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Interatrial block (IAB) (P waveor=110 ms) is a potential risk of atrial fibrillation (AF). However, few investigations have assessed the relevance of echocardiographic parameters, particularly the contribution of its known correlate, left atrial enlargement in this regard. We identified 32 consecutive patients with comparable echocardiographic parameters, such as left atrial dimension and left ventricular ejection fraction. Patients were evaluated for IAB and followed for 15 months for cardiovascular events (heart failure, transient ischemic attacks, and stroke), atrial tachyarrhythmias (AF/atrial flutter), and death. Preexisting AF and IAB (p = 0.02) were significantly associated with future AF events. However, logistic regression analysis indicated that IAB was not an independent predictor of future AF, only preexisting atrial tachyarrhythmias was (hazard ratio 39.5, 95% confidence interval 2.7 to 576.3, p = 0.007). In conclusion, in patients with comparable echocardiographic parameters, such as left atrial size and left ventricular ejection fraction, IAB remained associated with AF after a 15-month follow-up. Additional investigation is needed to confirm the extent of the association.

We investigated 500 consecutive, unselected electrocardiograms of outpatients for interatrial block (IAB) using all 12 leads rather than the usual recommendation in the literature, which is lead II, sometimes with another lead. IAB had been reported in 2 widely separated large general hospitals in40% of 1,000 patients in sinus rhythm in each. Because the P waves in IAB (durationor =110 ms) generally have low amplitude despite their excessive width, we used magnifying graticules and, for greater specificity, a minimal duration ofor =120 ms. Four hundred sixty-nine patients remained after excluding those with atrial arrhythmias or technically poor tracing. Two hundred three of these patients (40.6%) had IAB. Had we used lead II alone, only 110 cases would have been identified, which would have meant overlooking almost 1/2 the cases with this lesion, which is important (1) as a predictor of atrial fibrillation and other arrhythmias, and (2) represents a large, dysfunctional left atrium. Leads V3 and V4 yielded larger numbers of IAB than lead II. (The slightly smaller prevalence than in the 2 cited studies may be due to our using 1/2 the number of patients.) Electrocardiographic interpreters should seek IAB in all 12 leads and consider its anatomic functional and predictive correlates.

Recent generations of dual-chambered cardiac pacemaker pulse generators have included an interesting feature called rate smoothing, which is now starting to be used to good effect clinically. Rapid cycle-to-cycle variations in pacing rate are modulated by these devices by limiting permitted cycle length changes in both upper and lower chambers to some set fraction of the usual beat-to-beat interval, between 3 and 25%. Typically, it is believed that physicians are well-advised to limit upper rate settings in patients with coronary artery disease so as not to provoke ischemia while exercising. It has been reported recently that the use of rate smoothing, even to a very mild degree, allows higher degrees of exercise capacity, and moreover, permits it without the usual symptoms that limit exercise ability in patients with coronary artery disease. The feature functions by setting up independent atrial and ventricular windows on a beat-to-beat basis, within which the chambers are permitted to respond. In effect, a controlled atrioventricular dissociation is permitted. Thus, it may seem somewhat paradoxical in a era when synchrony of the upper and lower chambers is believed to represent a worthwhile goal physiologic pacing. However, it appears that rhythms that include short cycle intervals and irregular heart rate changes adversely affect the subjective ability of patients to exercise. Rate smoothing appears to be an effective means of achieving flexibility in the paced response to exercise especially in chronotropically competent patients. In addition, the rate-smoothing mechanism may be uniquely indicated for: (1) failure of sinus node function (sinus arrest, sinoatrial block, bradycardia-tachycardia syndrome); (2) premature atrial and ventricular contractions; (3) supraventricular tachycardia especially when intermittent, atrial flutter and atrial fibrillation; (4) retrograde P-wave conduction; and (5) nonphysiologic pacemaker influences such as myopotential sensing, electromagnetic interference and cross talk.

