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1.1. Two patients with a chronic auricular tachycardia which consisted of short recurrent attacks of paroxysmal auricular tachycardia are reported on. 2.2. The condition was refractory to ordinary therapy. 3.3. In one of the two patients it was possible to revert the rhythm to a normal sinus rhythm by full digitalization followed by the administration of quinidine. 4.4. In the other patient, the arrhythmia persisted although the ventricular rate could be partially controlled by digitalis.

Radionuclide angiography was used to study the hemodynamic effects of intravenous procainamide during stable monomorphic ventricular tachycardia. In four patients studied without procainamide, the ejection fraction was 25% +/- 2.4% during normal sinus rhythm, dropped to 11.3% +/- 2.2% (p less than 0.05) at the onset of ventricular tachycardia, increased to 16.7% +/- 1.7% after remaining in ventricular tachycardia for 10 minutes, and returned to 25.3% +/- 3.7% in sinus rhythm. In the 10 study patients, ejection fraction dropped from 36% +/- 5.8% in sinus rhythm to 25% +/- 5.1% in ventricular tachycardia (p less than 0.2). Ejection fraction decreased further (23% +/- 5.0%) following low doses of procainamide (140 +/- 52 mg) despite cycle length prolongation (354 +/- 18 msec versus 373 +/- 21 msec, p less than 0.5). In 8 of 10 patients, there was a progressive increase in the ejection fraction (28.8% +/- 4.1%). Ventricular tachycardia onset also resulted in a decrease in cardiac output and end-diastolic and end-systolic volumes. Two patients who tolerated procainamide in sinus rhythm showed hemodynamic collapse secondary to procainamide during ventricular tachycardia. We conclude that in some patients hemodynamic intolerance to an antiarrhythmic drug may only become evident during ventricular tachycardia.

There are limited data on prognosis and outcomes of patients with new-onset atrial fibrillation (AF) compared with those with a prior history of AF.We conducted a comparison of these 2 groups in the AFFIRM trial. New-onset AF was the qualifying arrhythmia in 1,391 patients (34%). Compared with patients with prior history of AF, patients with new-onset AF were more likely to have a history of heart failure. There was no mortality difference between rate control (RaC) and rhythm control (RhC) among patients with new-onset AF (17% vs 20%, P = .152). In the univariate model, new-onset AF was associated with increased risk of mortality compared with history of prior AF (RaC unadjusted hazard ratio [HR] 1.36 [P = .010], RhC unadjusted HR 1.39 [P = .003]). However, after multivariate adjustments, new-onset AF did not carry an increased risk of mortality (RaC adjusted HR 1.14 [P = .370], RhC adjusted HR 1.16 [P = .248]). Subjects with new-onset AF randomized to the RhC arm were more likely to remain in normal sinus rhythm at follow-up (adjusted HR 0.79, P = .012) compared with patients with prior history of AF.In a multivariable analysis adjusting for confounders, new-onset AF was not associated with increased mortality compared with prior history of AF regardless of the treatment strategy. Patients with new-onset AF treated with the rhythm control strategy were more likely to remain in normal sinus rhythm on follow-up.

Improvement in left ventricular (LV) performance after coronary artery bypass surgery remains the gold standard in myocardial viability assessment. The time-related changes, however, are not well known. This study examined the LV ejection fraction (EF) by gated blood pool imaging early (6 +/- 4 days) and late (62 +/- 24 days) after surgery in patients with normal preoperative EF (group 1, n = 12) and those with LV dysfunction (group 2, n = 15). There were no changes in the clinical status between the early and late studies, and all patients had normal sinus rhythm. Group 1 had no significant change in EF (preoperatively 62%, early postoperatively 64%, late postoperatively 63%; p = NS). In group 2, EF was 26% +/- 8% preoperatively; 30% +/- 10% early postoperatively; and 34% +/- 8% late postoperatively (p0.05). Postoperatively there wasor = 5% improvement in EF in 4 patients early and 11 patients late (p0.05). Patients who showed early improvement continued to do so in the late study but, additionally, 7 patients showed improvement only in the late study. Thus the timing of EF measurement after surgery is important in patients with LV dysfunction but not in patients with normal LV function. Early assessment may underestimate the prevalence and degree of recovery.

