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Introduction: The experimental concept that "atrial fibrillation (AF) begets AF" implies that atrial tachyarrhythmia (AT)/AF burden uniformly increases over time. However, the temporal patterns of paroxysmal AT/AF burden progression, its conversion to persistent AF, and the relationship to underlying disease in humans are unknown. We analyzed the average daily AT/AF burden in patients with concomitant bradycardia and paroxysmal AF to examine these issues., Methods: Three hundred thirty patients with a history of paroxysmal AF (mean age 70 +/- 10 years; 61% male) were implanted with a pacemaker that automatically recorded the cumulative daily AT/AF burden. Persistent AT/AF was defined as 7 consecutive days with >23 hours of AT on the device data logs. Antiarrhythmic drug therapy was required to be stable for at least 7 months., Results: Average follow-up was 401 +/- 123 days. Seventy-eight patients (24%) progressed to persistent AT/AF during the follow-up period with a mean interval of 147 +/- 149 days. Mean AT/AF burden increased progressively (slope 14 s/d, P < .001) over 500 days after implant, and median AT/AF burden also increased (P < .01) in this subgroup of patients. This increase was highly correlated with the presence of structural heart disease (P < .001). There was a concomitant decrease in atrial premature beat (APB) frequency. Most patients transitioning to persistent AF were in sinus rhythm with minimal AT/AF burden in the days immediately before persistent AF. Neither mean nor median AT/AF burden increased over time in patients remaining in paroxysmal AF (slope 0 s/d, P = .7) despite a higher APB frequency than in patients with heart disease (P =.003) and a higher likelihood of daily AT/AF events (P < .001)., Conclusions: Temporal patterns of AT/AF burden in patients developing persistent AF show a progressive increase with a sudden transition to persistent AF. This is more consistent with substrate changes, rather than increased density of triggering APBs or paroxysmal AT/AF events. Thus, progression to persistent AF is probably related to an AF substrate, which is undergoing progressive structural remodeling owing to heart disease and other factors and is now suddenly capable of sustaining prolonged or multiple ATs. Therapies directed at the atrial substrate may be needed to prevent persistent AF.

Background: The circadian onset patterns and cycle lengths of atrial tachyarrhythmias (AT) were determined in a group of patients with persistent atrial fibrillation., Methods: Fifteen patients, mean age 63 +/- 14 years and 80% male, were implanted with the Jewel AF atrial defibrillator (Medtronic, Minneapolis, Minn) for persistent atrial fibrillation only. Onset times of AT and median onset atrial cycle lengths were determined from device memory., Results: Over a follow-up period of 23.3 +/- 7 months, 227 episodes of persistent AT were treated by patient-activated atrial defibrillation. The peak onset of persistent AT was nocturnal, with 74% of episodes initiating between 8 pm and 8 am. Eighty-seven percent of the patients experienced an additional 403 paroxysmal AT episodes. These episodes showed a "double-peaked" pattern with the least number of episodes occurring between midnight and 8 am. The mean onset atrial cycle length of persistent AT was significantly shorter than the paroxysmal AT episodes (200 +/- 37 ms vs 240 +/- 39 ms, P <.005). The atrial cycle lengths at arrhythmia onset of both paroxysmal and persistent AT episodes also demonstrated circadian variation., Conclusion: There is a circadian distribution of onsets for persistent AT with predominance at night. Patients with persistent AF have >1 type of atrial arrhythmia with differences in the onset patterns and atrial cycle lengths, suggesting different triggers and onset mechanisms.

