Search

The case history of a patient with common ventricle associated with complete atrioventricular (A-V) canal, severe mitral insufficiency, and tricuspid insufficiency is described. Successful repair was accomplished through the right atrium by excising the A-V valves, partitioning the ventricular cavity with a patch, inserting two Braunwald-Cutter prostheses in the A-V position, and continuing the patch cephalad to close the atrial septal defect. A His bundle locater was employed, and normal sinus rhythm was preserved.

Data in 20 patients with normal sinus rhythm who, following induced premature atrial beats (PABs), manifested re-entry in the region of the sinus node are presented. PABs at coupling intervals ranging between 230-535 msec were followed by sinus node re-entry (SNR). Several criteria were applied to diagnose SNR: the temporal sequence of atrial excitation, the intra-atrial conduction time, the shape and polarity of the P waves, and manifestation of re-entry independent of atrioventricular (A-V) nodal delays. In 18 patients SNR lasting for one to several beats was observed. In the remaining two patients sustained SNR was manifested as supraventricular tachycardia (SVT), with cycle lengths ranging between 320-500 msec, which persisted for several minutes prior to its termination by properly timed atrial stimuli. In one of the latter two patients sustained SNR and SVT were produced only after atropine administration. Sinus node re-entry could be elicited at will in a specific echo zone with a duration ranging between 10-170 msec. In some cases SNR was also observed during and on cessation of regular atrial pacing. The latter observation provides a possible explanation for the unexpected sinus node acceleration seen sometimes on termination of atrial pacing. It is demonstrated that SNR for a single beat may fallaciously simulate sinus node entrance block. Simultaneous occurrence of re-entry at multiple sites, i.e., the sinus node and the A-V node, with resultant fusion P waves is also demonstrated. This study provides another mechanism for the genesis of regular and irregular SVT. The analysis and localization of the re-entry circuit may prove to be of clinical and therapeutic significance in selected patients.

Summary A case of Prinzmetal's variant angina pectoris was discovered mainly by the use of dynamic electrocardiography (DECG). This diagnosis prompted this patient's admission to the hospital where ventricular fibrillation was successfully converted to normal sinus rhythm. A coronary angiogram revealed a singular isolated stenosis of the left anterior descending coronary artery which was successfully bypassed with a saphenous vein graft. The validity of ST segments recorded by DECG is discussed. This report demonstrates that DECG may be the only way to diagnose variant angina pectoris.

In experiments conducted on anesthetized dogs, a single prolonged cardiac cycle caused an increase in the duration of the refractory period of the ventricular myocardium. The refractory period remained prolonged for one or two additional cardiac cycles after the basic cycle length was resumed. In concealed bigeminy, a 2:1 block in a reentry path is postulated. The compensatory pause that follows a manifest extrasystole results in a prolongation of the refractory period. If the refractory period exceeds the propagation time of the next ectopic impulse conducted through the reentry path, that ectopic impulse will be concealed. However, if the refractory period does not exceed the propagation time, another extrasystole will occur, and a bigeminal sequence will ensue. Consecutive compensatory pauses appear to exert a cumulative effect on refractory period duration, so that for critical propagation times, the bigeminal pattern will be terminated briefly when an ectopic impulse becomes concealed. A quadrigeminal pattern occurs when the propagation time in the reentry loop lies between the refractory period durations of the beat terminating a compensatory pause and the beat that occurs two sinus cycles later. In concealed bigeminy where an odd number of conducted beats greater than five lies between extrasystoles, the propagation time in the reentry path is just less than the refractory period of the ventricular cells during normal sinus rhythm at the prevailing heart rate. Random increases in propagation time or decreases in refractory period result in manifest extrasystoles.

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.

Atrial tachycardia in Wolff-Parkinson-White (W.P.W.) syndrome is usually treated by the administration of digitalis, quinidine, or procainamide, separately or in combination. Some instances of refractory tachycardia have been terminated by electroshock. This report describes a case of Wolff-Parkinson-White syndrome in which atrial tachycardia was promptly converted to normal sinus rhythm by the use of intravenously administered lidocaine.

