Atypical atrioventricular node reciprocating tachycardia masquerading as tachycardia using a left-sided accessory pathway.

OBJECTIVES: The study was performed to document that atrioventricular node reciprocating tachycardia (AVNRT) can be associated with eccentric retrograde left-sided activation, masquerading as tachycardia using a left accessory pathway. BACKGROUND: The eccentric retrograde left-sided activation during tachycardia is thought to be diagnostic of the presence of a left free wall accessory pathway. However, it is not known whether AVNRT can occur with eccentric retrograde left-sided activation. METHODS: We studied 356 patients with AVNRT who underwent catheter ablation. Retrograde atrial activation during tachycardia and ventricular pacing were determined by intracardiac recordings, including the use of a decapolar coronary sinus catheter. RESULTS: The retrograde atrial activation was eccentric in 20 patients (6%). Eight of these patients had the earliest retrograde atrial activation recorded in the lateral coronary sinus leads, and 12 had the earliest retrograde atrial activation recorded in the posterior coronary sinus leads, with the most proximal coronary sinus electrode pair straddling the coronary sinus orifice. These tachycardias were either the fast-slow or the slow-slow form of AVNRT. The slow-fast form of AVNRT was also inducible in 17 of the 20 patients. Successful ablation of the slow pathway in the right atrial septum near the coronary sinus ostium prevented the induction and clinical recurrence of reciprocating tachycardia in all patients. CONCLUSIONS: Atypical AVNRT with eccentric retrograde left-sided activation was demonstrated in 6% of all patients with AVNRT masquerading as tachycardia using a left-sided accessory pathway. Ablation of the slow pathway at the posterior aspects of the right atrial septum resulted in a cure in these patients.

Upper limit of vulnerability predicts chronic defibrillation threshold for transvenous implantable defibrillators.

INTRODUCTION: The upper limit of vulnerability (ULV) is the shock strength at or above which ventricular fibrillation cannot be induced when delivered in the vulnerable period. It correlates acutely with the acute defibrillation threshold (DFT) and can be determined with a single episode of fibrillation. The goal of this prospective study was to determine the relationship between the ULV and the chronic DFT. METHODS AND RESULTS: We studied 40 patients at, and 3 months after, implantation of transvenous cardioverter defibrillators. The ULV was defined as the weakest biphasic shock that failed to induce fibrillation when delivered 0, 20, and 40 msec before the peak of the T wave. patients were classified as clinically stable or unstable based on prospectively defined criteria. There were no significant differences between the group means for the acute and chronic determinations of ULV (13.5 +/- 5.3 J vs 12.4 +/- 6.8 J, P = 0.25) and DFT (10.1 +/- 5.0 J vs 9.9 +/- 5.7 J, P = 0.74). Five patients (15%) were classified as unstable. The strength of the correlation between acute ULV and acute DFT (r = 0.74, P < 0.001) was similar to that between the chronic ULV and chronic DFT (r = 0.82, P < 0.001). There was a correlation between the change in ULV from acute to chronic and the corresponding change in DFT (r = 0.67, P < 0.001). The chronic DFT was less than the acute ULV +3 J in all 35 stable patients, but it was greater in 2 of 5 unstable patients (P = 0.04). CONCLUSIONS: The strength of the correlation between the chronic ULV and the chronic DFT is comparable to that between the acute ULV and the acute DFT. Temporal changes in the ULV predict temporal changes in the DFT. In clinically stable patients, a defibrillation safety margin of 3 J above the acute ULV proved an adequate chronic safety margin.

Programming of implantable cardioverter-defibrillators on the basis of the upper limit of vulnerability.

