Sinus node electrogram in patients with the hypersensitive carotid sinus syndrome.

Sinus node electrograms were obtained in two patients with unexplained syncope and the cardioinhibitory form of the hypersensitive carotid sinus syndrome. Direct recordings of sinus node potentials were obtained using a transvenous electrode catheter. Sinus node function was normal in both patients during standard electrophysiologic evaluation. Carotid sinus massage was performed in both patients and the sinus node electrogram was continuously recorded. After the onset of carotid sinus massage, prolongation of sinoatrial time, slowing of sinus rate of depolarization, sinoatrial exit block and finally sinus node arrest were recorded. After termination of carotid sinus massage, sinus node potentials did not precede the first atrial impulse; subsequent beats showed markedly prolonged sinoatrial times as well as changes in the P wave on the surface electrocardiogram. Sinus rate and sinoatrial time returned to control values gradually, as did the P wave configuration. Intravenous atropine (1.0 mg) abolished the abnormal response to carotid sinus massage. It is concluded that the application of carotid sinus massage in patients with the hypersensitive carotid sinus syndrome produces profound changes in sinoatrial conduction including sinoatrial exit block, as well as shifts in primary pacemaker site and sinus node arrest. These alterations in conduction and automaticity are reversible with atropine and may be secondary to denervation sensitivity to acetylcholine.

The signal-averaged electrocardiogram as a screening test for inducibility of sustained ventricular tachycardia in high risk patients: a prospective study.

The role of the signal-averaged electrocardiogram in predicting the induction of sustained monomorphic ventricular tachycardia in high risk patients was assessed prospectively in 100 consecutive patients. Presenting diagnoses were syncope (38 patients), nonsustained ventricular tachycardia (24 patients), sustained ventricular tachycardia (25 patients) and sudden cardiac arrest (13 patients). Using programmed ventricular stimulation, 71 patients (group I) did not have and 29 patients (group II) did have inducible sustained monomorphic ventricular tachycardia. Using the signal-averaged electrocardiogram with filtering (6 dB/octave) at high pass corner frequencies of 67 and 100 Hz, the two groups were compared. The signal-averaged electrocardiogram was considered abnormal if all of the following criteria were satisfied: 1) the total filtered QRS complex duration was greater than 120 ms, 2) the duration of the terminal QRS complex of less than or equal to 20 microV was greater than or equal to 30 ms, and 3) at least one deflection (late potential) was present in this region. Differences between groups I and II in these three measures were highly significant (p less than or equal to 0.001). The sensitivity and specificity of signal averaging for predicting the induction of sustained ventricular tachycardia were 93 and 94%, respectively. Stepwise logistic regression analysis identified the signal-averaged electrocardiogram as the best predictor of induction of sustained monomorphic ventricular tachycardia, independent of left ventricular ejection fraction, presence of ventricular aneurysm, myocardial infarction and other clinical variables (chi-square = 93.2, p less than 0.0001). The signal-averaged electrocardiogram is a sensitive and specific test for the induction of sustained monomorphic ventricular tachycardia, having independent predictive value.

Closed chest catheter ablation of an accessory pathway in a patient with permanent junctional reciprocating tachycardia.

This report describes a 23 year old woman with a lifelong history of permanent junctional reciprocating tachycardia refractory to conventional antiarrhythmic medications who was successfully treated with closed chest, transvenous selective ablation of a posteroseptal bypass tract. Two 100 J (stored) direct-current shocks were delivered to the region of the os of the coronary sinus using a quadripolar catheter positioned in the coronary sinus. At a 2 month follow-up interval, the patient is asymptomatic without recurrence of the tachycardia. It is concluded that in patients with permanent junctional reciprocating tachycardia, selective catheter ablation of a posteroseptal accessory pathway is a feasible alternative to a difficult pharmacologic regimen or to ablative surgery.

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.

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.

Underdetection of ventricular tachycardia by algorithms to enhance specificity in a tiered-therapy cardioverter-defibrillator.