A case of heart block in rheumatic carditis has been electrocardiographically studied. Difficulties of diagnosing the condition without mechanical aid has been pointed out. The effects of atropin in removing the block has been graphically shown. An explanation has been offered for the unusual preferential behaviour of atropin in such a case in restoring normal sinus rhythm without having any effect on the rate of the heart.

The electrocardiographic, vectorcardiographic and hemodynamic data of 50 cases of isolated ventricular septal defect were analyzed. All but 1 patient had normal sinus rhythm. Ten per cent had first degree A-V block. Patients with rS in V 1 had the lowest right ventricular pressures and relatively small pulmonary to systemic blood flow ratio. The right ventricular systolic pressures were generally increased when V 1 revealed prominent R waves. In adults of this group there was a reduction in the ratio of pulmonary to systemic blood flow as compared to children. There was, however, poor correlation between the height of the R wave in V 1 and right ventricular systolic pressures. The incidence of combined ventricular hypertrophy by electrocardiographic criteria varied from 8 to 22 per cent, according to the criteria applied, and was 24 per cent by vectorcardiographic criteria. The vectorcardiographic features of combined ventricular hypertrophy are discussed.

Summary Repetitive paroxysmal tachycardia of auricular type with aberrant intraventricular conduction which simulated paroxysmal ventricular tachycardia is reported in an infant 7 months of age. Among the note-worthy features about the case were: (1) the bizarre ventricular complexes, (2) high and variable rate of discharge (up to 300 per minute) of the ectopic focus, (3) lack of evidence of ectopic auricular activity, (4) absence of sinus or extrasystolic beats between paroxysms, (5) increase in duration of the Q-T interval, and (6) development of persistent S-T-T segment abnormalities with restoration of normal sinus rhythm.

A forty-five year old patient suffered his second acute myocardial infarction and “died” suddenly. The presence of a physican during the catastrophe made possible immediate institution of closed chest cardiac massage, thus providing time for electrocardiographic diagnosis of ventricular fibrillation. Three defibrillator shocks restored normal sinus rhythm and the patient subsequently made an uncomplicated recovery.

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.

Summary1. Experimentally produced auricular fibrillation in the dog was successfully restored to normal sinus rhythm by the intravenous infusion of atabrine (average 2.17 mg per kg). 2. The mechanism by which atabrine might produce this effect is discussed. It is suggested that its action is similar to that of quinine or quinidine.

An implantable, synchronous cardiac pacemaker for long-term correction of complete heart block has been developed. It has been successfully used in dogs for periods up to eight months. The performance of the pacemaker during normal sinus rhythm and atrial arrhythmias is illustrated with electrocardiograms. After implantation of the pacemaker, the dogs have returned to completely normal activity and have tolerated all physical exercises well. [see figure in the PDF file]

Thioridazine hydrochloride was investigated in 10 dogs for its quinidine-like activity in experimental cardiac arrhythmias simulating clinical disorders. It was found to cause significant reduction in the duration of acetyl-choline-induced auricular fibrillation and to bring about reversion of auricular flutter to normal sinus rhythm. It exerted a long-lasting suppressor action on ventricular ectopic tachycardia produced by two stage coronary ligation. These findings coupled with the low toxicity of the drug are suggestive of the therapeutic usefulness of thioridazine in selected cases of cardiac arrhythmias.

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.