BACKGROUND: A patient-specific measure of defibrillation efficacy that requires a minimum number of ventricular fibrillation (VF) episodes would be valuable for programming implantable cardioverter-defibrillators (ICDs). The upper limit of vulnerability (ULV) is the weakest shock strength at or above which VF is not induced when a stimulus is delivered during the vulnerable phase of the cardiac cycle. It correlates with the defibrillation threshold (DFT) and can be determined with a single episode of VF. The objective of this study was to test the hypothesis that ICDs programmed on the basis of the ULV convert spontaneous ICD-detected VF reliably. METHODS AND RESULTS: We studied 100 consecutive patients at ICD implantation and during follow-up of 20 +/- 7 months. At implantation, the ULV and DFT were determined, and the ICD system was tested at a shock strength equal to the ULV + 3 J. During follow-up, the strength of the first shock was programmed to the ULV + 5 J for arrhythmias detected in the VF zone (cycle length < 292 +/- 17 ms). We reviewed stored detection intervals and electrograms from spontaneous episodes of ICD-detected VF to determine the success rate for appropriate first shocks. The programmed first-shock strength was 17.5 +/- 5.2 J. During follow-up, there were 120 appropriate first shocks in 37 patients. The arrhythmia was rapid monomorphic ventricular tachycardia (VT) in 70% of episodes (31 patients), VF in 11% (13 patients), polymorphic VT in 1%, and unclassified in 17% (15 patients). The first shock was successful in 119 of 120 episodes (99%; 95% CI, 93% to 100%). One unclassified episode required two shocks. No patient had syncope associated with an ICD shock or arrhythmic death. CONCLUSIONS: ICD shocks can be programmed on the basis of the ULV, a measurement made in regular rhythm, without a direct measure of defibrillation efficacy.

The zone of vulnerability to T wave shocks in humans.

INTRODUCTION: Shocks during the vulnerable period of the cardiac cycle induce ventricular fibrillation (VF) if their strength is above the VF threshold (VFT) and less than the upper limit of vulnerability (ULV). However, the range of shock strengths that constitutes the vulnerable zone and the corresponding range of coupling intervals have not been defined in humans. The ULV has been proposed as a measure of defibrillation because it correlates with the defibrillation threshold (DFT), but the optimal coupling interval for identifying it is unknown. METHODS AND RESULTS: We studied 14 patients at implants of transvenous cardioverter defibrillators. The DFT was defined as the weakest shock that defibrillated after 10 seconds of VF. The ULV was defined as the weakest shock that did not induce VF when given at 0, 20, and 40 msec before the peak of the T wave or 20 msec after the peak in ventricular paced rhythm at a cycle length of 500 msec. The VFT was defined as the weakest shock that induced VF at any of the same four intervals. To identify the upper and lower boundaries of the vulnerable zone, we determined the shock strengths required to induce VF at all four intervals for weak shocks near the VFT and strong shocks near the ULV. The VFT was 72 +/- 42 V, and the ULV was 411 +/- V. In all patients, a shock strength of 200 V exceeded the VFT and was less than the ULV. The coupling interval at the ULV was 19+/- 11 msec shorter than the coupling interval at the VFT (P < 0.001). The vulnerable zone showed a sharp peak at the ULV and a less distinct nadir at the VFT. A 20-msec error in the interval at which the ULV was measured could have resulted in underestimating it by a maximum of 95 +/- 31 V. The weakest shock that did not induce VF was greater for the shortest interval tested than for the longest interval at both the upper boundary (356 +/- 108 V vs 280 +/- 78 V; P < 0.01) and lower boundary (136 +/- 68 msec vs 100 +/- 65 msec; P < 0.05). CONCLUSIONS: The human vulnerable zone is not symmetric with respect to a single coupling interval, but slants from the upper left to lower right. Small differences in the coupling interval at which the ULV is determined or use of the coupling interval at the VFT to determine the ULV may result in significant variations in its measured value. An efficient strategy for inducing VF would begin by delivering a 200-V shock at a coupling interval 10 msec before the peak of the T wave.

The retropectoral transaxillary permanent pacemaker: description of a technique for percutaneous implantation of an "invisible" device.

This report describes a percutaneous, transaxillary approach for implanting permanent pacemakers in the retropectoral space. This approach was used in 17 patients; indications for the procedure included the need to find a new implantation site in patients with infections and multiple previous pacemaker pocket sites (2 patients), emaciation and absence of sufficient adipose tissue (4 patients), and cosmetic considerations (11 patients). No complications were encountered during the implantation and the results were uniformly excellent in all patients. The pacemaker was "invisible" in each case. We conclude that a percutaneous approach for implanting permanent pacemakers in the retropectoral region is safe and feasible. This approach is likely to be applicable to the implantation of transvenous antitachycardia devices.