Background: Atrial fibrillation (AF), the most common form of sustained arrhythmia, is associated with a frightening risk of embolic complications, tachycardia-related ventricular dysfunction, and often disabling symptoms. Pharmacologic therapy is the treatment used most commonly to restore and maintain sinus rhythm, to prevent recurrences, or to control ventricular response rate., Methods: This article reviews published data on pharmacologic treatment and discusses alternative systems to classify AF and to choose appropriate pharmacologic therapy., Results: AF is either paroxysmal or chronic. Attacks of paroxysmal AF can differ in duration, frequency, and functional tolerance. In the new classification system described, 3 clinical aspects of paroxysmal AF are distinguished on the basis of their implications for therapy. Chronic AF usually occurs in association with clinical conditions that cause atrial distention. The risk of chronic AF is significantly increased by the presence of congestive heart failure or rheumatic heart disease. Mortality rate is greater among patients with chronic AF regardless of the presence of coexisting cardiac disease. The various options available for the treatment of chronic AF include restoration of sinus rhythm or control of ventricular rate. Cardioversion may be accomplished with pharmacologic or electrical treatment. For patients in whom cardioversion is not indicated or who have not responded to this therapy, antiarrhythmic agents used to control ventricular response rate include nondihydropyridine calcium antagonists, digoxin, or beta-blockers. For patients who are successfully cardioverted, sodium channel blockers or potassium channel blockers such as sotalol, amiodarone, or a pure class III agent such as dofetilide, a selective potassium channel blocker, may be used to prevent recurrent AF to maintain normal sinus rhythm., Conclusions: The ultimate choice of the antiarrhythmic drug will depend on the presence or absence of structural heart disease. An additional concern with chronic AF is the risk of arterial embolization resulting from atrial stasis and the formation of thrombi. In patients with chronic AF the risk of embolic stroke is increased 6-fold. Therefore anticoagulant therapy should be considered in patients at high risk for embolization. Selection of the appropriate treatment should be based on the concepts recently developed by the Sicilian Gambit Group (based on the specific channels blocked by the antiarrhythmic agent) and on clinical experience gained over the years with antiarrhythmic agents. For example, termination of AF is best accomplished with either a sodium channel blocker (class I agent) or a potassium channel blocker (class III agent). In contrast, ventricular response rate is readily controlled by a beta-blocker (propranolol) or a calcium channel blocker (verapamil). Alternatively, antiarrhythmic drug therapy may be chosen based on the Vaughan-Williams classification, which identifies the cellular electrophysiologic effects of the drug.

Background: The relation between abnormalities in the signal-averaged P wave and atrial size has not been determined in patients with paroxysmal atrial fibrillation (PAF) without structural heart disease., Methods: Signal-averaged electrocardiograms of P waves were recorded in 38 patients with idiopathic PAF and 34 control subjects. Filtered P-wave duration (FPD) and root-mean-square voltages for the last 20 ms of the vector magnitude were measured. Atrial volume was calculated by cine magnetic resonance imaging., Results: FPD was longer (131.7 +/- 10.9 ms vs 120.8 +/- 8.6 ms, P <.0001) and root-mean-square voltage was lower (2.89 +/- 1.29 microV vs 3.62 +/- 1.48 microV, P <.05) in the PAF group than in control subjects. However, the various atrial volumes were similar in the 2 groups. In controls, FPD was significantly correlated with left (r = 0.593, P <.0001) and total (r = 0.492, P <.005) atrial volume but not with right atrial volume. In patients with PAF, no significant correlations were found between FPD and any of the atrial volumes. Elderly patients with PAF (age > or =60 years) showed longer FPD than younger patients with PAF (139.2 +/- 9.4 ms vs 125.6 +/- 8.0 ms, P <.0001)., Conclusions: FPD is influenced by the left and total atrial volumes in the normal heart without PAF. Prolonged FPD seems to be a useful predictor of idiopathic PAF among patients without atrial enlargement, especially in the elderly.

Background: The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (PAF)., Methods: To search for possible electrocardiographic markers that could serve as predictors of idiopathic PAF, we measured the maximum P-wave duration (P maximum) and the difference between the maximum and the minimum P-wave duration (P dispersion) from the 12-lead surface electrocardiogram of 60 patients with a history of idiopathic PAF and 40 age-matched healthy control subjects., Results: P maximum and P dispersion were found to be significantly higher in patients with idiopathic PAF than in control subjects. A P maximum value of 110 msec and a P dispersion value of 40 msec separated patients from control subjects, with a sensitivity of 88% and 83% and a specificity of 75% and 85%, respectively., Conclusions: P maximum and P dispersion are simple electrocardiographic markers that could be used for the prediction of idiopathic PAF.

Several acceptable options are available for the successful management of children either with an acute PSVT episode or with ongoing episodes. These options include the "no treatment" management approach. Although an example of an algorithm used in one center is provided for this Medical Progress article, other algorithms also are successfully practiced among pediatric cardiologists together with primary care pediatricians. Current and ongoing updated data related to the important factors of presenting symptoms, natural history, results of the treatment options, and the risk/ benefit ratios of the treatment options are essential when one is choosing the specific management approach.