Sixty-six patients were cardioverted 82 times for various arrhythmias. Eigthy-three per cent were successfully converted to normal sinus rhythm. Those with acute arrhythmias who were in unstable situations (postoperative and acute myocardial infarctions), and those with long-standing arrhythmias associated with severe heart disease were less likely to be converted. Complications of the procedure were minimal except for two cerebral emboli which left no significant impairment. Forty-seven per cent of patients were able to maintain a sinus mechanism during the period of follow-up (3 to 26 months). With two exceptions, those who reverted to the previous arrhythmia did so within three months. Rheumatic heart disease (64 per cent) and hypertensive cardiovascular disease (56 per cent) were less likely to maintain a normal mechanism than those with coronary artery disease (38 per cent).

HE PURPOSE of this study was to determine the effects of postural changes on the A-V conduction mechanism of the heart and on alterations in rhythm in patients subject to Adams-Stokes seizures during normal sinus rhythm and transient heart block. In studying the natural course of this syndrome, it became apparent that quite a few patients who were subject to syncopal seizures gave a history of dizzy spells, unsteadiness of gait and loss of consciousness with changes in bodily postures. It was hoped that postural changes would facilitate the recognition of patients who were subject to Adams-Stokes seizures when they presented themselves with normal sinus rhythm.

Summary A case of auricular flutter in a child 2 years old, which continued forthree years, is described. Administration of digitalis was followed by a definite recovery, a normal sinus rhythm resulted, and the symptoms of cardiac failure disappeared. The child is probably suffering from a patent foramen ovale. As far as we have been able to discover, this case is the fourth described in literature and the second cured by digitalis

Three cases of intermittent obstruction of the mitral prosthesis (Cutter-Smeloff) due to ball variance have been reported. The typical findings were marked variation in the arterial pulse and the intensity of the mitral closing sound and intermittent absence of the opening click. The phonocardiography revealed varying intervals from aortic closing sound to the opening click (A 2 - OC interval). Hemodynamic studies revealed fluctuating aortic and pulmonary artery wedge pressures in spite of normal sinus rhythm, due to impaction of the ball into the prosthetic ring, opening only with severe elevation of the left atrial pressure. At operation, the balls showed yellowish discoloration, but no disruption of sutures nor thrombosis of the prosthesis was found. The incidence of this phenomenon was 9% with the Cutter-Smeloff mitral prosthesis, but no such case was seen among patients with the Starr-Edwards mitral prosthesis.

Sixty cases of atrial fibrillation from the USAF flying population are reported. Follow-up information in 59 subjects averaged 41.2 months. Only three cases of persistent atrial fibrillation were detected and two of these had normal sinus rhythm prior to the onset of atrial fibrillation. There were 21 cases of recurrent paroxysmal atrial fibrillation and 36 cases of isolated acute atrial fibrillation associated with a variety of precipitating factors. Thyrotoxicosis was notable by its absence in any of these cases of atrial fibrillation. Symptomatology either related to the primary disorder precipitating atrial fibrillation or secondary to the arrhythmia itself was frequently observed. The hemodynamic effects of atrial fibrillation on cardiac output, and cerebral artery spasm with diminished cerebral blood flow are important aeromedical considerations.

1.1. Clinical and physiologic data are presented in thirteen cases of proved rheumatic tricuspid stenosis. 2.2. The physiologic data of significance included (a) exaggerated "a" waves in the right atrial pressure curves in patients with a normal sinus rhythm and, more important from a diagnostic point of view, (b) significant atrioventricular pressure gradient during ventricular diastole. 3.3. The significance of the clinical symptoms and signs is discussed. 4.4. A method for determining the size of the tricuspid orifice during the course of cardiac catheterization is suggested.

We report a patient with atrial fibrillation which reverted to normal sinus rhythm after treatment for hyperkalemia. The concept of a sino-ventricular rhythm, with sino-atrial discharge in the presence of hyperkalemic-induced apparent complete atrial depolarization, is presented and related to recent electrophysiologic findings in animals.

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.