Moricizine is a class I antiarrhythmic drug. In preclinical studies, it produces a concentration-dependent decrease in the maximal rate of phase 0 depolarization, speeds repolarization of phases 2 and 3, and decreases the action potential duration and effective refractory period duration in cardiac Purkinje fibers. It has no effect on the slope of phase 4 depolarization, but suppresses normal automaticity in vitro and in vivo and suppresses abnormal automaticity in depolarized Purkinje fibers. Also, it suppresses early afterdepolarizations, delayed afterdepolarizations and triggered activity. In patients, moricizine has minimal effects on the normal sinus node, slows conduction in the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium and has little effect on the atrial and ventricular refractoriness. The intensity of moricizine action on the atrioventricular node, His-Purkinje system and JT interval are dose-related. Co-administration of digoxin and moricizine intensified the lengthening of the PR, AH and HV intervals, and produced more shortening of the JT interval. Patients in whom moricizine was efficacious had a significantly greater lengthening of the AH and QRS intervals than those in whom moricizine was not efficacious. In some patients with sinus node dysfunction, moricizine produced sinus bradycardia, increased sinus node recovery time, and produced second-degree or complete sinoatrial block.

The M-mode echocardiogram of the right atrial (RA) wall can be easily recorded in each person from the subcostal location. In a normal RA wall motion pattern, atrial contraction is represented by a markedly prominent posterior motion. The presence or absence of atrial contractions in the subcostal RA wall echocardiogram, their amplitude, and their timing may help in the diagnosis of cardiac arrhythmias with the simultaneously recorded non-diagnostic electrocardiogram. Flat and hidden P waves can be accurately identified throughout the cardiac cycle. It is possible to distinguish between atrial, ventricular, and nodal premature beats and to recognize atrial fibrillation, atrial flutter, paroxysmal atrial tachycardia, paroxysmal atrial tachycardia with block, atrioventricular (AV) nodal tachycardia, and supraventricular tachycardias with aberrant ventricular conduction. The diagnosis of wandering pacemaker, AV dissociation, sinoatrial block, and AV block is facilitated. On the basis of study of 60 patients with various rhythm disturbances, it was concluded that analysis of the subcostal RA wall echocardiogram is a new, helpful noninvasive approach in the diagnosis of cardiac arrhythmias.

Since Jalife and Moe 1 reported the experimental modulation of a parasystolic focus, it has become evident that a parasystolic rhythm may manifest with features different from those classically described. The modulated parasystolic cycle may become irregular as a result of influence exerted by the sinus beats, and the interectopic intervals may therefore not be mathematically related. 2–5 We present a case of modulated ventricular parasystole in which the typical diagnostic features of parasystole are lacking and in which the distribution of the ectopic beats suggests a Wenckebach form of ectopic-ventricular block.

Twenty-one patients with long-term right bundle branch block and left posterior himiblock were studied electrophysiologically and then followed up prospectively. The group consisted of 19 men and 2 woman aged 61 +/- 2.7 years (mean +/- standard error of the mean). The majority of patients had either hypertensive cardiovascular disease (48 percent) or primary conduction disease (33 percent). Initial electrophysiologic studies revealed A-H intervals of 58 to 152 msec (mean 98 +/- 7.7) and H-V intervals of 40 to 80 msec (mean 52 +/- 2.1). Six patients (29 percent) had prolonged H-V intervals. The follow-up period ranged from 91 to 1,231 days (mean 671 +/-68). Three of 21 patients (14 percent) needed a permanent pacemaker after development of the following symptomatic conduction disease: sinoatrial block on day 3 of follow-up; second degree atrioventricular (A-V) block, site undetermined, on day 118; and second degree A-V block proximal to the His bundle on day 398. One patient died suddenly (on day 571), and two others died of noncardiac causes. In conclusion, combined right bundle branch block and left posterior hemiblock was associated with less trifascicular disease than reported previously. The clinical course of most of the patients was benign and the incidence of sudden death was relatively small. Symptomatic conduction disease occurred but could be definitely related to trifascicular disease in only one patient. These short-term data suggest that prophylactic pacemaker insertion is not routinely indicated in patients with chronic right bundle branch block and left posterior hemiblock.

