, respectively) or non-Q-wave infarct (1,112 + 28 and 3,730 + 266 ms, respectively), than in patients with anterior infarct (1,044 + 20 and 1,153 + 28 ms, respectively). The parameters were within the reported normal range. When corrected for heart rate (CSNRT), these differences were no longer present. The presence or site of residual ischemia during right atrial pacing did not affect the sinus nodes parameters. A-V nodal function, studied in all 220 patients, was assessed by the appearance of second-degree A-V block at pacing rates below 120 beats/min and by measuring the shortest atrially paced cycle length with 1:1 A-V conduction. Second-degree A-V block appeared at a similar frequency in different AMI locations. Thus, sinus and A-V node functional status in patients recovering from AMI are not affected by infarct site or by the presence or absence of residual myocardial ischemia.

Percutaneous transcatheter laser balloon ablation from the canine coronary sinus: implications for the Wolff-Parkinson-White syndrome.

Transcatheter direct current electrical shocks for ablation of left-sided accessory pathways in Wolff-Parkinson-White patients have led to serious complications. We report the feasibility of percutaneous transcatheter laser balloon ablation of left-sided accessory pathways from the coronary sinus using a 1,064-nm, continuous wave Nd:YAG laser triple lumen catheter with an optical fiber terminating in a cylindrical diffusing tip within a 2-cm-long, 3-mm-diameter balloon transparent to Nd:YAG laser radiation. In eight mongrel dogs (18 to 31 kg), the laser balloon catheter was positioned via an 8 French guide catheter in the distal and proximal coronary sinus. During balloon inflation, two to three consecutive laser doses of 30 W x 20 sec were applied to each site (cumulative energy, 1,200 to 1,800 J). Coronary angiography, left ventriculography, and coronary sinus injection were performed before and after laser exposure. After percutaneous transcatheter laser balloon ablation, there was no evidence of mitral regurgitation, left circumflex artery, coronary sinus obstruction, or perforation. Coagulation necrosis and/or polymorphonuclear infiltrates involving the atrioventricular groove and left atrial wall over a mean length of 17 mm were present in all eight dogs sacrificed 6 +/- 1 hr postablation. In conclusion, percutaneous transcatheter laser balloon ablation from the coronary sinus is free of immediate major complications and may be feasible for potential interruption of left-sided accessory pathways.