Optimal electrode configuration for pectoral transvenous implantable defibrillator without an active can.

A new 83 cm3 implantable cardioverter-defibrillator (ICD) designed for pectoral implantation has been implanted most frequently using right ventricular and superior vena cava (RV-->SVC) electrodes; a patch electrode (RV-->patch + SVC) has been added when necessary to decrease the defibrillation threshold (DFT). The goal of this prospective study was to compare biphasic waveform DFTs for 3 electrode configurations: RV-->patch, RV-->SVC, and RV-->patch + SVC in 25 consecutive patients. The patch was positioned in a left retro-pectoral pocket, and the SVC electrode was positioned with the tip at the junction of the SVC and innominate vein. In the first 15 patients, all 3 electrode configurations were tested in random order; in the last 10 patients, only the RV-->patch and RV-->patch + SVC configurations were tested. In the first 15 patients, the stored-energy DFT for the RV-->SVC configuration (15.2 +/- 7.7 J) was higher (p < 0.001) than the DFT for the RV-->patch configuration (11.3 +/- 6.2 J) and the RV-->patch + SVC configuration (10.0 +/- 5.8 J). For all 25 patients, the DFT was lower for the RV-->patch + SVC configuration (9.7 +/- 5.1 J) than for the RV-->patch configuration (12.4 +/- 6.6 J, p = 0.005). The pathway resistance was highest for the RV-->patch configuration (72 +/- 9 omega), lower for the RV-->SVC configuration (63 +/- 6 omega, p < 0.01), and lowest for the RV-->patch + SVC configuration (46 +/- 3 omega, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Upper limit of vulnerability reliably predicts the defibrillation threshold in humans.

BACKGROUND: The upper limit of vulnerability is the stimulus strength above which electrical stimulation cannot induce ventricular fibrillation even when the stimulus occurs during the vulnerable period of the cardiac cycle. The purpose of this study was to test the hypothesis that the upper limit of vulnerability can accurately predict the defibrillation threshold in patients undergoing implantable cardioverter-defibrillator (ICD) implantation using nonthoracotomy lead systems. METHODS AND RESULTS: We studied 77 patients at the time of ICD implantation. Multiple endocardial-endocardial and endocardial-subcutaneous shock pathways were used. Two different protocols were used to test the upper limit of vulnerability. In protocol 1 (n = 17), the upper limit of vulnerability was tested with two shocks on the peak or the up-slope of the T wave of paced rhythm. The shocks were given randomly either at the peak and 20 milliseconds before the peak of T wave (n = 7) or at 20 and 40 milliseconds before the peak of T wave (n = 10). In protocol 2 (n = 60), the upper limit of vulnerability was tested with three shocks delivered at 0, 20, and 40 milliseconds before the peak of the T wave. The weakest shock that failed to induce ventricular fibrillation by a 5-J step-down or step-up method was defined as the upper limit of vulnerability. The defibrillation threshold was also determined by a 5-J step-down or step-up method. In protocol 1, the upper limit of vulnerability (9 +/- 6 J) was significantly lower than the defibrillation threshold (13 +/- 7 J) with a correlation coefficient of .87 and P < .001. In protocol 2, the upper limit of vulnerability (13 +/- 6 J) was not significantly different from the defibrillation threshold (13 +/- 6 J) with a correlation coefficient of .85 and P < .001. In 45 of the 60 patients, the upper limit of vulnerability was < or = 15 J; all had a defibrillation threshold of < or = 20 J. In 51 of the 60 patients, the upper limit of vulnerability was within 5 J of the defibrillation threshold. The upper limit of vulnerability overestimated the defibrillation threshold by > 10 J in 8 patients and underestimated the defibrillation threshold by > 10 J in only 1 patient. The overestimation and underestimation occurred only in patients with the upper limit of vulnerability > 15 J. CONCLUSIONS: When tested with three shocks on and before the peak of the T wave, the upper limit of vulnerability accurately predicted the defibrillation threshold in patients undergoing ICD implantation using nonthoracotomy lead systems. This method required either one or no episodes of ventricular fibrillation in most patients.