The purpose of this study was to evaluate the correlates of spontaneous echo contrast in mitral stenosis and normal sinus rhythm. Spontaneous echo contrast is associated with clot formation and embolic phenomena. It has been noted in conditions involving blood stasis, especially mitral stenosis and atrial fibrillation, but the correlates of spontaneous echo contrast in patients with mitral stenosis and normal sinus rhythm have not been extensively evaluated. The transthoracic and transesophageal echocardiograms and clinical findings of 47 patients with mitral stenosis and normal sinus rhythm were reviewed. Left atrial size, mean transmitral gradient, and valve area were measured, and the presence or absence of spontaneous echo contrast in the left atrium was noted. Spontaneous echo contrast was found in the echocardiograms of 21 (45%, group 1) of 47 patients. There was no contrast in those of the other 26 patients (group 2). Mean transmitral gradient was significantly higher in group 1 (13.6 +/- 5.2 mm Hg) than in group 2 (10.5 +/- 4.9 mm Hg) (p0.05). Mitral valve area was significantly smaller in group 1 than in group 2 (1.0 +/- 0.5 vs 1.4 +/- 0.5 cm2; p0.02). There was a trend toward a higher prevalence of significant mitral regurgitation in group 2. There was no significant difference with respect to age, left atrial size, history of embolism, or warfarin therapy. We conclude that spontaneous echo contrast in the left atrium of patients with mitral stenosis and normal sinus rhythm is common and is associated with a significantly smaller mitral valve area and higher mitral gradient.(ABSTRACT TRUNCATED AT 250 WORDS)

The automatic implantable defibrillator is an electronic device programmed to monitor the cardiac rhythm continuously, to recognize ventricular fibrillation and ventricular tachyarrhythmias characterized by sinusoidal waveform, and to deliver corrective difibrillatory discharges when indicated. Three patients suffering from recurrent malignant ventricular arrhythmias refractory to medical therapy underwent permanent implantation of this device. Seven episodes of ventricular tachycardia and flutter-fibrillation were documented during the weeks following the implantations; two were induced at electrophysiologic studies and five occurred spontaneously. All were correctly identified and six were automatically reverted to normal sinus rhythm by the implanted device; one induced episode was cardioverted externally before the unit could recycle. Although many problems remain to be solved and the ultimate value of this therapeutic modality has to be determined, a new approach to prevention of sudden death in patients at high risk of developing lethal ventricular arrhythmias has become available.

Although the long-term prognosis of children with persistent supraventricular tachycardia (SVT) has been generally considered benign, recent reports have suggested that some of these patients may develop cardiac dysfunction secondary to their persistent SVT. The clinical course of six children demonstrating ECG criteria of persistent SVT are presented herein with follow-up data for 5 to 20 years. Persistent SVT was present in each patient from 2 to 19 years. Two patients had transient congestive heart failure early in their course of persistent SVT, and two others demonstrated continued roentgenographic evidence of mild cardiomegaly without associated symptomatology. Conventional antiarrhythmics administered briefly in five patients and chronically in two were without effect on their arrhythmias. Persistent SVT remains in three patients and a fourth continues to exhibit intermittent episodes of SVT; however, all six patients are currently asymptomatic with two in stable normal sinus rhythm. This investigation indicates that the persistent form of SVT (lasting more than 1 year) is uncommon among children with paroxysmal SVT, and long-term observation of the consequences of persistent SVT supports the view that this rhythm disturbance is generally well tolerated in such patients.

In animal experiments arrhythmias induced by cardiac glycosides which prove fatal if untreated can be terminated by administration of glycoside-specific antibodies. Immunotherapy with digoxin-specific antibody fragments had hitherto only been employed on one occasion, namely in a person who had taken a massive overdose of digoxin with suicidal intent and who had failed to respond to symptomatic treatment. The present paper describes the use of F(ab') 2 fragments of digoxin-specific antibodies in a female patient with lanatoside C intoxication to treat the associated life-threatening cardiac arrhythmia. The arrhythmia was rapidly terminated and normal sinus rhythm was restored. Treatment with the heterologous antibodies did not cause any side-effects.

1. 1. A method of obtaining rapid digitalization by the simultaneous administration of ouabain intravenously and digitalis leaf orally is presented. 2. 2. Digitalization was produced sixty times in fifty-nine cases. The patients had varying degrees of congestive heart failure and different types of heart disease; their ages ranged from 28 to 70 years. 3. 3. In the majority of the cases, improvement occurred within one hour. This improvement, once established, was progressive; the maximum effect was attained at the end of twenty-four hours. 4. 4. After the initial digitalization, it was not difficult to establish the maintenance dose of digitalis leaf. 5. 5. The method was found to be applicable to patients with normal sinus rhythm, as well as to those with auricular fibrillation. 6. 6. Evidences of toxicity were the least that could be expected, indicating that the method is a safe one.

