Bloqueo sinoauricular en el postoperatorio inmediato de cirugía de cataratas ¿Casualidad o causalidad? / Sino-auricular block immediately after cataract surgery. Casualty or causality?

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Deficient zebrafish ether-à-go-go-related gene channel gating causes short-QT syndrome in zebrafish reggae mutants.

BACKGROUND: Genetic predisposition is believed to be responsible for most clinically significant arrhythmias; however, suitable genetic animal models to study disease mechanisms and evaluate new treatment strategies are largely lacking. METHODS AND RESULTS: In search of suitable arrhythmia models, we isolated the zebrafish mutation reggae (reg), which displays clinical features of the malignant human short-QT syndrome such as accelerated cardiac repolarization accompanied by cardiac fibrillation. By positional cloning, we identified the reg mutation that resides within the voltage sensor of the zebrafish ether-à-go-go-related gene (zERG) potassium channel. The mutation causes premature zERG channel activation and defective inactivation, which results in shortened action potential duration and accelerated cardiac repolarization. Genetic and pharmacological inhibition of zERG rescues recessive reg mutant embryos, which confirms the gain-of-function effect of the reg mutation on zERG channel function in vivo. Accordingly, QT intervals in ECGs from heterozygous and homozygous reg mutant adult zebrafish are considerably shorter than in wild-type zebrafish. CONCLUSIONS: With its molecular and pathophysiological concordance to the human arrhythmia syndrome, zebrafish reg represents the first animal model for human short-QT syndrome.

[Symptomatic bradycardia with amiodarone in patients with pre-existing conduction disorders]. / Symptomatische Bradykardien unter Amiodaron bei Patienten mit präexistenter Reizleitungsstörung.

Amiodarone has been shown to improve survival in patients with impaired left ventricular function and ventricular trachyarrhythmias. The clinical applicability, however, is limited by numerous often serious adverse effects. 70 patients receiving the treatment with amiodarone for ventricular tacharrhythmias were investigated regarding the development of symptomatic bradycardia. Group 1 consisted of 25 patients with preexisting conduction disorders, 5 had first degree heart block, 10 had right bundle branch block, and 7 had left bundle branch block on electrocardiographic examination. The 3 remaining patients showed asymptomatic sinus node dysfunction defined as sinus arrest or sinuatrial block. Amiodarone caused symptomatic bradycardia in 6 of the group 1 patients (II degrees-III degrees AV block in 3 patients with preexisting I degree AV block or right bundle branch block; intermittent sinus arrest or SA block in the 3 cases with previous sinus node dysfunction). 45 patients had no conduction disorders before the administration of amiodarone (group II). None of these patients developed symptomatic bradycardia. The difference to group I was significant (p < 0.0005). Thus, patients with preexisting conduction disorders have a substantial risk of developing symptomatic bradycardia under amiodarone therapy, with an incidence of 24% in group I patients of our collective.

Xamoterol in sinus node disease.

A pharmacological alternative to pace-maker implantation would be useful in some patients with sinoatrial disorder particularly since the single lead ventricular system usually fitted has disadvantages. Xamoterol, a cardioselective beta-receptor partial agonist, has been shown to increase heart rate both in animals and in man. We, therefore, studied the effects of Xamoterol in patients with sinoatrial disease in a double blind, cross-over trial in 10 patients. Mean heart rates and number and duration of pauses were compared during the treatment phases of the trial with Holter monitoring. Mean heart rates were significantly increased between 01:00 h and 05:00 h (P < or = 0.02) and between 05:00 h and 09:00 h (P < or = 0.01) on Xamoterol. The number of sinus pauses were eliminated or reduced on Xamoterol in six patients, but there was an increased frequency in three patients. Xamoterol, therefore, does increase the heart rate and reduce the number of pauses in sinoatrial disorder, but only in some patients.

The therapeutic and diagnostic cardiac electrophysiological uses of adenosine.

Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.

[Efficacy and tolerance of disopyramide in arrhythmia associated with sinus node dysfunction]. / Efficacité et tolérance du disopyramide dans les troubles du rythme associés à une dysfonction du sinus.

The aim of this study was to assess the effect of delayed release Disopyramide 500 mg daily on sinus node function in 12 subjects with sinus node dysfunction and supraventricular and/or ventricular excitability. An ECG, Holter monitoring and electrophysiological studies of sinus node function with an oesophageal electrode were performed before and after 5 days treatment. The drug had to be discontinued in 1 patient because of urinary retention. The Disopyramide suppressed the clinical tachyarrhythmias in 8 out of the 11 subjects. The maximal sinus pause observed on Holter monitoring did not change significantly. It only increased in one subject. The mean sinus cycle length during electrophysiological study slightly decreased but there was a global increase in sinoatrial conduction time from 309 +/- 164 to 413 +/- 125 msec and of the corrected sinus mode recovery time from 470 +/- 168 to 605 +/- 303 msec. However, these changes were not significant. This study of delayed released Disopyramide shows a discordance between the tendency for sinus node function to deteriorate when assessed by electrophysiological studies and good clinical tolerance as assessed by Holter monitoring in the bradycardia-tachycardia syndrome.

