The mechanism of supraventricular tachycardia

In six successive patients, none of whom had the Wolf-Parkinson-White syndrome, recurrent episodes of paroxysmal supraventricular tachycardia (SVT) were analyzed to determine the mechanism by which this arrhythmia is initiated and sustained. In each patient, simultaneous intracavitary atrial electrograms and surface electrocardiograms were recorded during the onset of numerous spontaneous episodes of SVT. Atrial premature depolarizations (APD) produced by programmed stimulation sequences were used to measure atrioventricular refractory periods and to produce atrial echoes and episodes of SVT. Stimulated APDs introduced during sustained episodes of SVT either altered its behavior or terminated it. The electrophysiologic behavior of SVT in these patients strongly suggests that the mechanism responsible for paroxysmal supraventricular tachycardia is atrial reentry utilizing the A-V conducting system.     

Influence of age on the electrophysiological mechanism of paroxysmal supraventricular tachycardias

The purpose of this study was to evaluate the influence of age on the mechanism of paroxysmal supraventricular tachycardia (PSVT). Previous studies have shown age and sex differences between certain arrhythmias and especially changes in electrophysiological characteristics of Wolff-Parkinson-White syndrome. Four hundred and eighty five patients aged 9-86 years, with PSVT and without Wolff-Parkinson-White syndrome in sinus rhythm, were studied. The esophageal or intracardiac electrophysiological study used a standardized atrial pacing protocol. Paroxysmal junctional tachycardia was induced in 475 patients. The mechanism of tachycardia was not influenced by age and atrioventricular nodal reentrant tachycardia (AVNRT) was found as the main cause of PSVT in all ranges of age. Atrioventricular reentrant tachycardia (AVRT) using a concealed accessory pathway (AP) had a similar incidence from youth to elderly. The ratio male/female (M/F) and the inducibility of other arrhythmias (atrial flutter/fibrillation) (AF/AFl) were also found to be similar in all ranges of age. The age of the patients did not influence the mechanism of the tachycardia. Most of PVST were related to a AV nodal reentrant tachycardia. Concealed accessory pathway was identified with a similar incidence in young and old patients.     

Swallowing-induced supraventricular tachycardia.

A rare form of paroxysmal supraventricular tachycardia (SVT), associated with swallowing solid food, is described. Repeated triggering of the arrhythmia during esophagoscopy was produced by mechanical stimulation of the anterior esophageal wall, 30 cm from the incisors. Treatment with verapamil abolished this tachycardia. Esophagoscopic examination, the first of its kind in this setting, aided the investigation.     

Perinatal supraventricular tachycardia.

OBJECTIVE: To determine the incidence, therapy required and prognosis of perinatal supraventricular tachycardia (SVT). DESIGN: Retrospective chart review of eight years. SETTING: Tertiary level perinatal and pediatric centres in Halifax, Nova Scotia. PATIENTS: All newborn infants who developed SVT either in utero or in the first 30 days of life. RESULTS: SVT was present in 33 neonates, with a male:female ratio of 2.7:1 and an incidence of 1:4347. Fetal SVT was recorded in nine (group I) but these patients did not differ from those with postnatal SVT (group II) in birthweight, noncardiac illnesses and associated heart disease. Thirty-one of the babies (94%) received digoxin and eight (24%) also required propranolol. All were asymptomatic after 48 h. One late death occurred due to renal failure unrelated to the dysrhythmia. No major congenital heart disease was found in either group. Follow-up over 44 months revealed four late relapses requiring prolonged therapy. CONCLUSIONS: Perinatal SVT is a common disorder in a tertiary centre and may represent a transient adaptation phenomenon. It is usually benign, easily treated and rarely associated with major congenital heart disease.     

Prolongation of the tachycardia zone: a possible mechanism for medical failure in paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia in man has been considered to be due to either development of reentry utilizing AV junctional tissue or the presence of an ectopic pacemaker located within the atrium. Most contemporary information suggests that AV junctional reentry is the dominant mechanism for this arrhythmia in man. This present study identifies that the frequence of tachycardia episodes may be correlated with the width of a tachycardia zone as determined by the atrial extrastimulus technique. Moreover, pharmacological therapy directed toward the elimination of this arrhythmia can be assessed utilizing this atrial stimulation technique. Findings in this present study identify that, in patients with widened tachycardia zones, propranolol therapy may not be efficacious. This latter finding is no contrast to the previous observations suggesting that propranolol therapy is the drug of choice for reentrant arrhythmias in man.     