1. 1. A patient with coronary artery disease and intraventricular block who suffered from fifteen seizures of unconsciousness during a period of eight hours with spontaneous recovery is reported. 2. 2. The syncopal attacks were shown to be the result of transient ventricular fibrillation. 3. 3. Spontaneous revival from a seizure of ventricular fibrillation was ushered in by the appearance in the electrocardiogram, of a postundulatory pause followed by idioventricular rhythm, and ventricular ectopic beats and finally by normal sinus rhythm.

1. 1. Auricular flutter is a common result of quinidine therapy given for conversion of auricular fibrillation to normal sinus rhythm. 2. 2. The appearance of auricular flutter is in itself not a contraindication to continue quinidine therapy. In most instances if the dosage of quinidine is maintained or increased, conversion to a regular sinus rhythm will result. 3. 3. Cardiac enlargement and congestive heart failure in themselves are not contraindications to quinidine therapy. The danger of embolic phenomena remains a possibility, but since this occurs even more commonly if the auricular fibrillation persists, it cannot be considered a definite contraindication.

1. 1. Lanatoside C, which is a stable, crystalline glycoside derived from digitalis lanata, caused no anatomic changes in the heart muscle of the dog when it was given in therapeutic doses daily for a period of three months. 2. 2. Lanatoside C, when administered intravenously to patients with auricular fibrillation, reduces the heart rate to normal within a period of two minutes to two hours. When administered orally, lanatoside C reduces the rate of the heart to normal within twenty-four to forty-eight hours. 3. 3. Lanatoside C is efficacious in the treatment of congestive heart failure when normal sinus rhythm is present. In fact, the efficacy of lanatoside C in the presence of normal sinus rhythm is almost as great as when the heart failure is associated with auricular fibrillation. 4. 4. Lanatoside C will often restore normal rhythm in cases of supraventricular paroxysmal tachycardia and auricular flutter. In eight of our 102 cases of nonparoxysmal auricular fibrillation, normal sinus rhythm became established spontaneously during treatment with lanatoside C. 5. 5. Lanatoside C will reduce the pulse rate to normal in some cases of auricular fibrillation associated with hyperthyroidism, and, in at least one case, the venous pressure was brought down from 22 cm. of water to 9 cm. of water within forty-eight hours. 6. 6. Lanatoside C seems definitely less toxic than preparations of digitalis purpurea. Some patients who cannot tolerate digitalis purpurea can take lanatoside C in sufficient doses to aid in the relief of their heart failure.

A woman with hypertension and repeated paroxysms of 1:1 auricular flutter received 20.8 grams of quinidine sulphate within nine days, in total doses ranging from 0.4 gram to 4.8 grams a day with the purpose of abolishing this abnormal rhythm. The doses ranged from 0.2 gram of the drug at two hour intervals to 0.4 gram at hour intervals. On the fourth day, after 9 grams of quinidine had been administered, the auricular flutter was temporarily abolished and normal sinus rhythm was restored for a few hours. Following the reestablishment of auricular flutter, the patient went into circulatory collapse on several occasions when there was a return of the 1:1 flutter. A ventricular rhythm with widely aberrant complexes resembling those seen in ectopic ventricular tachycardias was found on the ninth day, and the drug was then discontinued. All these abnormal complexes then disappeared. On the tenth day, one day after the drug had been discontinued, the patient complained of blindness which gradually disappeared, and normal vision returned after four days.

Two cases of transient complete heart block are reported in which there was a supernormal phase in the conductivity of the depressed region. In the first case, penetration of the depressed zone by an impulse arising in the ventricle produced a supernormal phase during which A-V conduction occurred. The conducted impulse in turn gave rise to a supernormal phase which permitted the next impulse to pass, so that normal sinus rhythm was established. It was maintained until auricular slowing caused the auricular impulse to fall outside of the period of supernormal conductivity. In the second case, impulses arising in the auricle produced in the depressed zone a supernormal phase which permitted retrograde conduction.