SummaryRapid intravenous administration of procaine amide was found effective in reverting ventricular tachycardia, produced in dogs by large doses of cardiac glycosides, to normal sinus rhythm. In most instances, the reversion was temporary and additional injections of procaine amide were necessary in order to maintain the normal rhythm. Such additional injections, repeated several times in these experiments, did not produce electrocardiographic signs of cumulative toxicity.Although procaine amide effectively reverted ventricular tachycardia in the dog experiments, the same agent failed to increase the lethal dose as determined by limited “cat unit” studies. A similar relation was noted by Emerson in studies on procaine(6) and by Stanbury and Farah(7) in studies on magnesium.The development of slow idioventricular rhythms and cardiac arrest in several experiments following procaine amide administration demonstrates a danger of drug termination of digitalis-induced ventricular tachycardia. As Gold(8) has ...

9 children with supraventricular tachycardias refractory to conventional therapy were treated with propranolol. In 3 children normal sinus rhythm was restored. In 3 others frequency of paroxysmal arrhythmias was decreased. In 1 reduction of ventricular response to the ectopic rhythm was achieved, and in 2 remaining patients, propranolol had no effect. The dosage of propranolol ranged from 0·5 to 4·0 mg/kg per day, given orally, with few side effects. It appears that propranolol can play an important role in treatment of supraventricular arrhythmias of childhood unresponsive to conventional therapy.

In the course of a study of electrocardiograms which show a large Q-3 deflection, we noted what appeared to be a relative frequency of inversion of the P deflection in the third lead of these tracings. This appeared to be consistent with the finding of Carr, Hamilton and Palmer1 that inversion of P-3 is occasionally associated with the production of a large Q-3 wave in electrocardiograms taken from pregnant women.We undertook to determine the frequency with which an inverted P-3 wave is found in an indifferent series of electrocardiographic tracings and in a series of electrocardiograms which contain a large Q-3 wave.No attempt was made in this study to exclude or separate electrocardiograms showing auricular fibrillation, auricular flutter, paroxysmal auricular tachycardia or nodal rhythm. In tracings where extrasystoles were present these were ignored—the P-waves associated with the normal sinus rhythm alone were examined. No attention was paid to diphasic P-waves or to isoelectric P-intervals. Only whe...

In a case of Wolff-Parkinson-White syndrome, type B, the electrocardiogram displayed the same broad QRS configuration during an episode of paroxysmal atrial fibrillation as during normal sinus rhythm

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.

Phonocardiographic and Cinefluorographic methods were used to study the mechanism of closure of the Starr-Edwards mitral prosthetic valve (model 6320) in 41 patients with a normal QRS interval. Atrial fibrillation was present in 23 patients and normal sinus rhythm in 18. The following intervals were measured: QRS to mitral closing click (Q-Mc), QRS to onset of closure (Q-Oc) and QRS to completion of closure (Q-Cc) of the prosthetic valve. Ball travel time was measured as Q-Cc minus Q-Oc. Mean Q-Oc was shorter in the group with normal sinus rhythm. In 8 patients in this group, Q-Oc occurred before ventricular systole and, in 2, completion of closure occurred before the QRS interval. Early closure in the group with normal rhythm was related to a prolonged P-R interval. In this group, values for Q-Mc and Q-Cc intervals did not differ significantly. Q-Cc in the groups with atrial fibrillation and normal sinus rhythm were not significantly different. Ball travel time was significantly longer in the latter group. Long R-R intervals in the group with atrial fibrillation may be associated with partial and occasionally complete premature closure of the valve. Q-Mc was inversely related to the R-R interval in this group. This study indicates 3 mechanisms for closure of the mitral prosthetic valve. Atrial or ventricular contraction alone may close the valve. The contribution of each is dependent on the time interval separating the contraction of these chambers. Spontaneous partial or complete closure may occur before ventricular systole during a prolonged R-R interval.