To evaluate arrhythmogenicity in patients who receive a modified direct-current (DC) shock ablation (distal pair of electrodes connected in common as the cathode) or radiofrequency (RF) ablation of supraventricular tachycardia, a prospective study was performed with signal-averaged ECG, 24-hour Holter monitoring, electrophysiologic study (EPS) for ventricular tachycardia (VT), and treadmill exercise test. Sixty-nine consecutive patients with documented paroxysmal supraventricular tachycardia were included. Twenty-eight patients proved to have atrioventricular nodal reentrant tachycardia, and 41 patients had atrioventricular reciprocating tachycardia that involved accessory atrioventricular pathways. The first 34 patients received DC shock ablation and the other 35 patients received RF ablation. Signal-averaged ECG, Holter monitoring, and EPS for VT were performed before ablation, immediately after ablation, then 1 week, 2 weeks (Holter monitoring), 1 month (except EPS), and 3 months after ablation. Treadmill exercise testing was performed before ablation, and at 1 week and 3 months after ablation. The root mean square, low-amplitude signal and QRS duration of signal-averaged ECG disclosed no significant change after either DC or RF ablation up to 3 months. Late potential developed in only one patient in the DC shock group and it was considered to be innocuous because neither VT nor ventricular fibrillation was noted or induced. Increases in the number of ventricular premature contractions and in short-run VT were detected by Holter monitoring in the first week after either mode of ablation (p < 0.001 for the DC shock group; p < 0.05 for the RF group), which were greater (p < 0.05) and lasted longer in the DC shock group than in the RF group.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to determine the effects of quinidine and mexiletine on the adaptation of ventricular refractoriness to a change in heart rate. The ventricular effective refractory period was measured at a basic drive cycle length of 500 msec with basic drive train durations of two beats, eight beats, 20 beats and 3 minutes. The ventricular refractory periods were measured in the baseline state and after oral treatment with quinidine or mexiletine in 20 subjects each. In the baseline state, there was progressive shortening of the ventricular refractory period as the drive train duration increased from two beats to 3 minutes. Quinidine prolonged refractoriness by 5% (p less than 0.001) at each drive train duration. Mexiletine did not affect the ventricular effective refractory period at any of the drive train durations. In a control group of 20 subjects, there were no significant differences between two determinations of refractoriness at each basic drive train duration. In conclusion, neither quinidine nor mexiletine affect the adaptation of ventricular refractoriness to an increase in rate. Although the ventricular effective refractory period measured with a conventional basic drive train duration of eight beats is often more than 20 msec longer than the actual ventricular effective refractory period measured with a drive train duration of 3 minutes, the effects of quinidine and mexiletine on the conventionally measured ventricular effective refractory period accurately reflect the effects of these drugs on the actual ventricular effective refractory period.

Twenty children and adolescents treated orally with atenolol for chronic paroxysmal ventricular tachycardia (n = 10) or Long QT Syndrome (n = 10) over a 5 year period were retrospectively evaluated to ascertain the efficacy of arrhythmia suppression, the effective dosage, the cardiovascular effects, and the incidence of adverse effects. Patients with paroxysmal ventricular tachycardia were classified by their response to exercise or catecholamines. Atenolol was effective in each patient (n = 5) whose tachycardia was precipitated or exacerbated by exercise or catecholamines when the patient was receiving a dosage of approximately 1.7 mg/kg/day. In those patients (n = 4) in whom exercise or catecholamines either suppressed or had no effect on the tachycardia, none were effectively treated in spite of receiving comparable dosages. Three of these four patients also had structural abnormalities or myocardial dysfunction. Atenolol was effective in treating 4 of 10 patients with long QT syndrome with a dosage of approximately 1.5 mg/kg/day. Six ineffectively treated patients received similar dosages, and four required either additional medication or surgical sympathectomy for persistent syncope. The other two patients died suddenly. Cardiovascular side effects included bradycardia in three patients and hypotension in one. Noncardiovascular effects included mild fatigue (four patients) headache (two), sleep disturbance (two), and difficulty concentrating (one). The medication was discontinued because of side effects in two patients. Atenolol is more likely to be effective in the suppression of paroxysmal ventricular tachycardia in children if the tachycardia is exacerbated by exercise or catecholamines and if the heart is otherwise normal.