1. 1. Electrocardiograms which were taken before, and at intervals during, resection of the pericardium in six cases of chronic constrictive pericarditis have been described. 2. 2. Two patients who had auricular fibrillation developed both right and left ventricular premature contractions and short runs of ventricular paroxysmal tachycardia. In one case of normal sinus rhythm, auricular premature contractions which had been present beforehand increased in frequency. Moreover, paroxysms of auricular fibrillation, auricular flutter, and auricular paroxysmal tachycardia were recorded. Two patients with normal sinus rhythm and one with auricular fibrillation developed neither premature contractions nor other changes in rhythm. In only one case did the electrocardiograms which were taken before and after operation show appreciable changes in the amplitude and form of the T waves. 3. 3. These observations demonstrate the remarkable amount of manipulation and mechanical stimulation of its surface that the heart can tolerate without the occurrence of prolonged abnormalities of rhythm and without embarrassment of its function. These observations should give assurance to surgeons who undertake the surgical treatment of chronic constrictive pericarditis.

1. 1. An unusual auricular rhythm is described. It fulfilled the major criteria for the identification of paroxysmal auricular tachycardia, with the exception of the fact that the rate was comparatively slow at 86 per minute. The rate of the normal sinus rhythm at the time, however, was only 70 per minute. 2. 2. Theoretical implications are discussed, and it was concluded that the underlying mechanism of this arrhythmia was parasystole.

Acceleration of the sinoatrial rate leading to complete heart block is reported as an unusual cause of the Adams-Stokes syndrome. It is postulated that the maximal rate of impulse transmission of the atrioventricular conduction system was exceeded when the atrial rate reached 100 per minute, and complete heart block resulted. The re-establishment of 1:1 A-V conduction was dependent upon the atrial rate slowing to 100 per minute or less. Many of the clinical features which tend to characterize individuals with the Adams-Stokes syndrome in whom normal sinus rhythm predominates between syncopal attacks were evident in this patient. The diagnosis was delayed because of the transient nature of the syncopal attacks and the cardiac arrhythmias responsible for them. Medical therapy, once initiated, failed to decrease the frequency or severity of the Adams-Stokes attacks. In fact, there was the suggestion that Isuprel led to an exacerbation of the episodes of heart block, presumably by increasing the atrial rate. The surgical implantation of an artificial cardiac pacemaker was followed by the appearance of multiple ectopic ventricular premature beats and by ventricular fibrillation as a terminal event.

1. 1. The electrocardiographic findings of myxedema heart have been reviewed. These are, briefly: (a) low voltage of all complexes, (b) flattening and inversion of the T waves, and (c) reversion toward normal on thyroid therapy. 2. 2. The various arrhythmias and disturbances in auriculoventricular conduction associated with myxedema heart are mentioned. 3. 3. A case of complete auriculoventricular block with reversion to normal on thyroid therapy is reported. 4. 4. Possible etiologic factors for the above changes are discussed.

In two cases of paroxysmal tachycardia of supraventricular origin the intravenous administration of digitalis produced a pronounced slowing of the heart rate followed by the return of the normal sinus rhythm. The significance of these observations is discussed.

1. 1. Three cases are presented with aberrant ventricular conduction which simulated ventricular tachycardia. Two of these cases did not respond to moderate doses of quinidine and treatment was ineffective until adequate digitalization was carried out. One of these had a basic rhythm of normal sinus rhythm, and in the other two patients the basic rhythm was auricular fibrillation. One case with a basic rhythm of auricular fibrillation exhibited supraventricular tachycardia with aberrant ventricular conduction during surgical manipulation of the heart. 2. 2. Prompt recognition of this arrhythmia is desirable since on superficial analysis it simulates paroxysmal ventricular tachycardia. Digitalis is usually contraindicated in the management of paroxysmal ventricular tachycardia but appears to be the drug of choice in paroxysmal supraventricular tachycardia displaying aberrant ventricular conduction. 3. 3. The mechanism of production and the recognition of aberrant ventricular conduction is discussed.

1. 1. Six hypertensive patients receiving protoveratrine developed various forms of cardiac arrhythmias on nine occasions. These arrhythmias consisted of sinus bradycardia, sinus arrest, wandering pacemaker, first-degree atrioventricular block, and partial and complete atrioventricular dissociation. All of these mechanisms reverted to normal sinus rhythm with time or with the administration of atropine. 2. 2. These arrhythmias are believed to result from excessive vagal stimulation by the drug, producing depression of the sinoauricular and atrioventricular nodes of the heart. A direct toxic effect of protoveratrine on the myocardium cannot definitely be excluded. 3. 3. It is emphasized that protoveratrine may produce either atrioventricular block or atrioventricular dissociation, or both. Atrioventricular dissociation may occur by virtue of excessive sinus slowing and ventricular escape (default) or increased ventricular automaticity (usurpation). In the present series of cases, the effect in depressing the sinoauricular node was paramount. 4. 4. At times these toxic effects appeared to be related to a certain critical threshold dosage of the drug; at other times, they occurred on maintenance dosage previously tolerated without toxic symptoms. 5. 5. Digitalis preparations were being used concomitantly in four of the six patients. No definite conclusion as to the possible synergistic action of these two drugs in the production of these arrhythmias can be made from this small series of cases.