Left atrial volume and its change during cardiac cycle were studied in 49 patients with various heart diseases and 8 normal individuals by simultaneous use of cineangiocardiography at 400 fps and film changer at 6 fps. Methods Calculation of left atrial volume was performed as described by Sauter et al. assuming that the left atrium might be represented by an ellipsoid, and it was corrected for nonparallel X-ray beams in each case. Results Left atrial volume was calculated by two different methods: 1) using both A-P and lateral projections and 2) using only A-P projection. When the left atrial volume was less than about 200ml, it could be calculated from the following formula; Y = 0.55X + 0.8 where Y is the true left atrial volume and X is the value calculated from A-P projection. When the left atrial volume was more than 300ml, the value calculated from A-P projection was much the same as the value calculated from both A-P and lateral projections. As the left atrial volume became large, the length of two axes became equal especially in the lateral projection. There was a statistically significant correlation between maximal left atrial volume and left atrial cyclic volume change, but in cases with atrial fibrillation there was no significant correlation between them. There was no significant correlation between the left atrial volume and the mean PC pressure. The large left atria could be found in mitral valvular diseases, but a gigantic one was usually seen in the mitral regurgitation. In general, the left atrial volume was larger in cases with atrial fibrillation than in cases with normal sinus rhythm. In mitral valvular diseases with auricular fibrillation contraction of the left atrium was insufficient. Left atrial cyclic volume change was close to left ventricular stroke volume in mitral regurgitation with atrial fibrillation but the former never exceeded the latter in all cases. On making observation of the left atrium by using high speed cineangiography, the length of both longer and shorter axes changed parallel to its volume during cardiac cycle in cases with normal sinus rhythm, but they changed quite irregularly in cases with atrial fibrillation. In cases with mitral regurgitation, it was observed that the expansion of the left atrium was due to regurgitant flow from the left ventricle is spite of the presence of the atrial ribrillation.

The therapeutic efficacy of Atabrine in ventricular tachycardia has not yet been clearly demonstrated. In this case report, Atabrine stopped ventricular tachycardia and restored normal sinus rhythm following the fifth two-hourly oral dose of 0.30 Gm. Nausea and vomiting were the only toxic effects noted. Ventricular tachycardia, in this case, occurred as a complication of acute myocardial infarction. The latter's characteristic electrocardiographic picture became obvious as the arrhythmia was corrected.

An assessment was made of cardiac function by means of right heart catheterization before and immediately after conversion of atrial fibrillation to sinus rhythm in 11 studies on 10 human subjects. Comparable data during exercise were available in five studies. Medical management of patients in this study was identical to that employed routinely for this procedure. After conversion to normal sinus rhythm cardiac output response was significantly increased only during exercise. The relationship of mean right atrial and mean pulmonary wedge pressures to right and left ventricular stroke work was uniformly improved both because of decreases in these pressures and increases in work. Indirect evidence of mitral valvular regurgitation was diminished to absent after conversion. "A" waves and the pulse pressure of atrial contraction were very small in the right atrial tracings after conversion and these contours were usually inapparent on pulmonary wedge tracings. It is concluded that over-all cardiac performance was improved with re-establishment of sinus rhythm and that diminutions in atrial-venous pressure behind each ventricle may be important in explaining symptomatic improvement following electroconversion. Measures of both pressure and flow were required for complete description of the alterations induced by this intervention.

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.

