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Blocked atrial premature contractions simulated 2:1 sinoatrial block because those were superimposed on the T wave of the preceding sinus heats and were not visible on the surface electrocardiogram of our patient. Additionally, His bundle recordings and premature atrial stimulation demonstrated the presence of an atrio-His anomalous pathway. The premature atrial contractions traveled anterograde via the anomalous pathway and were blocked distally to the His bundle. The term, pseudosinoatrial block, is used to describe the arrhythmia because there was no evidence of an intrinsic abnormality of sinus node function and sinoatrial conduction.

We studied atrial arrhythmias during the first 12 h of admission to the hospital in 266 consecutive patients with acute myocardial infarction who subsequently underwent coronary angiography. Ten patients developed atrial fibrillation, one atrial flutter, and one supraventricular tachycardia. Another five developed sinus dysrhythmias. All of the above patients had an acute inferior myocardial infarction, and in 10 of the 12 patients with supraventricular arrhythmias and in four of five with sinus dysrhythmias, the origin of the sinus node artery started just after an occluded right coronary or left circumflex artery or was involved in the occlusion. Thus, ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was a likely cause of these arrhythmias.

We describe the criteria for differential diagnosis between 3:2 sinoatrial block from atrial bigeminy due to an ectopic focus in the sinus or parasinus zone. In the 3:2 sinoatrial block the RR interval of the basic rhythm is similar to the short R-R interval of the paired rhythm. In atrial bigeminy, the R-R interval of the basic rhythm is similar to the long R-R interval of the paired rhythm. (Chest 1991; 99:735–36)

Fifty-two patients with disease of the sinoatrial node were reviewed for the purpose of clarifying the natural history of the sinoatrial nodal dysfunction. Of these, 38 were observed for periods of time ranging from 1 to 23 years (average, six years). All available electrocardiograms of each patient were analyzed. A long duration of the disease was more frequently observed in patients with sinus bradycardia with sinoatrial block or sinus arrest and in patients with persistent atrioventricular junctional rhythm. The duration of the disease in patients with the latter condition with total sinus arrest ranged from 7 to 29 years (average, 13 years). Patients with a normal sinus rate with concomitant sinoatrial block or sinus arrest did not have a different average duration of the disease, as compared with those observed in who had sinus bradycardia as the basic rhythm. One-third of the patients had documented paroxysmal supraventricular tachycardia, which occurred irrespective of the underlying arrhythmias. Occasional complete recovery of normal sinus mechanism and rate could be noted during a long course of the disease and irrespective of the underlying electrocardiographic manifestations. Only one patient died in relation to the dysfunction of the sinoatrial node. We concluded that only with difficulty was the sinoatrial node destroyed by the disease process, and dysfunction of the sinoatrial node seemed to have a better prognosis than advanced atrioventricular block.

Persisting symptoms, consisting of palpitations, dizziness, or syncope, were found in 49 of 570 consecutively followed patients (8.6 percent) with permanent pacemakers (PM). Among 540 patients with ventricular PM, 19 had syncope and 24 dizziness; among 30 patients with dual-chamber PM, five had palpitations and one dizziness. Symptoms were PM-related in 17, caused by tachyarrhythmias in 12, of noncardiac origin in 16, and of unknown origin in four patients. Holter monitoring was necessary for evaluating the persisting symptoms in 36 patients and helpful in 32 studies (89 percent). Symptoms were relieved in all patients with PM-related causes but only in 6/16 patients (38 percent) with syncope or dizziness of noncardiac origin despite various therapeutic measures. In patients with either documented tachyarrhythmias or unknown cause of syncope or dizziness, antiarrhythmic drugs led to symptomatic improvement in 11 of 12 treated patients during an average follow-up of 15 months. We concluded that: (1) persistent syncope, dizziness, or palpitations occurred in 8.6 percent of 570 patients after PM-implantation; (2) symptoms were more frequent but less severe in patients with dual-chamber PM than in those with ventricular PM; (3) tachyarrhythmias as a possible cause of symptoms were found in 25 percent of patients; (4) symptomatic improvement was noted in 28 of 29 patients when a PM-related cause or tachyarrhythmias were treated.

en a long pause follows sinoatrial block or atrioventnicular block, A-V junctional escape beat ensues. The same holds true for marked sinus bradycardia. Thus, it is natural that escape beats are encountered frequently in sick sinus syndrome. Ifsinus impulse resumes control ofthe ventricles, ie, “captures” the ventricles, and “escape-capture” occurs in succession, then “escape-capture” bigemmny is the result. Alternatively, mfthe next sinus beat is further detamed, junctional impulse can be conducted retrogradely to the atria and then back to the ventricles, eliciting a reciprocal beat. The underlying mechanism is reentry. Occurring in pairs and in succession, the phenomenon is “escape-reentry” bigeminy. Both “escape-capture” and “escape-reentry” bigemmny are common in sick sinus syndrome; however, the sequence of “escape-reentry-capture” trigeminy is a rarity. Recently, we encountered a case of bradycardiatachycardia syndrome displaying an ECG pattern of “escape-reentry-capture” during 24-hour telemetric ECG on the second day of hospitalization.

In a clinical case of 2:1 sinoatrial block, carotid massage, paradoxically, released the sinoatrial block and doubled the manifest sinus rate. This resulted from a deceleration of the sinus discharge rate which allowed consecutive sinus impulses to traverse the sinoatrial junction. (Chest 1988; 94:650-52)

The findings in two patients with interpolated ventricular extrasystoles showing 2:1 exit block are reported. In these patients the blocked impulses appear to penetrate into the ectopic-ventricular junction (or reentrant pathway) to a varying extent, and the coexistence of a distal 2:1 exit block and a proximal (concealed) Wenckebach phenomenon in the ectopic-ventricular junction is suggested.