OBJECTIVES: The goal of this study was to determine the incidence and clinical significance of underdetection in 125 patients treated with a tiered-therapy cardioverter-defibrillator, the Medtronic PCD. BACKGROUND: Underdetection, distinct from undersensing, is a unique, potential complication of new algorithms that enhance specificity in tiered-therapy cardioverter-defibrillators. These algorithms may delay or prevent recognition of ventricular tachycardia even though electrograms are sensed accurately and RR intervals meet the programmed interval criterion. METHODS: Underdetection was defined as delay in detection > 5 s at electrophysiologic study or symptomatic delay or detection failure at follow-up of 15 +/- 8 months. RESULTS: We identified six specific mechanisms of underdetection caused by algorithms to discriminate sustained ventricular tachycardia from sinus tachycardia, atrial fibrillation, ventricular fibrillation and nonsustained ventricular tachycardia. Underdetection caused detection delays in 13 (1.9%) of 677 induced ventricular tachyarrhythmia episodes in 12 patients (9.6%). During follow-up, underdetection occurred in 7 (9.9%) of 71 patients in whom ventricular tachycardia therapies were programmed. Failure to detect ventricular tachycardia occurred in 6 (0.6%) of 988 spontaneous ventricular tachycardia episodes in four patients (5.6%); 2 episodes required external cardioversion. After defibrillator reprogramming, underdetection did not occur. CONCLUSIONS: Algorithms to enhance specificity cause underdetection of ventricular tachycardia in a significant minority of patients with tiered-therapy cardioverter-defibrillators. Optimal programming can minimize underdetection.

High dose oral amiodarone loading: electrophysiologic effects and clinical tolerance.

Although amiodarone is an effective drug for the treatment of life-threatening ventricular arrhythmias, no standard oral loading dose protocol has been defined, and patients often undergo prolonged hospitalization for amiodarone loading. High dose (greater than 1,800 mg/day) oral loading has usually been reserved for unstable patients with incessant ventricular tachyarrhythmias. The current study was designed to 1) examine the clinical and electrophysiologic effects of a high dose oral amiodarone loading regimen in more stable patients; and 2) ascertain its safety and tolerance, possibly allowing shortened amiodarone loading periods and potentially decreased length of hospital stay. The study group included 16 patients with a history of recurrent ventricular arrhythmias and decreased left ventricular function, who were refractory to prior antiarrhythmic drug therapy. The oral loading protocol was 50 mg/kg per day of amiodarone for 3 days, then 30 mg/kg per day for 2 days, followed by maintenance therapy of 300 to 400 mg twice daily. Electrophysiologic testing was performed at baseline, on days 1 and 5 and during week 6. Amiodarone and desethylamiodarone levels were measured and symptoms monitored. Clinically, the high dose loading protocol was well tolerated in 15 of the 16 patients. Arrhythmias were rendered noninducible by day 1 in three patients and remained noninducible throughout the study period in two of the three. The remaining patients continued to have inducible ventricular tachycardia. Ventricular tachycardia cycle length and right ventricular effective refractory period both progressively increased significantly over baseline, starting on day 1. The 15 patients who remained in the study had no significant side effects during the loading period.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic influences on sinus node recovery time: effects of autonomic blockade.

Ten patients with normal sinus node function were evaluated prospectively, to determine whether the decrease in blood pressure during rapid atrial pacing shortens the corrected sinus node recovery time. All patients had 30 seconds of atrial pacing at cycle lengths from 600 to 300 ms, with continuous arterial pressure monitoring, before and after intravenous administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In the control state, a decrease in corrected sinus node recovery time was recorded with faster atrial pacing rates, which was significantly related to the initial drop in systolic blood pressure at the onset of atrial pacing. Specifically, as the initial pressure drop increased from 15 mm Hg or less to 16 to 45 and 45 to 100 mm Hg, corrected sinus node recovery time decreased from 272 +/- 79 to 205 +/- 70 ms (p less than 0.04) and to 134 +/- 120 ms (p less than 0.04), respectively. In contrast, after autonomic blockade, the corrected sinus node recovery time was prolonged, in a near linear fashion, as atrial pacing rates increased. The magnitude of blood pressure drop with atrial pacing did not differ significantly from that in the control state at similar pacing rates. These findings suggest that hypotension during rapid atrial pacing activates autonomic reflexes that significantly shorten the corrected sinus node recovery time. Autonomic blockade negates this effect and the corrected sinus node recovery time prolongs with faster atrial pacing.

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.

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.

A model of chronic ischemic arrhythmias: the relation between electrically inducible ventricular tachycardia, ventricular fibrillation threshold and myocardial infarct size.

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a "clinical" stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction. Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean +/- standard deviation 29 +/- 11 to 10 +/- 5 mA, p less than 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct. It is concluded that: (1) inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.

Effects of timolol and propranolol on inducible sustained ventricular tachyarrhythmias in dogs with subacute myocardial infarction.