The effects of potassium canrenoate on arrhythmias induced by long-term progressive digoxin toxicity were studied in eight conscious beagle dogs. Sinus bradycardia and sinoatrial block, as well as atrioventricular (A-V) conduction disturbances, were consistently alleviated by administration of potassium canrenoate. Premature supraventricular (including junctional) and ventricular depolarizations as well as ventricular tachycardias were also suppressed. Although potassium canrenoate always terminated the digitalis-induced arrhythmias, it usually converted the rhythm to sinus arrhythmia rather than to normal sinus rhythm. Equimolar sodium canrenoate, but not potassium chloride, had similar reversal effects on arrhythmias induced by long-term digoxin intoxication. These data indicate that canrenoate, a diuretic agent with reported positive inotropic effects, may be useful in the treatment of digitalis-induced arrhythmias in man.

The effect of ventricular premature contractions on atrioventricular (A–V) conduction of the following sinus beat was studied in 25 patients with use of His bundle electrography. Facilitation of A–V conduction (shortening of the A–H interval) in the postextrasystolic beat was observed in 17 patients. This facilitation was believed to be due to a longer recovery period of the A–V node after its premature retrograde (and frequently concealed) depolarization by the ventricular premature contraction. Slowing of A–V conduction (prolongation of the A–H interval) after interpolated or repetitive ventricular premature contractions occurred in five patients. In these instances, after retrograde depolarization by the ventricular premature contraction, the A–V node was still partially refractory and conduction of the postextrasystolic beat was delayed. Retrograde P waves without resetting of the A–V node were documented; in these cases, the interval after the retrograde P wave was fully compensatory, suggesting retrograde and antegrade sinoatrial block.

The tachycardia-bradycardia syndrome consists of paroxysmal atrial fibrillation, flutter or tachycardia followed by sinoatrial block or sinus arrest resulting in Stokes-Adams attacks. Detailed histologie findings of the conduction system of 2 patients with this entity correlated well with the clinical observation of cardiac rhythm disturbances in the sinus node, atria and atrioventricular (A-V) junction. Eight other patients with the syndrome were studied clinically. The mechanisms (as revealed by the electrocardiogram) producing the bradycardia phase include depression of pacemaker function (arrest) or of conduction (exit block) of the sinus impulse, or both, plus depression of A-V junctional impulse formation. Proper therapy usually requires electrical pacing in conjunction with administration of digitalis or propranolol, or both. Our findings suggest that the term “sick sinus syndrome” is an inaccurate and inappropriate synonym for the tachycardia-bradycardia syndrome.

A case of a 29 year old female patient with sinoatrial block, first degree A-V heart block and Adams-Stokes seizures since the age of 11 is reported. The mechanism of the syncopal attacks was established by continuous radioelectrocardiographic monitoring as episodes of sinoatrial heart block or arrest, or both. There was no evidence of inflammatory, degenerative or congenital heart disease, and the patient had never received drugs assocated with the production of Adams-Stokes seizures. From the etiologic standpoint exaggerated vagal effects undoubtedly played a role; the existence of a congenital abnormality of the conduction system must, however, be taken into consideration. Treatment with artificial pacemaker stimulation proved effective and prevented further Adams-Stokes attacks.

Fatty infiltration has only rarely been reported as a cause of a cardiac conduction defect. A case of chronic sinoatrial block and atrial fibrillation with severe fatty infiltration of the myocardium and the conduction system is reported. The literature on conduction defects due to fatty infiltration is reviewed.

A new technique for the transvenous implantation of a specially designed atrial sensing electrode is described. In combination with a ventricular stimulating electrode and an atrial-controlled pacemaker, the method enables synchronization of atrial with ventricular activity. The atrial sensing electrode is put into the right atrial appendage through a preshaped radiopaque Teflon applicator catheter. Two hooks on the electrode tip provide for safe and secure anchoring of the electrode tip to trabeculae of the atrial appendage. The technique has been used for synchronous P wave pacing in 12 patients with complete atrioventricular block, most of them suffering from AdamStokes attacks. Three additional patients with sinoatrial block were treated by means of anchored atrial electrodes. Observation periods of up to 39 months showed no dislocation of any of the anchored atrial electrodes, and performance in all patients was faultless.