The material comprised the data of 146 patients with tetralogy of Fallot treated by corrective intracardiac surgery. Electrocardiograms were recorded in all cases before and in 108 cases after operation. The majority of the patients were between 5 and 20 years of age at the time of surgery and have been followed for an average of 1.5 years. Arrhythmias, mostly extrasystoles, were recorded in eight cases before operation and in 14 cases on the last follow-up examination. The amplitude of the P wave in lead II decreased by 1 mm. or more after surgery in one third of the cases. Seventeen patients developed complete AV block postoperatively, seven died; of the 10 who survived operation, in all but two the electrocardiogram reverted to normal sinus rhythm. The electrocardiogram showed right axis deviation and right ventricular hypertrophy in the majority of cases. A balanced axis and signs of combined ventricular hypertrophy were commonest in acyanotic patients and more common in cyanotic patients who had had previous shunt procedures than in cyanotic patients who had had no previous shunt. Two patients showed electrocardiographic signs of left ventricular hypertrophy. After corrective cardiac surgery, the mean electrical axis and the pattern of the QRS complex in V 1 and V 6 changed toward normal in the eight patients in whom intraventricular conduction defects did not appear and in the 26 patients with incomplete right bundle-branch block. Two of nine surviving patients in whom a small coronary artery was divided at surgery developed the pattern of myocardial infarction in the postoperative electrocardiogram. Conduction disturbances frequently appeared during operation; they were considered to be caused mainly by direct trauma to the conduction system during closure of the ventricular septal defect or during infundibulum resection. Complete right bundle-branch block appeared in 74 (69 per cent) and incomplete right bundle-branch block developed in 20 (19 per cent) of surviving patients. Only eight patients showed no disturbances of conduction after surgery. The right bundle-branch blocks persisted throughout the follow-up period. The conduction disturbances have not adversely affected the postoperative course, nor have they caused any discomfort to the patients.

The antiarrhythmic effect of Ro 2–5803 was investigated in thirty-four patients with various cardiac arrhythmias. The results obtained were excellent in thirteen patients in whom the drug restored and then maintained normal sinus rhythm. A good effect was achieved in an additional six patients in whom the frequency of extrasystoles was decreased by at least 75 per cent. In four patients with paroxysmal atrial fibrillation and in an additional patient with paroxysmal atrial tachycardia, normal sinus rhythm was restored. The incidence of side effects and untoward reactions was low.

His bundle (BH) electrograms were recorded in 123 patients. The electrocardiogram showed only left axis deviation (LAD) in ten, right bundle branch block (RBBB) with a normal axis in thirty, RBBB and LAD with or without old myocardial infarction in sixty-eight and RBBB with right axis deviation (RAD) in fifteen. Thirteen of these patients were restudied at intervals of six months to two years. The conduction times through the atrioventricular (A-V) node (A-H) and His-Purkinje system (H-V) were measured during normal sinus rhythm and atrial pacing. In all but four patients with sinus rhythm in whom second degree A-V block developed only during atrial pacing at rapid rates (range 100 to 180/minute) the block was localized in the A-H interval (A-V node). In the other four with sinus rhythm the second degree block was localized distal to the BH deflection (H-V). Most of the patients with RBBB (normal axis) and first degree A-V block had a normal H-V time with delay localized in the A-V node (A-H), indicating that this combination in the electrocardiogram does not necessarily mean bilateral bundle branch block. In none of the ten patients with only LAD was the H-V time abnormal (normal range=35 to 45 msec). In seven (23 per cent) of the thirty patients with RBBB (normal axis) the H-V time was abnormal. Forty-nine (72 per cent) of the sixty-eight patients with RBBB and LAD with or without myocardial infarction had an abnormal H-V time. Furthermore, patients with similar electrocardiographic patterns (RBBB and LAD) may or may not have an abnormal H-V time. All fifteen patients (100 per cent) with RBBB and RAD had abnormal H-V times. This study demonstrates that (1) the surface electrocardiographic criteria for assessing quantitative damage in the His-Purkinje system are frequently of limited value, and (2) the majority of the patients (72 per cent) with RBBB and LAD, besides RBBB and anterior hemiblock, have additional damage in the remaining fascicles of the His-Purkinje system. This would suggest partial bilateral bundle branch block or trifascicular block.