Timolol and propranolol reduce the incidence of cardiac death after myocardial infarction (MI). To explore possible mechanisms of this reduction in mortality, the antiarrhythmic effects of these 2 beta blockers were compared in a dog model of inducible sustained ventricular tachycardia (VT) or fibrillation (VF) 4 to 6 days after experimental closed-chest MI. Dogs with inducible VT or VF underwent drug studies with timolol and propranolol; the sequence of drug administration was randomized. Timolol doses were 0.1, 0.3, and 1.0 mg/kg; propranolol doses were 1.0, 3.0 and 10.0 mg/kg. Timolol and propranolol were equally effective in abolishing inducible VT or VF: 77% of instances of inducible VT or VF responded to 1 or both beta blockers. The VF threshold was significantly elevated by both timolol and propranolol; the elevation in the VF threshold was significantly greater in "responders," i.e., dogs in whom VT was prevented by beta blockade (15 +/- 9 vs 8 +/- 9 mA, p less than 0.05). The ventricular effective refractory period was prolonged by both drugs; again, more so in the responders than in the nonresponders (16 +/- 9 vs 8 +/- 14 mA, p less than 0.05). The QTc interval was not significantly affected by either beta blocker. Among the responders, no difference was detected between timolol and propranolol in the extent to which the effective refractory period was prolonged or the VF threshold elevated. However, the highest dose of propranolol decreased the mean blood pressure significantly more than the comparable dose of timolol. In conclusion, timolol and propranolol are equally effective in abolishing inducible VT or VF in the dog after subacute MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Rate-dependent effects of procainamide on His-Purkinje conduction in man.

Microelectrode studies in isolated cardiac tissues have shown that the depressant effect of several antiarrhythmic drugs on the maximal upstroke velocity of the cardiac action potential is rate-dependent. To determine whether this effect of antiarrhythmic drugs is seen in humans, 14 patients undergoing atrial pacing at several rates were prospectively studied before and after the infusion of procainamide (15 mg/kg). The HV interval (His-Purkinje conduction rate) and the QRS duration (intraventricular conduction rate) were measured. Before procainamide infusion, atrial pacing did not significantly prolong the maximal HV interval (from 54 +/- 15 to 58 +/- 13 ms). After procainamide infusion (mean serum level 10.0 +/- 3 micrograms/ml) atrial pacing at an average of 5 pacing rates significantly prolonged the HV interval (from 67 +/- 18 to 80 +/- 20 ms, p less than 0.001). The extent of HV prolongation with atrial pacing after procainamide infusion was independent of the HV interval at rest before procainamide. The duration of the QRS complex also tended to prolong with atrial pacing after procainamide infusion, but this prolongation was not statistically significant. Thus, procainamide produces a rate-dependent depressant effect on His-Purkinje and intraventricular conduction, confirming observations made in isolated tissue preparations.

Electropharmacologic testing in sustained ventricular tachycardia associated with coronary heart disease: value of the response to intravenous procainamide in predicting the response to oral procainamide and oral quinidine treatment.

Twenty patients with inducible, sustained ventricular tachycardia (VT) were prospectively evaluated to determine whether the response to intravenous procainamide administration, as assessed by programmed ventricular stimulation, predicted the response to oral procainamide and oral quinidine treatment. Six patients (30%) responded to intravenous procainamide (fewer than 10 beats of inducible VT). Ten of 20 patients (50%) responded to oral quinidine and 5 (25%) responded to oral procainamide. Mean drug serum levels were 11.3 +/- 2.1 micrograms/ml for intravenous procainamide, 5.4 +/- 0.8 micrograms/ml for oral quinidine and 11.7 +/- 3.4 micrograms/ml for oral procainamide. There was no significant difference in serum levels between those who responded and those who did not. Fifteen patients (75%) had a concordant drug response for intravenous and oral procainamide. Ten patients (50%) had a concordant response for intravenous procainamide and oral quinidine. Fifteen patients (75%) had a concordant drug response for oral procainamide and oral quinidine. Thus, in patients with sustained VT, the response to intravenous procainamide does not reliably predict the response to oral quinidine or oral procainamide, and serial day drug testing with these agents is necessary. Furthermore, high-dose quinidine therapy may be more effective in controlling VT in these patients than procainamide.

Detection of late potentials on the surface electrocardiogram in unexplained syncope.