To increase the limited knowledge of the effects of digitalis on sinus nodal function in patients with sinus nodal dysfunction and to initiate an investigation into the mechanisms underlying its effects, 34 patients with sinus nodal dysfunction were studied. Twenty patients underwent determination of sinus cycle length, estimated sinoatrial conduction time and maximal corrected sinus recovery time before and after the administration of 0.75 mg of intravenous digoxin. For the group, sinus cycle length did not change, sinoatrial conduction time increased insignificantly and maximal corrected sinus recovery time shortened; however, individual variation occurred. The effects of acute digitalization appeared to predict the effects of chronic digitalis administration on sinus nodal function in the eight patients who subsequently continued to take digoxin. Fourteen patients received digoxin after vagal blockade with atropine. After vagal blockade, digoxin lengthened sinus cycle length, sinoatrial conduction time and maximal corrected sinus recovery time. The effects of digoxin administered after atropine could be antiadrenergic, direct, or both, and are opposite to those induced by atropine alone. Because these effects are similar to those of vagotonia yet are not apparent when the vagi are unblocked, digoxin may have direct excitatory, adrenergic or previously unrecognized vagolytic effects on sinus nodal function in man and their manifestation may be dependent on heart rate or autonomic tone.

Twenty-one patients with long-term right bundle branch block and left posterior himiblock were studied electrophysiologically and then followed up prospectively. The group consisted of 19 men and 2 woman aged 61 +/- 2.7 years (mean +/- standard error of the mean). The majority of patients had either hypertensive cardiovascular disease (48 percent) or primary conduction disease (33 percent). Initial electrophysiologic studies revealed A-H intervals of 58 to 152 msec (mean 98 +/- 7.7) and H-V intervals of 40 to 80 msec (mean 52 +/- 2.1). Six patients (29 percent) had prolonged H-V intervals. The follow-up period ranged from 91 to 1,231 days (mean 671 +/-68). Three of 21 patients (14 percent) needed a permanent pacemaker after development of the following symptomatic conduction disease: sinoatrial block on day 3 of follow-up; second degree atrioventricular (A-V) block, site undetermined, on day 118; and second degree A-V block proximal to the His bundle on day 398. One patient died suddenly (on day 571), and two others died of noncardiac causes. In conclusion, combined right bundle branch block and left posterior hemiblock was associated with less trifascicular disease than reported previously. The clinical course of most of the patients was benign and the incidence of sudden death was relatively small. Symptomatic conduction disease occurred but could be definitely related to trifascicular disease in only one patient. These short-term data suggest that prophylactic pacemaker insertion is not routinely indicated in patients with chronic right bundle branch block and left posterior hemiblock.

Eighty-three patients with paroxysmal supraventricular tachycardia (Wolff-Parkinson-White syndrome in 47 patients and atrioventricular nodal reentry in 36 patients) underwent electrophysiologic study before and after intravenous administration of flecainide. Sixty-seven of these 83 patients entered an open clinical trial to evaluate the efficacy and safety of long-term oral treatment with flecainide. Efficacy was evaluated by a patient diary of spontaneously occurring attacks during flecainide treatment and periods of withdrawal. In 24 patients, electrophysiologic study was repeated during oral therapy. During a mean follow-up of 22.8 months, the therapeutic response to flecainide (mean dose 263 mg/day) was good in 48 patients (71%) and fair in 7 patients (10%). In 8 patients (10%), an arrhythmogenic effect was seen (increased number and prolonged duration of supraventricular tachycardia episodes in 4 patients, spontaneous episodes of atrial fibrillation in 2 patients and sinoatrial block in 2 patients). No consistent abnormalities were seen in the laboratory tests. Extracardiac side effects were of minor importance and usually subsided spontaneously or disappeared after reduction of dosage. It is concluded that flecainide is a useful addition to the drugs already available for short- and long-term treatment of supraventricular tachycardia due to Wolff-Parkinson-White syndrome and atrioventricular nodal reentry.