Characteristics of the action potential and stimulus conduction in the A-V nodal region were studied electrophysiologically, especially in connection with the histological findings by means of ultramicroelectrode technique. The intracellular records in each case of normal sinus rhythm and A-V conduction disturbance were obtained. And situation of the tip of the microelectrode was ascertained by using immigration of cobalt ion. The specific muscle fibers were recognized in the vicinity of the A-V node. The action potentials of those fibers represented an inter-mediate type between the nodal type and the ordinary atrial muscle type. When the recording microelectrode was moved from the upper part of the node to the His' bundle, the shape of the action potential changed from the typical nodal type to the His' type, and the onset of the activation was gradually delayed. Disturbances of the A-V conduction were made using the effects of acetylcholine. And incomplete A-V block, complete A-V dissociation, and A-V dissociation with nodal or ventricular capture were observed and the boundary of characteristic changes of the action potential in all cases was found at the atrial margin of the A-V node which is netlike in structure.

Diphenylhydantoin (DPH) has been demonstrated to be an effective agent in the treatment of cardiac arrhythmias of various etiologies. It appears to have special utility in the treatment of ventricular arrhythmias, especially those which are digitalis-induced. The drug has been shown to be ineffective in converting atrial fibrillation and flutter to normal sinus rhythm. DPH counteracts the arrhythmic action of digitalis. It depresses ventricular automaticity, enhances A-V conduction and does not significantly effect intraventricular conduction. Also, DPH counteracts the depressant effects of procaine amide. Limited observations, thus far, indicate that DPH is effective when given prophylactically in clinical situations which predispose to the production of cardiac arrhythmias. Side effects of DPH are generally of a mild and transient nature and may be minimized by administering the drug at a rate not to exceed 25–50 mg./min.

Rapid atrial pacing, at rates of 150 to 600/min with stimulus strength up to 15 ma, was attempted in 15 patients with atrial flutter. In 13 of the patients, atrial capture was achieved with changes in both atrial and ventricular rates. In 7 of these, flutter resumed upon cessation of pacing. In the other 6, rapid atrial pacing produced atrial fibrillation which persisted until cardioversion. In 2 patients, atrial capture could not be obtained because of increased atrial refractoriness secondary to flutter. Thus, rapid atrial pacing was ineffective in converting atrial flutter to normal sinus rhythm in all 15 patients. This was in contrast to direct-current cardioversion which was successful in 12 of the patients, in all of whom stable sinus rhythm developed. The 3 patients who did not undergo cardioversion subsequently experienced spontaneous conversion to sinus rhythm. These results suggest that rapid atrial pacing has little place in the management of atrial flutter.

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.

Left ventricular ejection time (LVET; indirect carotid pulse) was studied in 48 patients with atrial fibrillation. In comparison with normal individuals in normal sinus rhythm, ejection times for similar cycle lengths were usually short in patients with atrial fibrillation. Patients without mitral valve disease usually show increasing ejection times following increasing cycle lengths until a certain cycle length is reached (usually around 0.85 sec). Further prolongation of cycle length will not further lengthen the LVET. By contrast, patients with significant mitral stenosis show a continuously sloping curve, i.e. continue to show prolongation of ejection times with progressive lengthening of cycles, eventually reaching ejection times (if cycles are sufficiently long) which exceed those of patients without mitral stenosis. Conversion to normal sinus rhythm (six patients) produced variable results, usually lengthening of ejection time for similar cycle length. Postconversion lengthening of LVET was most pronounced in those cases which lacked progressive increase in LVET with longer cycles during atrial fibrillation. This effect was evident in those patients manifesting relatively slow sinus rates after conversion. Our results indicate that in order to derive information from ejection times in atrial fibrillation one must plot these values against cycle lengths. Moreover, he cannot use data obtained from patients in normal sinus rhythm to interpret ejection times in those manifesting atrial fibrillation.

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.

A case of idiopathic auricular flutter in a male newborn infant is presented. Twenty published cases of auricular flutter in the newborn infant were reviewed and the therapy discussed. Digitalis, the drug of choice, was successful in only 9 of 14 cases. Cardioversion to normal sinus rhythm with the D.C. defibrillator was performed in our case without significant side effects. The method appears to be a safe procedure in the newborn.

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.