Transmyocardial impedance during single and multiple internal ventricular defibrillation shocks.

Little is known about the transmyocardial impedance during internal ventricular defibrillation. In a canine model, using high rate on-line digitization, random shock delivery, and titanium electrodes, we determined the relationship among voltage, current, and impedance, delivered energy, and defibrillation success within the individual and within successive defibrillation shocks. Impedance decreased with repeated defibrillation in 10 of 11 dogs. Impedance always increased during trapezoidal discharges, whereas voltage decreased. Impedance was lower with high energy-voltage shocks in all dogs. Visually, voltage and current waveform did not show a phase shift. There was no difference in the total energy delivered and the energy converted into heat by the resistive part of the impedance. With a formula valid only for resistive loads, the capacitance of the defibrillator was calculated to be within the measurement accuracy and tolerance of the factory-provided value of 132 microF. Polarization voltage was consistently observed. Thus the transmyocardial impedance during defibrillation is primarily resistive, nonlinear voltage dependent, and declines with successive shocks. Defibrillation success was not influenced by these phenomena.

Relation between upper limit of vulnerability and defibrillation threshold in humans.

BACKGROUND: In the canine model, an upper limit of shock strength exists that can induce ventricular fibrillation during the vulnerable period of the cardiac cycle. This shock strength (the upper limit of vulnerability) closely correlates with the defibrillation threshold and supports the "upper limit of vulnerability" hypothesis of defibrillation. It is not known whether an upper limit of vulnerability exists in humans or whether this limit correlates with the defibrillation threshold. METHODS AND RESULTS: In 13 patients undergoing implantable cardioverter-defibrillator implantation, the shock strengths associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) and a 50% probability of reaching the defibrillation threshold (DFT50) were determined by the up-down algorithm. The ULV50 was determined only for the mid-upslope of the positive T waves and for the mid-downslope of the negative T waves. No major complications occurred during surgery. An upper limit of vulnerability was demonstrated in each patient. The ULV50 was 300 +/- 138 V or 6.8 +/- 5.8 J, which was significantly lower than the DFT50 of 347 +/- 167 V (p = 0.038) or 9.1 +/- 7.3 J (p = 0.013). The correlation between the ULV50 and the DFT50 was significant (r = 0.90, p < 0.001 for voltage; r = 0.93, p < 0.001 for energy). CONCLUSIONS: An upper limit of vulnerability is present in humans. There is a significant correlation between the ULV50 and the DFT50, and the ULV50 is significantly lower than the DFT50.

Selection of patients for programmed ventricular stimulation: a clinical decision-making model based on multivariate analysis of clinical variables.

OBJECTIVE: This study was conducted to assess the utility of clinical variables in predicting the inducibility of sustained ventricular arrhythmias in a heterogeneous group of patients undergoing programmed ventricular stimulation. METHODS: Variables were considered in a simulated chronologic order to determine the incremental information added by the signal-averaged electrocardiogram (ECG) and left ventricular ejection fraction. All patients undergoing baseline programmed ventricular stimulation for induction of ventricular tachyarrhythmia during a 30-month period were included in the study. Fourteen historical, ECG, signal-averaged ECG and left ventricular wall motion variables were evaluated for their ability in predicting inducibility of a sustained ventricular arrhythmia, a "positive" event, at programmed ventricular stimulation. RESULTS: On univariate analysis of the clinical variables, comparison between patients with positive or negative results showed significant differences in 10 of the 14 clinical variables: major cardiac diagnosis, history of ventricular tachycardia, myocardial infarction by history or ECG, all five signal-averaged ECG variables, left ventricular ejection fraction and presence of left ventricular aneurysm. On multivariate analysis, five independent variables were determined to be important: history of ventricular tachycardia, historical or ECG evidence of myocardial infarction, history of loss of consciousness, filtered QRS duration on the signal-averaged ECG and left ventricular ejection fraction. However, with sequential multivariate analysis, a model based only on historical and conventional ECG data was found to do as well as a model that included signal-averaged ECG and left ventricular ejection fraction data. CONCLUSIONS: Routinely available noninvasive historical, ECG, signal-averaged ECG and left ventricular wall motion variables can be used to accurately predict the outcome of programmed ventricular stimulation. The majority of the predictive power was obtained with the routine model, using only historical and ECG data. The signal-averaged ECG and left ventricular wall motion analysis added no significant incremental information.