To assess the usefulness of signal averaging of the surface electrocardiogram for detecting hitherto undocumented ventricular tachycardia (VT) in patients with unexplained syncope, 24 such patients were evaluated by electrocardiography and programmed ventricular stimulation. The surface electrocardiograms of 15 normal volunteers and 22 patients with documented sustained VT were also examined. No study subject had a bundle branch block or a QRS duration longer than 120 ms. Sustained VT was recorded in 9 of the 24 patients with syncope (8 patients with inducible VT and 1 with a spontaneous episode of recorded sustained VT). The signal-processed electrocardiogram contained late potentials and a filtered QRS duration longer than 120 ms in 8 of these 9 patients (89% sensitivity). None of the remaining 15 patients had these electrocardiographic abnormalities. Similar results were found in the patients with previously documented sustained VT (82% sensitivity) and in normal volunteers (no instances of abnormal recordings). In patients with unexplained syncope, signal processing of the surface electrocardiogram may be a sensitive and specific noninvasive test for detecting a high-risk subset of patients prone to lethal ventricular tachyarrhythmias.

Effects of voltage and respiration on impedance in nonthoracotomy defibrillation pathways.

The effects of applied voltage and phase of respiration on impedance of pathways used by implantable cardioverter-defibrillators were investigated. Patients were studied at implantation of cardioverter-defibrillators using epicardial (n = 12) or transvenous and subcutaneous (SQ) (n = 30) electrodes. Transvenous-SQ pathways were right ventricular cathode to SQ anode and coronary sinus cathode to SQ anode. Transvenous-transvenous pathways were right ventricle to coronary sinus and right ventricle to superior vena cava. Patients with nonthoracotomy electrode systems were studied at end-expiration and end-inspiration. Five shocks of 65 to 745 V (0.2 to 34 J) were given in random order in sinus rhythm. Over this range, end-expiratory impedance decreased monotonically for all pathways. This effect was greatest for transvenous-SQ pathways (13 +/- 3% to 17 +/- 4%, p < 0.001), intermediate for transvenous-transvenous pathways (5 +/- 4% to 8 +/- 5%, p < 0.001), and least for epicardial pathways (3 +/- 3%, p = 0.006). Paired data in inspiration and expiration showed that inspiration increased impedance in transvenous-SQ pathways (p < 0.001) but not in transvenous-transvenous pathways. Further, the effects of respiration and voltage on impedance in transvenous-SQ pathways were interactive (p < 0.001): Inspiration increased voltage-dependence of impedance. The magnitude of the inverse relationship between voltage and impedance depends on type of defibrillation pathway. The effect of respiration on impedance suggests that voltage-dependence of impedance is greatest in the lungs. These findings have potential relevance for intraoperative testing of cardioverter-defibrillators and selection of pathways for low-energy cardioversion.

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.

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)

Response to programmed ventricular stimulation: sensitivity, specificity and relation to heart disease.

This prospective study of 100 patients evaluated the sensitivity and specificity of the repetitive ventricular response and ventricular tachycardia induced by programmed electrical stimulation for identifying patients with spontaneous ventricular tachyarrhythmias. The influence of underlying heart disease on such sensitivity and specificity was also evaluated. The repetitive ventricular response was sensitive (92 percent) for detecting patients with prior spontaneous ventricular tachyarrhythmias, but lacked specificity (57 percent); the rate of false positive responses was 43 percent. Inducible ventricular tachycardia was less sensitive (65 percent) but more specific (98 percent); the rate of false positive responses was only 3 percent. Among the 100 patients, 71 had heart disease, 29 did not. The presence of underlying heart disease had no significant effect on the sensitivity and specificity of repetitive ventricular responses or ventricular tachycardia induced by programmed stimulation; it did not increase the rate of false positive responses. It is concluded that (1) ventricular tachycardia induced with programmed ventricular stimulation is an excellent basis for guiding the management of clinically significant ventricular tachyarrhythmias, regardless of underlying heart disease; and (2) the repetitive ventricular response is not useful for this purpose because of its high rate of false positive responses among patients with or without significant heart disease.

Orthodromic tachycardia initiation dependent on 1:2 atrioventricular conduction in the presence of a left lateral bypass tract.

This report describes a patient who presented with atrial fibrillation associated with a rapid ventricular response (270 bpm) and wide QRS complexes. At the time of electrophysiology study, a left lateral bypass tract with both anterograde and retrograde conduction was demonstrated. Orthodromic tachycardia with atrial premature impulses was initiated and was dependent on two ventricular responses to one atrial impulse. Intravenous procainamide administration had little effect on anterograde or retrograde conduction in the accessory pathway; however, it prevented orthodromic tachycardia initiation with atrial premature impulses by prolonging atrial muscle refractoriness.