Cases reported "Sinoatrial Block"

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1/9. Sinus escape-capture bigeminy and sinus extrasystolic bigeminy.

    Blocking conduction between the sinus node and the atria (SA block) can be responsible for symptomatic rhythm problems. However, in atrial escape-capture bigeminy with SA block, when atrial escape P waves originate in a site within or close to the sinus node, the diagnosis of SA block is not easy. Electrocardiograms were selected from 7 people with atrial bigeminy because (1) all atrial deflections (P waves) were almost the same in shape and in length of PR intervals, (2) comparatively long PP intervals alternated with comparatively short PP intervals, and (3) occasionally the atrial bigeminy changed to normal regular sinus rhythm in which 2 or more sinus P waves were found in succession. An attempt is made to clarify the mechanism for these cases. When regular sinus rhythm changed to bigeminal rhythm, the long PP interval introduced the bigeminy in 3 cases, indicating the presence of "sinus" escape-capture bigeminy; whereas the short PP interval introduced the bigeminy in the other 4 cases, indicating the presence of "sinus" extrasystolic bigeminy. In cases of sinus escape-capture bigeminy associated with SA block, the cases may occasionally be diagnosed wrongly as ordinary sinus arrhythmia not associated with SA block. Therefore, it seems that sinus escape-capture bigeminy is not so rare as is generally believed. patients with SA block often require implantation of the artificial pacemaker. Thus, the authors believe that differentiation of sinus escape-capture bigeminy from other forms of "sinus" bigeminy is clinically important.
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2/9. Evidence of sinoatrial block as a curative mechanism in radiofrequency current ablation of inappropriate sinus tachycardia.

    Inappropriate sinus tachycardia is a nonparoxysmal tachycardia characterized by high resting heart rates and a disproportionate response to activity. Sinus node modification with radiofrequency current has been used successfully as treatment for this arrhythmia. However, the electrophysiologic mechanisms leading to successful modification are not yet fully elucidated. We report a case of a patient with drug-resistant inappropriate sinus tachycardia in whom successful treatment of the arrhythmia was achieved by documented sinoatrial exit block induced by radiofrequency current applications.
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3/9. sinoatrial block during lithium treatment.

    lithium is known to produce T wave changes in the ECG, whereas effect upon the conducting system of the heart has not been described. In our patient lithium produced sinoauricular block and possibly tachycardia. The correlation between lithium treatment and tachyarrhythmias is discussed. When during lithium treatment block is found, the treatment should preferably be stopped, but if this is not possible it is important to realize that digitalis should not be used as a prophylactic drug against tachycardia, as it worsens the block and therefore increases the frequency of arrhythmia, even leading to Adams-Stokes attacks.
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4/9. Atrial escape-capture bigeminy in dominant atrial rhythm with 2:1 exit block.

    A 27-year-old woman with atrial bigeminy is reported in whom long PP intervals alternate with short PP intervals. All P waves are negative in lead II and all PR intervals measure 0.12 s. In the 12-lead electrocardiogram, however, these P waves were definitely different in configuration from each other, and were divided into two groups. Namely, these negative P waves are divided into those of dominant atrial rhythm J1 with 2:1 exit block, and those of atrial escape J2. Long J1-J2 intervals alternate with short J2-J1 intervals. These electrocardiographic findings show the presence of atrial escape-capture bigeminy. Such atrial escape-capture bigeminy in dominant atrial rhythm with 2:1 exit block has never been reported before.
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5/9. Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome.

    Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.
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6/9. Alternating sinus rhythm and intermittent sinoatrial block induced by propranolol.