Relation between acute ventricular arrhythmias, ventricular late potentials and mortality in acute myocardial infarction.

The relation between ventricular late potentials and the occurrence of acute (in-hospital) and hyperacute (before hospital admission) ventricular tachycardia or fibrillation was studied in 281 consecutive patients with uninterrupted acute myocardial infarction. The prevalence of late potentials was significantly higher in patients with than without ventricular tachycardia/fibrillation (65 vs 22%; p less than 0.01). These relations persisted among patients with left bundle branch block, although a different definition was used for identifying late potentials in these patients. Multivariate analysis showed that presence of late potentials and peak creatine kinase enzyme level were the only 2 independent variables associated with early ventricular tachycardia/fibrillation. Total in-hospital mortality, as well as in-hospital cardiac mortality, was significantly higher among patients with than without acute ventricular tachycardia/fibrillation. However, at 1 year, mortality rates did not differ between the 2 groups. The following conclusions were drawn from this study: (1) Late potentials are closely related to ventricular tachycardia/fibrillation in hyperacute and acute phases of infarction. (2) Presence of left bundle branch block does not mitigate against the finding of late potentials in these patients. (3) Early ventricular tachycardia/fibrillation in acute infarction is related to large infarctions and to a high in-hospital mortality rate.

Acute effects of intravenous propafenone on the internal ventricular defibrillation threshold in the anesthetized dog.

In 10 treated and 2 control dogs, the short-term effects of intravenous propafenone (2 mg/kg/10 minutes, followed by 1 mg/min [n = 2] or 25 micrograms/kg/min [n = 8]) on the internal ventricular defibrillation energy requirements (DER) were investigated. Multiple stored energy levels were randomly tested and the percent successful defibrillation was plotted against the stored energy, and the raw data were fit by logistic regression. The energy at 50% (E50) and 80% (E80) defibrillation success increased after propafenone by a mean of 75% (8.4 +/- 2.4 to 14.7 +/- 5.9 joules, p less than or equal to 0.05) and 59% (11.1 +/- 3.5 to 17.6 +/- 6.7 joules, p less than or equal to 0.05), respectively. Plasma propafenone levels ranged from 778 to 2554 ng/ml (1495 +/- 592 ng/ml) at the beginning to 833 to 2193 ng/ml (1297 +/- 389 ng/ml) at the end of the defibrillation trials. Two dogs served as controls and received Ringer's solution instead of propafenone and showed the temporal stability of the preparation. In conclusion, intravenous propafenone increases the internal ventricular DER in this canine model. This may have important clinical implications in patients with automatic implantable cardioverter-defibrillators (AICDs) receiving concomitant antiarrhythmic drug therapy and in patients undergoing therapy with intravenous propafenone.

Age-related changes in the clinical and electrophysiologic characteristics of patients with Wolff-Parkinson-White syndrome: comparative study between young and elderly patients.

The natural history of patients with Wolff-Parkinson-White (WPW) syndrome remains an intriguing question with respect to clinical decision-making, since serial electrophysiologic data spread over several decades in the same patient are not available in the literature. To study the age-related changes in WPW syndrome, we compared two separate groups of patients referred to this Medical Center for electrophysiologic studies because of a clinical presentation with significant arrhythmias. An elderly group of 42 patients aged 50 years or more were compared with a younger group of 51 patients aged 15 to 30 years. The groups were comparable in terms of clinical presentation, including the number of patients who had reported syncopal episodes and those requiring cardioversion of their tachyarrhythmias. Baseline electrophysiologic variables such as sinus rate; sinoatrial conduction time; corrected sinus node recovery time; AH interval; and effective refractory periods of the right atrium, atrioventricular (AV) node, and right ventricular muscle, were significantly greater in the elderly group. Similarly, the anterograde effective refractory period of the bypass tract, the shortest atrial pacing cycle length with 1:1 anterograde conduction via the bypass tract, retrograde effective refractory period of the bypass tract, the shortest ventricular pacing cycle length with 1:1 retrograde conduction via the bypass tract, the shortest consecutive preexcited R-R interval during atrial fibrillation, and the cycle length of orthodromic atrial ventricular reciprocating tachycardia were significantly greater in the elderly group.(ABSTRACT TRUNCATED AT 250 WORDS)

Increasing the yield of ventricular tachycardia induction: a prospective, randomized comparative study of the standard ventricular stimulation protocol to a short-to-long protocol and a new two-site protocol.