1. 1. The application of the salt-bridge method of esophageal electrocardiographic registration to the development of a simple and clinically reliable bipolar esophageal lead has been outlined. The results of multichannel, multilevel esophageal lead surveys made with this device upon 26 subjects with normal sinus mechanism and 74 with various cardiac arrhythmias are reported here. The leads which were routinely recorded simultaneously in these surveys include unipolar registration from the proximal and distal members of the lead assembly (VE P and VE D ), the difference in potential between these two members (Lead BE), and a conventional extremity lead (usually Lead II). 2. 2. A careful and extensive analysis of the group of subjects with normal sinus rhythm confirms that both the unipolar and bipolar esophageal leads greatly exceed the capability of conventional body surface leads in depicting the forces of atrial depolarization and repolarization. In this group the bipolar esophageal leads appeared to have certain advantages as compared to the unipolar leads, and in no instance did they prove inferior to the unipolar leads. 3. 3. In our evaluation of the group of subjects with cardiac arrhythmias the esophageal leads offered unsurpassable diagnostic superiority as compared to the conventional leads. In a number of cases the bipolar esophageal lead was decidedly better than the unipolar leads, although this was not invariably so. 4. 4. Our clinical observations of the unipolar and bipolar esophageal electrocardiograms appear to confirm the theoretical principles which were previously developed in this laboratory. As anticipated, the bipolar lead has proved to be particularly sensitive to alterations in the time course of atrial depolarization. It also provides a ready means for sorting atrial from ventricular deflections, especially in situations in which they occur concomitantly. 5. 5. On the basis of the experiences reported here, we believe that no complicated or perplexing arrhythmia will have been studied adequately without the benefit of esophageal tracings. The relative technical simplicity of the salt-bridge principle as applied to unipolar and bipolar esophageal registration greatly minimizes the demands which such a procedure would ordinarily impose upon the physician's time and energy.

A case is presented of a patient in whom eyeball pressure was applied to terminate an attack of paroxysmal supraventricular tachycardia with resulting short runs of ventricular fibrillation followed by return to normal sinus rhythm. The implication that myocardial irritability even to the point of ventricular fibrillation may be a hitherto unconsidered danger in the clinical use of vagal cardiac stimulation is offered.

The spatial ventricular gradient was obtained from 71 ECG records exhibiting both normal sinus beats (NSB) and premature ventricular contractions (PVC). The difference in gradients between normal and extra beats was compared statistically with beat-to-beat variability of normal sinus rhythm. A significant difference was found, and Wilson's hypothesis on the constancy of the ventricular gradient in spite of changes in the ventricular activation pathway could be rejected. Two different corrected orthogonal lead systems were used in order to minimize the effect that a particular lead design might have had upon results. Methods for obtaining ECG time integrals were studied for accuracy and consistency. In planimetric determinations the width of records was found to influence results considerably. Digital or analog computations were found to be a preferable procedure for quantitative applications. Furthermore, the averaging of time integrals over at least one respiratory cycle was found to be necessary in order to eliminate beat-to-beat variability of the ventricular gradient. Since methods for obtaining ECG time integrals were found to be very critical, the question was raised whether simpler ECG measurements, such as maximal QRS vectors, are not preferable for clinical use.

1. 1. Procaine amide was given intravenously to sixteen patients during twenty-two episodes of tachycardia of various origins with conversion to normal sinus rhythm in fourteen instances. 2. 2. Ventricular tachycardia was successfully treated in all of five attempts. 3. 3. Supraventricular tachycardias responded in eight out of twelve episodes. Two cases of atrial tachycardia with 2:1 block included in this group did not revert to normal rhythm. 4. 4. In four cases of recent atrial fibrillation with rapid ventricular rates, one returned to normal sinus rhythm and in two instances atrial flutter appeared. 5. 5. Aberrant ventricular conduction at a rapid rate complicated two cases of atrial fibrillation. Isolated ventricular aberration appeared in one case of atrial tachycardia with 2:1 block when treated with both procaine amide and Quinidine Sulfate. 6. 6. It would appear advisable to fully digitalize all patients with atrial fibrillation before giving procaine amide. 7. 7. The intravenous route of administration is a safe method and results are accomplished rapidly.