Patients with acute myocardial infarction and transient complete atrioventricular (A-V) block in association with right bundle branch block and left anterior hemiblock have a high incidence rate of late sudden death presumably due to recurrent A-V block. Over a 5 year period, 18 patients demonstrated right bundle branch block and left anterior hemiblock and had transient complete block during an acute myocardial infarction and survived to hospital discharge. Of six patients who did not have permanent pacing, five died suddenly (one was lost to follow-up) with a mean survival time of 2.4 months after hospital discharge. Twelve subsequent patients received permanent demand pacemakers and had a significantly improved prognosis with a mean survival time of 18 months (P less than 0.001). Six patients were still alive at an average follow-up time of 20 months. Prophylactic permanent pacing significantly improves the prognosis after acute myocardial infarction in this select subgroup of patients.

Amiodarone is a benzofuran derivative with potent electrophysiologic effects on the impulse generation and conduction system of the heart. 1 The effects of amiodarone on the sinus node, in particular, are well described. 2,3 Sinus arrest 4 and sinoatrial block(5) with oral therapy have been demonstrated; we describe a patient with acute sinus arrest after intravenous amiodarone therapy.

With use of 24-hour ambulatory electrocardiographic monitoring, the effect of 1 hour of cigarette smoking on cardiac rhythm in 73 patients with coronary heart disease was studied. Fifteen subjects had no arrhythmia; 37 subjects had fewer than 2 atrial or ventricular premature complexes (APCs or VPCs)/hour, with APCs possibly related to smoking in 2 and VPCs related to smoking in 1. Nineteen subjects had more than 2 VPCs/hour (range 4 to 368) and had 16 +/- 29 VPCs/hour (+/- standard deviation) less during than before smoking (p less than 0.05), associated with an increase in heart rate of 4.6 +/- 6.8 beats/min (p less than 0.01). In none of the 9 subjects with unifocal VPCs did multiform beats develop during or after smoking, whereas 3 of 10 subjects with multiform VPCs had only unifocal beats during and immediately after smoking. In 1 of these 19 subjects, frequent APCs developed during smoking. One other subject had frequent APCs unaffected by smoking and another had sinoatrial block, which disappeared during smoking on 1 of 3 monitorings. In conclusion, no sustained or high-grade ventricular arrhythmia was provoked by smoking; although APCs may have been related to smoking in a few persons, the frequency and complexity of VPCs tended to be reduced in these subjects with coronary artery disease.

Sinus node (SN) refractoriness can be measured indirectly by observing the return responses after the introduction of progressively earlier atrial premature beats. The SN effective refractory period (ERP) is defined as the longest premature interval resulting in an interpolated atrial return response. In the present study, SNERP was analyzed in 71 subjects--51 control persons and 20 patients with evidence of SN dysfunction. SNERP could be measured in 40 of 51 control subjects and was shown to prolong at shorter basic pacing cycle lengths. At a basic cycle length of 600 ms, SNERP was 330 +/- 40 ms, whereas at 500 ms it was 350 +/- 50 ms (p less than 0.05). At a basic cycle length of 600 ms, SNERP was measured in 31 control subjects and 7 patients with SN dysfunction. The values of 330 +/- 40 and 520 +/- 20 ms, respectively, in these 2 groups suggested that this method can be used to differentiate patients with SN dysfunction (p less than 0.001). In 12 control subjects, SNERP was measured before and after partial autonomic blockade with propranolol and atropine. SNERP shortened from 360 +/- 40 to 320 +/- 40 ms (p less than 0.05). It shortened with atropine and prolonged with propranolol. Thus, SNERP prolongs with a shorter basic pacing cycle length and is affected by autonomic manipulation, in a fashion analogous to the atrioventricular node.