An unusual form of tachycardia circuit is described. The circuit incorporates a concealed nodoventricular fiber that conducts in a retrograde path, connects the atrioventricular node and the right ventricle, and also includes the distal portion of the atrioventricular node, the His-Purkinje system, and the ventricle. The study patient was first seen with paroxysmal tachycardias of normal QRS duration, complete right bundle branch block, and complete left bundle branch block. Electrophysiologic studies disclosed poor anterograde atrioventricular nodal conduction with a block proximal to His deflection that occurred at an atrial paced cycle length of 600 msec with no ventriculoatrial conduction. The tachycardias were inducible with two ventricular extrastimuli, had a His deflection that preceded each QRS complex and an HV interval identical to that during sinus rhythm, and revealed ventriculoatrial dissociation. Tachycardia with QRS patterns of right bundle branch block had a cycle 30 to 35 msec longer than tachycardias with either normal QRS duration or complete left bundle branch block. Tachycardias could be entrained by appropriate right ventricular pacing at rates slightly faster than the rate of tachycardia. Tachycardias could be terminated abruptly by an intravenous bolus of either adenosine triphosphate or verapamil.

This study prospectively assessed the electrophysiologic effects of parenteral magnesium sulfate administration on paroxysmal atrioventricular (AV) reentrant supraventricular tachycardia and the efficacy of magnesium to terminate these arrhythmias. Eleven normomagnesemic patients, seven with orthodromic reentrant supraventricular tachycardia that used an accessory AV pathway, and four with typical AV nodal reentry were examined. All patients had a history of sustained supraventricular tachycardia requiring pharmacologic therapy or electrical cardioversion for termination of tachycardia. After baseline electrophysiologic study, including documentation of sustained supraventricular tachycardia that was reproducibly induced, parenteral magnesium sulfate (a bolus of 0.3 mEq/kg of elemental magnesium infused over a 10-minute period followed by a maintenance infusion of 0.2 mEq/kg/hr) was administered during sustained supraventricular tachycardia. The serum magnesium concentration increased from (mean +/- standard deviation) 1.9 +/- 0.2 mg/dl to 4.0 +/- 0.6 mg/dl (p = 0.0001). Except for flushing and mild diaphoresis during infusion of the magnesium sulfate bolus, and dry heaves in one patient, there were no untoward effects or significant changes in systolic blood pressure. During administration of magnesium, the tachycardia cycle length increased from 319 +/- 39 msec to 348 +/- 43 msec (p = 0.0001). Slowing of the tachycardia occurred predominantly in the antegrade limb of the circuit at the level of the AV node with the AH interval increasing from 171 +/- 66 msec to 197 +/- 68 msec (p = 0.0001), whereas there was no significant change in the HV interval (43 +/- 3 msec to 43 +/- 4 msec, p = NS) or the VA interval (106 +/- 43 msec to 110 +/- 47 msec, p = NS) during tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular conduction patterns suggestive of dual A-V nodal pathways have been reported in patients with and without a history of paroxysmal A-V nodal re-entrant tachycardia (PSVT). The purpose of this study was to determine whether significant association exists between this conduction pattern and the occurrence of PSVT in man. The pattern of A-V conduction was evaluated at similar pacing rates in 13 patients with documented PSVT and 135 patients with PSVT. Patients without PSVT were divided into groups with normal PR intervals (106 patients), PR intervals of 120 msec. or less (12 patients), and PR intervals of 200 msec. or greater (17 patients). Evidence of dual A-V nodal pathways was found in seven of 13 patients with PSVT and nine of 135 patients without PSVT, including eight of 106 patients with normal PR intervals, none of 12 patients with short PR intervals, and one of 17 patients with PR intervals of 200 msec. or greater. The incidence of dual A-V nodal pathways was significantly greater (P less than 0.01) in patients with PSVT when compared with all other groups. In two of four patients with PSVT, propranolol was found to unmask evidence of dual pathways; no evidence of dual pathways was produced by propranolol in 23 patients without PSVT. The data show that the pattern of dual A-V nodal pathways is common only in patients with PSVT and is significantly less frequent in patients without PSVT regardless of the presence of short or long PR intervals. The results of this study establish a strong association between this conduction pattern and the occurrence of PSVT in man.