Two reports of paroxysmal supraventricular tachycardia have been presented in which the patients developed ventricular tachycardia following carotid sinus stimulation before reverting to normal sinus rhythm.

Preliminary animal studies indicate that celiprolol has antiarrhythmic properties. Animal and clinical electrophysiologic studies suggest that the antiarrhythmic activity is from celiprolol β-blocking effects (class II antiarrhythmic). Studies with anesthetized dogs show that celiprolol elevates the ventricular fibrillation threshold. An unexpected finding in the canine infarct drug model is the spontaneous conversion of ventricular fibrillation to normal sinus rhythm. The β 2 -agonist property of celiprolol may account for this observation. In a clinical study celiprolol has been found to decrease ventricular rate in patients with chronic atrial fibrillation. In the same study, the compound decreased the occurrence of premature ventricular contractions by 50%. Animal and clinical studies demonstrate that celiprolol does not adversely interact with digitalis glycosides.

Echocardiography was used to evaluate the late diastolic filling period of the left ventricle in 30 normal individuals, 25 patients with left ventricular hypertrophy, normal sinus rhythm, and either a normal or delayed mitral valve closure, and 15 patients with atrial fibrillation. The echocardiographic ventricular A wave (VAW) was defined as the difference between the end-diastolic and an earlier late-diastolic internal left ventricular dimension, and it was felt to primarily reflect the atrial contribution to late diastolic filling of the left ventricle. It disappeared during ventricular pacing and was significantly smaller than normal in patients with atrial fibrillation. The VAW was significantly larger in patients with left ventricular hypertrophy and normal mitral valve closure reflecting the greater contribution by atrial contraction to late diastolic filling in these patients. In patients with left ventricular hypertrophy and delayed mitral valve closure, the VAW was normal reflecting lesser ventricular enlargement with atrial contraction than in the other patients with left ventricular hypertrophy. This suggested a greater impairment to left ventricular filling in these patients. Therefore, the VAW appears to be an indicator of abnormalities of late diastolic filling caused by left ventricular hypertrophy.

In BOTH man and experimental animal, the fact has been established that only a fraction of the normal P-R interval represents passage of the excitation impulse across the auricular myocardium. Lewis 1 calculated that the speed of the impulse in the dog's auricle during normal sinus rhythm is approximately 1,000 mm. per second. By means of simultaneous esophageal leads, the normal impulse in the human auricle has been found to travel at a rate of at least 500 mm. per second 2 . If these determinations are accurate, the cardiac impulse traverses the auricles from the sinoauricular node to the A-V node in approximately 0.05 second, or in about one-third of the period occupied by the P-R interval in the normal electrocardiogram. The purpose of this communication is to present new data concerning the delay in conduction responsible for the remaining portion of the normal P-R interval.

Two cases of upper nodal rhythm associated with auriculoventricular heart block or antegrade block are presented. The first case shows the transitory development of an upper nodal rhythm with first degree auriculoventricular heart block, in an elderly hypertensive patient, soon after an attack of acute pulmonary edema. The second case is of unusual interest, exhibiting as it does phases of (1) normal sinus rhythm, (2) uncomplicated upper nodal rhythm, (3) nodal tachycardia with 2 to 1 auriculoventricular antegrade block, and (4) nodal tachycardia with instances of 2 to 1 block, first degree heart block, and nodal pauses. Another feature of unusual interest is the regular appearance of a coronary S-T-T pattern during phases of nodal rhythm.

1. 1. Development of atrial flutter is a common result of quinidine therapy given for conversion of atrial fibrillation to normal sinus rhythm. 2. 2. The fact that atrial fibrillation can be changed during quinidine therapy to atrial flutter or tachycardia before final conversion to sinus rhythm, and that when reversion takes place the rhythm again proceeds from sinus through atrial premature systoles, atrial tachycardia, and atrial flutter to atrial fibrillation lends support to the theory of unitary nature of the atrial arrhythmias.

This case report demonstrates the therapeutic effect of the combination of propranolol and procainamide upon recurrent paroxysmal ventricular tachycardia in a 10-year-old boy. When used as a single agent, procainamide, diphenylhydantoin, and propranolol proved ineffective in suppressing the arrhythmia. The child has been in normal sinus rhythm for 20 months without side effects, while receiving a combination of propranolol and procainamide. The etiology and therapy of this condition was discussed.