In a clinical case of 2:1 sinoatrial block, carotid massage, paradoxically, released the sinoatrial block and doubled the manifest sinus rate. This resulted from a deceleration of the sinus discharge rate which allowed consecutive sinus impulses to traverse the sinoatrial junction.

Persisting symptoms, consisting of palpitations, dizziness, or syncope, were found in 49 of 570 consecutively followed patients (8.6 percent) with permanent pacemakers (PM). Among 540 patients with ventricular PM, 19 had syncope and 24 dizziness; among 30 patients with dual-chamber PM, five had palpitations and one dizziness. Symptoms were PM-related in 17, caused by tachyarrhythmias in 12, of noncardiac origin in 16, and of unknown origin in four patients. Holter monitoring was necessary for evaluating the persisting symptoms in 36 patients and helpful in 32 studies (89 percent). Symptoms were relieved in all patients with PM-related causes but only in 6/16 patients (38 percent) with syncope or dizziness of noncardiac origin despite various therapeutic measures. In patients with either documented tachyarrhythmias or unknown cause of syncope or dizziness, antiarrhythmic drugs led to symptomatic improvement in 11 of 12 treated patients during an average follow-up of 15 months. We concluded that: (1) persistent syncope, dizziness, or palpitations occurred in 8.6 percent of 570 patients after PM-implantation; (2) symptoms were more frequent but less severe in patients with dual-chamber PM than in those with ventricular PM; (3) tachyarrhythmias as a possible cause of symptoms were found in 25 percent of patients; (4) symptomatic improvement was noted in 28 of 29 patients when a PM-related cause or tachyarrhythmias were treated.

Automaticity (postpacing impulse recovery time) of the sinus node or subsidiary pacemakers (or both) was determined by intracardiac recordings and atrial overdrive pacing in three patients with disease of the sinus node. Their electrocardiographic manifestations included sinus bradycardia, sinoatrial block, sinus arrest, atrioventricular junctional rhythm, and atrioventricular dissociation. One patient, who initially had syncope, demonstrated prolonged time for recovery of the sinus node (maximum corrected value, 3,485 msec) and impaired atrioventricular junctional automaticity (maximum corrected junctional recovery time, 1,460 msec). Of the remaining two patients without syncopal attacks, one had an adequate low atrial or junctional escape mechanism following cessation of pacing. The maximum low atrial escape interval was 1,660 msec, and the maximum junctional recovery time was 1,770 msec (corrected value, 140 msec). The third patient disclosed a prolonged maximum corrected recovery time for the sinus node (870 msec), while the maximum junctional recovery time was only 1,810 msec (corrected value, 160 msec). We conclude that automaticity of the subsidiary pacemakers in disease of the sinus node can be determined in the presence of atrioventricular dissociation or total sinus arrest, and that determination of the recovery time of the subsidiary pacemakers may be useful in identifying symptomatic patients with sinus nodal dysfunction.

We report the findings in a patients with the Wolff-Parkinson-White syndrome (type A) who initially had recurrent fainting episodes. It appeared that they were caused by prolonged posttachycardiac depression of the sinus node, which was induced by treatment with propranolol. The possibility of covert dysfunction of the sinus node in patients with Wolff-Parkinson-White syndrome should be considered before commencing therapy with beta-adrenergic blocking agents.

We present a patient in whom administration of aprindine on two occasions was responsible for clinically significant sinus node dysfunction and QTc prolongation. Knowledge of the drug's potential for influencing these characteristics, with the resultant possibility of adverse consequences, may be of clinical importance.

Thirty-four patients (mean age 64 years) with this syndrome are reviewed. Common symptoms relate to transient cerebral ischemia with syncope, episodes of rapid palpitations, or both. Usually no definite etiology was found but ischemic heart disease was present in 12 of the 34. Thirty patients had objective evidence of other cardiac disease besides, the sinoatrial block. Additional conduction disturbances were present in 14 subjects. Calcification was found in the mitral or aortic annulus in nine cases. It is likely that sinoatrial block is only symptomatic and important if other processes are present which may decrease the automaticity of lower pacemaker areas. This may take the form of associated cardiac disease or excessive vagal tone as in three cases of reversible chronic sinoatrial block with peptic ulcer. Treatment with drugs alone is almost always unsuccessful. Long-term cardiac pacing either alone or in combination with drugs usually alleviates the major symptoms.

An arrhythmia displaying the phenomenon of exit block around a junctional pacemaker in a patient with atrial tachycardia and complete A-V block at the junctional level is described. The importance of the exit block concept for a rational interpretation of cardiac arrhythmias is discussed.

This presentation reflects an atypical manifestation of si> noatrial block in a patient with chronic renal failure and hyperkalemia (7.S mEq/L). An allorhythmic distribution of P-P intervals permits the interpretation of sinoatrial block complicated by sinoatrial reciprocation.

A 78-year-old man developed sinoatrial block with Wenckebach phenomenon and ventricular parasytole after a myocardial infarction. Each of these arrhythmias is rare and the odds of both occurring together are astronomical. The mechanism and genesis of each arrhythmia correlated well with the site of infarction.

A case of Prinzmetal type of repetitive transient myocardial ischemia was observed in a 71-year-old man who presented with Stokes-Adams attacks, associated with complete heart block and intermittent sinoatrial block. He exhibited frequent transient episodes of marked RS-T segment elevation in leads 2, 3 and aVF with depression in leads 1, aVL and V1 through V4, which occurred entirely without chest pain. A permanent demand cardiac pacemaker was placed, with disappearance of further syncopal attacks.