Fifty-two patients with sinoatrial disturbances causing syncope, dizzy spells, heart failure or predisposition to ventricular tachyarrhythmias were treated with permanent cardiac pacing between January 1966 and June 1970. They were followed up from 12 to 60 months. The rhythm disorders treated with permanent pacer implantation were: (1) sinus bradycardia (27 patients); (2) sinoatrial block or arrest (10 patients); (3) brady-tachyarrhythmia syndrome (11 patients); and (4) sinus bradycardia with ventricular tachyarrhythmia (4 patients). Forty-seven patients had ventricular and 5 had coronary sinus pacemakers. Two of the five patients with coronary sinus pacemakers subsequently required ventricular pacing because of failure of the coronary sinus electrode to capture the atrium. One patient died 3 weeks after pacemaker implantation because of renal failure. Eleven others died of natural causes 3 to 38 months after implantation of the pacemaker. Long-term pacemaker complications such as perforation of the right ventricle, displacement or fracture of the pacing electrode, infection at the site of the powerpack and raised threshold were observed in nine patients. Syncopal or near syncopal episodes were abolished in 32 of 35 patients, chronic congestive heart failure was alleviated in 7 of 12 patients, and recurrent ventricular tachyarrhythmias were controlled in 3 of 4 patients by pacing and antiarrhythmic agents. We conclude that permanent ventricular pacing is an effective therapeutic approach in sinoatrial disturbances causing symptoms such as syncope, dizzy spells, brady-tachyarrhythmia syndrome, heart failure or recurrent ventricular arrhythmias.

A case is presented of second degree sinoatrial block with Wenckebach periods, and a rate-conditioned left bundle branch block masking an acute anteroseptal myocardial infarction which is revealed in the normally conducted beats occurring in the pauses caused by the second degree sinoatrial block. The mechanisms underlying this unusual tracing are discussed.

S ~NOATRIAL BLOCK is diagnosed when pauses appearing during regular heart action are approximately double the length, or a multiple, of the normal period and there is no evidence of ventricular and atria1 activity. If the pause is an exact multiple of the normal period, the disturbance is comparable to a type II atrioventricular (A-V) block; if less than double the normal period with certain irregularities, it is said to be an analog of a type I A-V block. Although sinoatrial block doubtless exists, its mechanism is difficult to explain, partly because it cannot be reproduced easily in experiments.1 This paper will consider four possible explanations, as well as a fifth modus operandi bearing on its genesis. The first possibility is that sinoatrial block results from a disturbance of impulse formation. The structure of the sinus node consists of thousands of specialized fibers possessing automaticity. Temporary failure of all these fibers to form impulses is improbable. When certain fibers cease to lead the heart, others take over. Evidence indicates that impulses may even arise in different areas of the sinus node without altering the electrocardiogram. Since it is difficult to conclude that all of the specialized fibers cease simultaneously to form an impulse for one beat, this explanation for sinoatrial block can be discarded. A second possibility, that sinoatrial block results from abnormal conduction between the sinus node and atria, is equally difficult to accept. Of the many connections between the sinus node and atria, numerous junctional fibers supplement the special preferential pathways. It is inconceivable that the impulse would be blocked in all these pathways simultaneously for one beat only. If different pathways are blocked temporarily, a continuous variation of the P waves would be expected, but in many instances of sinoatrial block the form of the P waves does not change. Anyone who has attempted to eliminate sinus node activity by clamping off the sinus node or by isolating it with ligatures knows how difficult it is to obtain a pertianent A-V junctional rhythm. Of course, a conduction disturbance must be postulated to account for beats periodically dropped between the sinus node and atria (Wenckebach periods). However, it is difficult to accept the existence of such periods as proved, for several reasons: (1) sinus node activity in our patients cannot be registered; (2) similar pauses may appear in simple respiratory arrhythmias; (3) the frequent diagnosis of periodically dropped beats between sinus node and atria in clinical tracings rests only on conjectures inferred from the duration of the atria1 periods; and (4) diagrams to indicate periodically dropped beats just because they are easily drawn do not demonstrate the presence of this conduction disturbance. The third possibility, advanced by Lewis,” is that sinoatrial block results from an increased uagal tone. He held that the long refractory period of the sinus node allowed a higher vagal tone to block the sinus node as it does the A-V node. Opposed to this explanation is the observation that the rate of the sinus beats is frequently regular in clinical instances of sino