Corticosteroids in the management of sinoatrial block.

This report presented our experience in the treatment of sinoatrial (S-A) conduction disturbances with corticosteroids. Three patients with intermittent second-degree S-A block who failed to respond to atropine and isoproterenol were treated with prednisone for 6-17 weeks. Sustained improvement in S-A conduction following prednisone administration was confirmed by repeated Holter monitoring on and off therapy. Two patients eventually regained permanent sinus rhythm, while therapy led to marked diminution in S-A block in the 3rd patient. The possible mechanisms by which steroids may improve S-A conduction are discussed. Our observation is based on a small case series, each patient serving as his own control, and as such constitutes an indication for further confirmatory studies.

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.

[Effect of ethmozine on the automatic function of the sinus node and sinoatrial conduction in patients with normal and impaired function of the sinus node]. / Deistvie étmozina na avtomaticheskuiu funktsiiu sinusovogo uzla i sinoatrial'noe provedenie u bol'nykh s normal'noi i narushennoi funktsiei sinusovogo uzla.

In this study involving 45 patients with the normal function of the sinus node and 10 patients showing signs of its damage (n-10), intravenous administration of ethmozine in a dose of 150 mg (1.5-2 mg/kg) exerted atropine like action. In four cases with dysfunction of the sinus node the drug significantly increased the time of the restoration of sinus node function. Ethmozine induced a Stage II sinoatrial block in 3 out of 10 patients with sinus node dysfunction. The above data suggest that ethmozine produces an atropine-like effect on the sinus node. In some patients with sinus node dysfunction, ethmozine may impair the function of the sinus node which calls for caution while employing the drug in such cases. The inhibitory effect of the agent on the sinoatrial conduction in the patients studied suggests that ethmozine may prove an effective antiarrhythmic drug for treating patients with paroxysmal sinoatrial tachycardia.

[Beta-adrenergic stimulation with prenalterol in sick sinus syndrome]. / Beta-adrenerge Stimulation mit Prenalterol beim Syndrom des kranken Sinusknotens.

The effect of beta-adrenergic receptor stimulation on sinus node function in patients with sick-sinus syndrome was investigated. Electrophysiological studies were performed in 14 patients (5 males and 9 females) aged 18-81 years before and after intravenous administration of 50 micrograms Prenalterol per kilogram body wt. Prenalterol decreased spontaneous cycle length by 26% (p less than 0.01), which corresponded to an increase in heart rate of 21 beats/min. The corrected sinus node recovery time was shortened by 23% (n.s.) in 10 patients, and was abnormal in 12 patients before and in 10 patients after Prenalterol. Secondary pauses occurred in 8 patients at control and in 9 patients after drug administration, in 2 of them for the first time after Prenalterol. In the sick-sinus syndrome the pronounced chronotropic response to beta-adrenergic receptor stimulation with Prenalterol doses not indicate improvement of impaired sinus node function.

Electrophysiologic effects of disopyramide phosphate on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered disopyramide (2 mg/kg) on three parameters of sinus node function were examined in 16 symptomatic patients with sinus node dysfunction. Based on their ECG data before study, patients were subdivided into group A (n = 8), those with sinus pauses and/or sinoatrial (SA) exit block; and group B (n = 8), those with sinus bradycardia. Disopyramide shortened spontaneous cycle length in 10 of 16 patients and lengthened it in six--markedly so (91%) in one patient. Estimated SA conduction time decreased in seven of 14 patients and increased in seven. Two patients developed second degree SA exit block after disopyramide. Maximum sinus node recovery time was prolonged by disopyramide in 11 of 16 patients and markedly so in four. For the group as a whole there was no significant difference in spontaneous cycle length, maximum sinus node recovery time or estimated SA conduction time. P-wave and QRS durations and H-V intervals were significantly lengthened by disopyramide. Marked depression of the three parameters of sinus node function occurred in three group A patients and in one group B patient who had persistent severe sinus bradycardia. These four patients also had secondary pauses after termination of rapid atrial pacing under control conditions. Disopyramide should be administered cautiously to patients with sinus node dysfunction, particularly those with sinus pauses, SA exit block or secondary pauses.