Adenosine and the treatment of supraventricular tachycardia.

Adenosine has recently become widely available for the treatment of paroxysmal supraventricular tachycardia. In order to evaluate its role in the management of arrhythmias, we have reviewed the literature on the cellular mechanisms, metabolism, potential for adverse effects, and clinical experience of the efficacy and safety of intravenous adenosine. Adenosine produces transient atrioventricular nodal block when injected as an intravenous bolus. This is of therapeutic value in the conversion to sinus rhythm of the majority of paroxysmal supraventricular tachycardias, which involve the atrioventricular node in a re-entrant circuit. The mean success rate was 93% from over 600 reported episodes. Compared with other antiarrhythmic agents, adenosine is remarkable for its rapid metabolism and brevity of action, with a half-life of a few seconds. It commonly produces subjective symptoms, particularly chest discomfort, dyspnea, and flushing, which are of short duration only. No serious adverse effect has been reported. Arrhythmias may recur within minutes in a minority of patients. Comparative studies have shown that adenosine is as effective as verapamil in the treatment of supraventricular tachycardia, and has less potential for adverse effects. Patients with supraventricular tachycardia should initially be treated using vagotonic physical maneuvers. Immediate electrical cardioversion is indicated if the arrhythmia is associated with hemodynamic collapse. Adenosine is the preferred drug in those patients in whom verapamil has failed or may cause adverse effects, such as those with heart failure or wide-complex tachycardia. The safety profile of adenosine suggests that it should be the drug of first choice for the treatment of supraventricular tachycardia, but only limited comparative data to support this view are available at present.     

Nonpharmacological treatment of supraventricular tachycardia.

Although pharmacological treatment is often effective in preventing or controlling attacks of tachycardia it is palliative rather than a cure. Some Arrhythmias are refractory to drug therapy and long-term antiarrhythmic agents are associated with side-effects, life-threatening toxicity, poor patient compliance and considerable cost. On the other hand, enhanced knowledge of electrophysiological mechanisms and advanced technology have resulted in the more and more widespread use of several nonpharmacological methods of treating arrhythmias. It is the purpose of this review to discuss the present status of nonpharmacological therapy of supraventricular tachycardia and comment upon its current role in the management of patients presenting with these arrhythmias.     

善得定中止阵发性室上性心动过速机制和疗效的探讨

为探讨善得定中止阵发性室上性心动过速(室上速)的机制和疗效,本文采用膜片钳全细胞记录方法观察生长激素抑制因子(SS)对心室肌细胞L型钙通道的作用;窦性心律、室上速时静注善得定,观察A-H间期及中止室上速的方式、效果。结果显示SS对心室肌细胞L型钙通道均有明显抑制作用;静注善得定后A-H间期延长,14例室上速中8例(57.1％)以房室结顺向传导阻滞方式转复为窦性心律。表明善得定中止室上速疗效肯定,副作用小,但容易复发。     

Mechanisms of supraventricular tachycardia

Programmed electrical stimulation of the heart in combination with intracardiac recordings has contributed a wealth of new information on the mechanisms and pathways of supraventricular tachycardia in humans. This knowledge has resulted in better treatment approaches to these patients. Questions still remain, however, about the mechanisms of atrial flutter and fibrillation and of some types of atrial tachycardia. The location of the circuit in paroxysmal atrioventricular nodal tachycardia also continues to puzzle investigators. The use of refined mapping techniques during cardiac surgery should provide answers to these questions in the near future.     

Mechanism of supraventricular tachycardia and pharmacological effects on it.

Electrophysiologic study in 30 patients with documented SVT, 16 of whom had preexcitation, and in 24 control subjects were reported. The mechanism of SVT were found to be various and to include reentry confined to the AV node, SA node or the atrium, reentry through accessory pathway and ectopic atrial automaticity. It was noted that some of SVT might use concealed accessory pathway in VA direction while the some of SVT in WPW syndrome might not utilize accessory pathways. Electrophysiological properties in cases with SVT did not differ from those observed in controls. There were no differences in the mode of electrophysiological action of drugs between XVT and control groups. Both propranolol and procaine amide slightly depressed AV conduction. However, the action of the drugs on echo zone were not the same. The basic mechanisms of the action of the drugs in SVT were discussed.