Programmed ventricular stimulation with a standard protocol that used up to three extrastimuli was compared prospectively with a short-to-long protocol and a two-site protocol in 77 consecutive patients undergoing electrophysiologic study in an attempt to increase the yield of ventricular tachycardia (VT) induction. The short-to-long protocol uses a train of eight stimuli at a short cycle length and up to two extrastimuli. The two-site protocol is similar to the standard protocol but delivers the last extrastimulus via a second spatially separated right ventricular catheter. Patients were divided into two groups based on indications for study: group 1 included 45 patients with syncope, nonsustained VT, or both, and group 2 included 32 patients with a history of sustained VT, sudden cardiac death, or both. The yield of VT induction with the short-to-long protocol was less than that with the standard protocol. In none of the patients in group 1 in whom the standard protocol results were negative did the short-to-long protocol produce sustained VT. Only two patients, both in group 2, had sustained arrhythmias induced by the short-to-long protocol when the standard protocol results were negative: one had sustained VT induced and one with long QT syndrome had ventricular fibrillation (VF) induced with the short-to-long protocol. However, the short-to-long protocol failed to induce sustained VT in seven patients in whom the standard protocol produced sustained VT. All seven of these patients required three extrastimuli with the standard protocol for induction of VT.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of signal-averaged electrocardiography in predicting patients at high risk for sudden death.

Delayed and inhomogeneous ventricular depolarization is found in patients with ventricular tachycardia. This abnormal activity may be discerned as a ventricular late potential (LP) by applying special signal-averaging techniques to the surface electrocardiogram. The presence of LPs after acute myocardial infarction (AMI) is associated with an increased risk of serious ventricular arrhythmias and sudden cardiac death during the subsequent year. Thus the signal-averaged ECG (SAECG) can identify a high risk subset of patients following AMI for whom more intensive diagnostic and/or therapeutic measures are indicated. Patients with findings ordinarily indicative of a relatively poor prognosis, such as reduced left ventricular ejection fraction, may be more precisely classified into high or low risk based on the presence or absence of LPs. The SAECG may be helpful in selecting patients with other types of presentations, such as syncope, who are likely to benefit from electrophysiological testing.

Benefit and risks of long-term amiodarone therapy for sustained ventricular tachycardia/fibrillation: minimum of three-year follow-up in 145 patients.

Our experience with amiodarone therapy in 145 consecutively referred patients with medically refractory sustained ventricular tachycardia and/or fibrillation treated for at least 3 years was reviewed. Ninety-seven had sustained ventricular tachycardia; the remaining 48 patients were survivors of sudden cardiac death. The patients had a mean of 3.7 +/- 1.4 unsuccessful anti-arrhythmic drug trials before initiation of amiodarone. The initial doses of amiodarone averaged 845 +/- 258 mg for the first 2 weeks and 56% of all patients received a type I antiarrhythmic drug in addition to amiodarone during the initial phase of therapy. The average maintenance dose of amiodarone was 410 +/- 187 mg per day. All patients were followed for a minimum of 3 years or until death or withdrawal from therapy. The maximum follow-up was a period of 8 years. Thus, the average duration of amiodarone therapy was 39 +/- 26 months, representing 472 patient years of therapeutic time on amiodarone. The incidence of deaths either caused by a documented ventricular tachyarrhythmia or presumed to result from an arrhythmic cause was 5.5% in the first year and 3.4% in each of the second and third years of follow-up. During the entire period of follow-up, 56 patients died of all causes (38.6% of the study population). Survival over the follow-up period was influenced significantly by left ventricular function, as judged by either New York Heart Association Functional Class or objective assessment of left ventricular ejection fraction, which was available in 102 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction.