    Alternating sinus rhythm and intermittent sinoatrial (S-A) block was observed in a 57-year-old woman, under treatment for angina with 80 mg propranolol daily. The electrocardiogram showed alternation of long and short P-P intervals and occasional pauses. These pauses were always preceded by the short P-P intervals and were usually followed by one or two P-P intervals of 0.92-0.95 s representing the basic sinus cycle. Following these basic sinus cycles, alternating rhythm started with the longer P-P interval. The long P-P intervals ranged between 1.04-1.12 s and the short P-P intervals between 0.80-0.84 s, respectively. The duration of the pauses were equal or almost equal to one short plus one long P-P interval or to twice the basic sinus cycle. In one recording a short period of regular sinus rhythm with intermittent 2/1 S-A block was observed. This short period of sinus rhythm was interrupted by sudden prolongation of the P-P interval starting the alternative rhythm. There were small changes in the shape of the P waves and P-R intervals. S-A conduction through two pathways, the first with 2/1 block the second having 0.12-0.14 s longer conduction time and with occasional 2/1 block was proposed for the explanation of the alternating P-P interval and other electrocardiographic features seen. atropine 1 mg given intravenously resulted in shortening of all P-P intervals without changing the rhythm. The abnormal rhythm disappeared with the withdrawal of propranolol and when the drug was restarted a 2/1 S-A block was seen. This was accepted as evidence for propranolol being the cause of this conduction disorder.
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7/9. Infra-His blocked premature atrial contractions simulating 2:1 sinoatrial block in a patient with an atrio-His bypass tract.

    Blocked atrial premature contractions simulated 2:1 sinoatrial block because those were superimposed on the T wave of the preceding sinus beats 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.
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8/9. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia: further evidence for microeentry as the underlying mechanism.

    INTRODUCTION: Idiopathic left ventricular tachycardia with a QRS pattern of right bundle branch block and left-axis deviation constitutes a rare but electrophysiologically distinct arrhythmia entity. The underlying mechanism of this tachycardia, however, is still a matter of controversy. This report describes findings in a 42-year-old man who underwent successful radiofrequency catheter ablation of idiopathic left ventricular tachycardia. methods AND RESULTS: On electrophysiologic study, the tachycardia was reproducibly induced and terminated with double ventricular extrastimuli. Intravenous verapamil terminated the tachycardia whereas adenosine did not. Detailed left ventricular catheter mapping during sinus rhythm revealed a fragmented delayed potential at the mid-apical region of the inferior site near the posterior fascicle of the left bundle branch. At the same site, continuous electrical activity throughout the entire cardiac cycle was recorded during ventricular tachycardia. Repeated spontaneous termination of this continuous electrical activity in late diastole was followed immediately by termination of the tachycardia. Single application of radiofrequency current for 20 seconds at this site completely abolished inducibility of the tachycardia. After catheter ablation, at the identical site of preablation recording of the fractionated potential during sinus rhythm, no fragmented delayed activity could be recorded. There was no complication from the ablation procedure. CONCLUSION: The preablation recordings of fragmented delayed potentials during sinus rhythm and continuous diastolic electrical activity during tachycardia, together with ablation characteristics and previously reported electrophysiologic properties of this arrhythmia, may further support microreentry as the underlying mechanism in idiopathic left ventricular tachycardia.
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9/9. Mechanism of atrial escape-capture bigeminy: second-degree sinoatrial exit and entrance block.

    Two women with atrial escape-capture bigeminy were reported in whom sinus P waves and escape P waves alternated with each other. Their electrocardiographic findings showed that, during the bigeminal rhythm, 2:1 exit block of sinus impulses associated with entrance block of escape impulses occurred in the sinoatrial junction. Three phenomena are suggested to explain the observations. (1) Seeming bradycardia-dependent sinoatrial exit block may have occurred, probably as a result of phasic changes in vagal tone due to respiration, with decreased vagal tone depressing conductivity in the sinoatrial junction to a greater degree than automaticity in the sinus node. (2) In case 1, type II second-degree entrance block in the sinoatrial junction may have occurred, reflecting the presence of sinus parasystole with incomplete entrance block. (3) Sinus escape also may have occurred, especially in case 2. These phenomena have never been reported before.
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