Efficacy of acute intravenous verapamil, 10 mg, and chronic oral verapamil, 320 mg, daily were studied electrophysiologically in 15 patients with paroxysmal supraventricular tachycardia (PSVT). Plasma verapamil concentrations were measured concurrently. Both intravenous and oral verapamil significantly increased the AV node conduction time, the cycle length producing a Wenckebach period, and the refractory period of the AV node. These changes were reflected in changes in plasma verapamil concentration. The echo zone and the supraventricular tachycardia (SVT) zone markedly narrowed after administration of both intravenous and chronic oral verapamil. Verapamil's efficacy was found to be related to the type of SVT. For instance, verapamil was more effective in SVT due to AV nodal re-entry than in SVT due to concealed accessory pathway. Fourteen patients were followed from 3 to 31 months and all except one were well controlled. In conclusion, verapamil was effective in prophylaxis of paroxysmal SVT.

A closed technique, using thoracotomy without cardiopulmonary bypass and atriotomy, for cryosurgical ablation of the atrioventricular node-His bundle junction is described. The technique was used in 34 patients selected from among 136 patients with disabling supraventricular tachyarrhythmias refractory to drug therapy in whom atrioventricular block was produced. After thoracotomy, four methods can be used to determine the site of cryoinstrument application: palpation of the internal anatomic landmarks, a "mechanical test," use of a cryoprobe, or recording of the His bundle electrogram. The cryoprocedure lasts 160 to 180 seconds at temperatures of -60 degrees to -80 degrees C and is repeated once or twice. Complete atrioventricular block was induced in 29 of the 34 patients. Paroxysmal tachycardia was terminated in 31. There were no operative deaths. The frequency of surgical complications was nearly three times lower than in the group of 77 patients subjected to open cryodestruction of the atrioventricular junction, and the length of hospital stay after the operation was an average of 4.7 days shorter. The follow-up for up to 6.5 years (mean 34 months) failed to show postoperative paroxysmal tachycardia or tachyarrhythmia in 31 patients. In my opinion, this rather safe method for ablation of the atrioventricular junction could be more widely used, especially if there are contraindications for extracorporeal circulation or if transvenous catheter ablation has failed.

Verapamil is considered by many investigators to be the drug of choice for the acute management of uncomplicated PSVT. Several clinical investigators have demonstrated termination of PSVT in more than 90% of their patients within minutes following IV drug administration. The incidence of reported severe adverse reactions has been less than 1%. PSVT may be complicated by underlying heart disease, or by antegrade accessory pathway conduction in individuals with pre-excitation syndrome. Such conditions, or the prior use of beta-blocking agents, may contraindicate the use of verapamil. However, the history of recent myocardial ischemia or the prior use of digitalis does not appear to contraindicate verapamil therapy. Guidelines for the emergency management of the patient in PSVT are presented.

Atrial reentrance as a mechanism of the tachycardia was demonstrated in a 28-year-old patient suffering from chronic repetitive supraventricular tachycardia. Criteria for diagnosis included the following: (1) Repetitive supraventricular tachycardia was induced and terminated by properly timed atrial extrastimuli. (2) Return cycles of all atrial extrastimuli not abolishing the tachycardia were fully compensatory. (3) A-H prolongation was not a prerequisite to induce the tachycardia. (4) The contours of P and A waves during tachycardia differed from those in sinus rhythm, but atrial activation remained antegrade. (5) A concealed anomalous pathway could not be proved.

This study examines the clinical setting, characteristics, and follow-up of 173 patients who had slow paroxysmal atrial tachycardia (SPAT) (greater than 4 beats, rate less than 150 bpm) during 24-hour Holter monitoring. These episodes were classified by probable mechanism according to recognized ECG criteria and included AV nodal reentry (AVNR), sinoatrial nodal reentry (SANR), and automatic (A). There were 76 males (44%) with a mean age of 72 years and 97 females (56%) with a mean age of 73 years. The indications for Holter recording revealed that the SANR and A subgroups had a higher frequency of cerebral symptoms compared to AVNR (p less than 0.01). Chest pain was more common in the SANR group as compared to the other two groups (p less than 0.01). There was no difference in the frequency of palpitation in the three subgroups. The mean rate of SPAT for the entire group was 115.2 +/- 14 and these episodes had a mean duration of 5.58 +/- 3.07 seconds. The SANR subgroup had a significantly slower rate (107.1 +/- 9.2) as compared to the AVNR subgroup (p less than 0.01). One hundred fourteen patients were available for follow-up. The average period of follow-up was similar for all three groups. At follow-up the frequency of sick sinus syndrome as determined clinically and permanent pacemaker insertion was significantly greater in the SANR subgroup (p less than 0.01) as compared to the other subgroups which did not differ from each other.