In some patients with acute myocardial infarction, low-amplitude potentials that prolong the QRS complex, termed "late potentials," can be recorded on a signal-averaged electrocardiogram. The presence of these late potentials is known to be associated with an increase in the risk of ventricular tachycardia and sudden death. Because patients with acute myocardial infarction who receive thrombolytic therapy have a reduced incidence of ventricular tachyarrhythmia and sudden death, we sought to determine whether such patients also have a decreased incidence of late potentials. We studied 106 patients less than 75 years of age who were admitted with a first myocardial infarction and in whom a signal-averaged electrocardiogram was recorded within 48 hours of admission. Within four hours of the onset of chest pain, tissue plasminogen activator (t-PA) was given to 44 patients, and 62 were treated conventionally. In the t-PA group, late potentials were recorded in 2 of 44 patients (5 percent), as compared with 14 of 62 (23 percent) in the conventionally treated group (P = 0.01). Furthermore, among the patients treated with t-PA, continued occlusion of the infarct-related artery was related to the presence of late potentials. In the t-PA group, late potentials were recorded within 24 hours of angiography in 2 of the 6 patients with an occluded infarct-related artery, as compared with none of the 38 patients with a patient infarct-related artery. Our data suggest that successful thrombolytic therapy is associated with a marked reduction in the incidence of late potentials on the signal-averaged electrocardiogram. Long-term follow-up will be required to determine whether this finding predicts a reduced incidence of subsequent ventricular tachyarrhythmia and sudden death.

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia.

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.

Utility of the signal-averaged electrocardiogram in patients presenting with sustained ventricular tachycardia or fibrillation while on an antiarrhythmic drug.

The utility of the signal-averaged electrocardiogram (SAECG) for predicting ventricular tachycardia (VT) induction in patients presenting with sustained VT or ventricular fibrillation (VF) while on an empirically chosen antiarrhythmic agent was assessed in 17 patients. At the time of presentation with a malignant arrhythmia, 12 patients were taking quinidine, three patients were taking procainamide, and two patients were taking flecainide. All patients underwent programmed ventricular stimulation when not taking antiarrhythmic drugs; 12 patients had no inducible sustained VT and five patients had inducible sustained monomorphic VT. The SAECG done in the control state without antiarrhythmic agents was negative for late potentials in 11 of 12 patients in the noninducible group and positive for late potentials in four of five patients in the inducible group (sensitivity = 80% and specificity = 92%). We conclude that in patients presenting with life-threatening ventricular arrhythmias while taking an antiarrhythmic drug, the SAECG distinguishes patients with possible proarrhythmic events from those who have the substrate for inducible sustained VT.

Decline in ventricular fibrillation threshold after successive premature extrastimuli: a possible explantation for the induction of ventricular fibrillation during programmed stimulation with multiple extrastimuli.

To examine the relation between the ventricular fibrillation threshold and the number of premature extrastimuli delivered to the right ventricle during programmed ventricular stimulation, a clinical stimulation protocol was performed in nine normal, anaesthetised, closed chest dogs. In addition, the ventricular fibrillation threshold was measured in each dog after a train of eight paced (S1) beats (VFT-S2), after a single premature extrastimulus (VFT-S3), and after two extrastimuli (VFT-S4). The VFT-V3 was 32% lower than the VFT-S2 (16(7) mA vs 24(9) mA, p less than 0.001). The VFT-S4, or the current required by the S4 extrastimulus to induce ventricular fibrillation, was 25% lower than the VFT-S3 (12(8) mA vs 16(7) mA, p less than 0.05). The cumulative reduction in the ventricular fibrillation threshold measured by the S1S2S3S4 stimulation protocol was approximately 50%. Although in most dogs the VFT-S4 was still considerably higher than twice threshold current intensity, the results of the study suggest that a possible mechanism for the induction of non-clinical ventricular fibrillation in the clinical electrophysiology laboratory may be the progressive lowering of the ventricular fibrillation threshold caused by the addition of multiple extrastimuli. This may be particularly relevant in patients with an already reduced fibrillation threshold.