This vignette illustrates the application of electrophysiological principles to the clinical problems of acute trifascicular A-V block occurring during an acute MI. Paroxysmal trifascicular A-V block that occurs transiently during an acute MI can be explained electrophysiologically as being due to tachycardia-dependent or bradycardia-dependent A-V block or both. Tachycardia-dependent A-V block also referred to as phase 3 A-V block is a term used when a premature beat occurring during repolarization of the preceeding beat causes conduction failure. Bradycardia-dependent A-V block or phase 4 block is used to explain the slowing of conduction or block after a longer diastolic interval. Physicians and nurses can improve their care of the critically ill cardiac patient through a better understanding of pathophysiology.

We have noted that inflation of the military antishock trousers (MAST) successfully converted five of six patients with paroxysmal supraventricular tachycardia to normal sinus rhythm. In all patients the usual "vagal" maneuvers were tried first and were unsuccessful. MAST inflation may be a safe and useful addition to the traditional vagal maneuvers used to treat paroxysmal supraventricular tachycardia.

Paroxysmal BBB may be either tachycardia-dependent which is referred to as "phase 3 block" or bradycardia-dependent, referred to as "phase 4 block." Tachycardia-dependent BBB is related to prolonged recovery. Bradycardia-dependent BBB is related to hypopolarization and SDD. These fundamental electrophysiological properties aid in understanding of transient BBB occurring during an acute MI.

Electrophysiologic drug testing was performed in nine patients with severely symptomatic sporadic (2 to 13 [mean 4.2] attacks/24 months) paroxysmal atrial fibrillation (PAF). All patients had control inductions of sustained (greater than 30 seconds) AF by high right atrial stimulation, and attempted inductions following serial administration of drugs. Drugs tested were intravenous procainamide (1.0 to 1.5 gm) (five patients), intravenous propranolol (0.1 mg/kg) (three patients), oral quinidine (1.6 to 2.4 gm/day) six patients), oral disopyramide (1.2 to 1.6 gm/day) (four patients), and oral aprindine (100 to 250 mg/day) (four patients). In all patients, one or more drugs prevented induction of sustained AF: procainamide (one patient), quinidine (five patients), disopyramide (four patients), and aprindine (four patients). All patients were treated with drugs which prevented induction of sustained AF and followed for 8 to 40 (mean 24) months. Seven patients tolerated their drugs: six had no AF and one had several short nonsustained attacks. Two patients did not tolerate their drugs: one had paroxysmal palpitation (on decreased aprindine dosage), and one had AF (while off of aprindine). In conclusion, electrophysiologic drug testing is feasible in patients with sporadic PAF. Inability to induce sustained AF following drug administration suggests successful prophylaxis of spontaneous PAF with the same drug.

The interpretation of IE recorded in children has been hampered by a lack of agreement regarding normal values. We recorded IE in 158 children and young adults (ages, three days to 33 years) to define the various conduction intervals in normal and disease states. The HBP was recorded in 156 subjects. In 85 subjects with normal conduction indicated by surface ECG, including 19 subjects with normal hearts, there were no statistically significant age-related differences in internodal, A-V nodal, or His-Purkinje conduction intervals. Therapeutic levels of digitalis did not alter the conduction intervals. In 11 subjects with first degree A-V block and in five subjects with congenital complete A-V block, the site of block as determined by IE could not be predicted from the surface ECG. No abnormalities in conduction intervals were found in 18 subjects with right bundle branch block (surgically induced in 17 cases). Intracardiac electrography with recording of the HBP was found to be a safe, informative technique for electrophysiologic investigations in children and young adults.

Five patients are reported with SN echoes which could be produced by the technique of APD. The RA was paced at the basic rate and the SEI was measured repeatedly. SN echoes were diagnosed on the basis of: (1) A1A3 interval shorter than the SEI; (2) upright P-waves in Leads II and III; (3) activation of high RA preceding the activation of low RA; (4) lack relation to critical delay in the A-V node or HPS; (5) definite echo zone. In one of the cases, attacks of reciprocating tachycardia through the SN occurred spontaneously and also could be initiated by an SN echo. These were terminated by a single APD or by atrial pacing.

Controversy exists as to which of several ECG criteria are necessary for the diagnosis of left atrial (LA) rhythm. We performed invasive electrophysiologic study in five patients (6 to 15 years-of-age) who had symptomatic supraventricular tachycardia (SVT) that could not be controlled by aggressive pharmacologic treatment. All patients were found to have automatic atrial tachycardia with the earliest site of activation during SVT in the LA. The ECG of each patient demonstrated negative P waves in lead I. The frontal plane P wave axis ranged between +90 to +270 degrees in each of our patients. Spontaneous "dome-and-dart" P waves occurred in lead V1 in two of our patients. We conclude that the necessary criterion for the diagnosis of LA rhythm should be negative P waves in lead I. The finding of "dome-and-dart" P waves in V1 is an additional useful and definitive criterion but is not present in each case.

His bundle electrocardiography has increased our understanding of the electrophysiology of the conducting system and has confirmed a number concepts which evolved from analysis of surface electrocardiograms. Electrophysiologic evaluation of conduction disease in the cardiac catheterization laboratory has become an accepted diagnostic procedure in determining the site of atrioventricular and ventriculo-atrial block as well as in the evaluation of patients with pre-excitation resulting from conduction through Kent and James bundles. Recent reports suggest that His bundle electrograms may prove to be of clinical and therapeutic significance in determining the site of re-entry in patients with PSVT as well as in determining the short-term prognosis of patients with acute myocardial infarction complicated by incomplete bundle branch block. As our knowledge and understanding of the basic mechanisms, specific therapy, and prognosis of cardiac arrhythmias are expanded, the data derived from His bundle electrocardiography will become more useful in the clinical practice of cardiology.

Sinus node re-entry (SNR) usually appears as a single beat. Tachycardias (SNRT) consistent with sustained SNR were seen in six patients and were initiated by premature stimulation of the high right atrium (six patients) and coronary sinus (four patients), and after continuous pacing from the high right atrium (four patients) or right ventricle (one patient) at rates of 130 to 200 per minute. During SNRT: (1) atrial beats exhibited a high-to-low atrial activation sequence, (2) the P-waves were similar in morphology to P-waves during sinus rhythm, and (3) re-entry in the A-V node or at the site of stimulation could be excluded. The cycle length of SNRT ranged from 625 to 320 msec. and SNRT either terminated spontaneously (six patients) or after premature atrial capture and/or vagal maneuvers (two patients). The electrophysiologic characteristics of SNRT and differentiation of SNRT from A-V nodal re-entry are discussed.

Electrophysiologic effects of intravenous ethmozin (1.5 to 2 mg/kg) were evaluated in 16 patients (10 with Wolff-Parkinson-White [WPW] syndrome and six with concealed accessory pathway [AP]) with ventricular preexcitation syndrome. Ethmozin terminated induced supraventricular tachycardia (SVT) in 9 of 14 patients and atrial flutter with anterograde conduction 2: 1 over AP in one patient. The drug prevented induction of sustained SVT in 8 of 14 patients (four with WPW syndrome and four with concealed AP). The drug significantly lengthened the cycle length of induced SVT in WPW syndrome (381 +/- 24 to 421 +/- 27 msec) and in concealed AP (313 +/- 19 to 343 +/- 15 msec), mainly because of prolongation of the ventriculoatrial (VA) interval; the drug increased SVT atrial zone in WPW syndrome and removed or decreased it in patients with concealed AP. The drug abolished anterograde (6 of 10 patients) and retrograde (3 of 16 patients) conduction over AP, and/or increased anterograde and retrograde refractoriness of AP in all patients. Ethmozin significantly lengthened the following: PA (27 +/- 2 to 40 +/- 3 msec), AH (92.6 +/- 6 to 107 +/- 8 msec), and PR intervals (175 +/- 9 to 202 +/- 15 msec), and refractoriness of VA conduction systems. The refractoriness of atrioventricular node, HV, QRS, and QT intervals and the spontaneous sinus cycle length did not change significantly. Thus intravenous ethmozin terminated induced SVT and prevented the induction of sustained SVT in most patients with preexcitation syndrome due to a suppressive effect of the drug on AP.

A 71-year-old woman with an episode of paroxysmal supraventricular tachycardia (PSVT) complicated by angina pectoris and hypotension had her arrhythmia abruptly terminated by digital rectal massage (DRM) after other vagotonic maneuvers had failed. DRM termination of PSVT has not been heretofore reported. In treating PSVT by physical vagotonic maneuvers, DRM may be preferable to other techniques because of the decreased likelihood of complications noted with other such maneuvers.