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At least 19 recordsLinked to original sources
PubMed1979

Atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction: diagnostic and therapeutic implications.

The diagnostic and potential therapeutic value of rapid right atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction, was examined. The effect of right atrial pacing at incremental rates beginning 10 bpm above the rate of the tachycardia was studied in five patients with ventricular tachycardia, and in four patients with supraventricular tachycardia with rate-related bundle branch block aberration, the mechanism of tachycardia having been demonstrated at electrophysiology study. Atrial pacing resulted in persistent (four) or occasional (one) normalisation of the QRS complexes to that seen in sinus rhythm in those five patients with ventricular tachycardia. The intraventricular conduction pattern persisted with atrial pacing in those patients with supraventricular tachycardia and aberrant intraventricular conduction. This confirms that atrial pacing is a useful and simple diagnostic test in wide QRS tachycardia, which does not require sophisticated electrophysiological facilities. In three of the patients with ventricular tachycardia, atrial pacing terminated the arrhythmia, suggesting potential therapeutic use of rapid atrial pacing in such patients.

Adult↗
PubMed1977

Atrial tachycardia without P waves masquerading as an A-V junctional tachycardia.

Two patients who presented by scalar ECG with an A-V junctional tachycardia were demonstrated during an electrophysiologic evaluation to have an atrial tachycardia without P waves in the surface ECG. Case 1 had an atrial tachycardia that conducted through the A-V node with a Wenckebach block. Atrial activity was recorded only from the proximal portion of the coronary sinus and from right atrial areas near the tricuspid valve. Case 2 had an atrial tachycardia that abruptly began and terminated following carotid sinus massage. Atrial activity was recorded only in the coronary sinusos, and pacing at that site resulted in atrial capture, with Wenckebach conduction to the ventricles. These observations demonstrate that an atrial tachycardia without P waves can simulate A-V junctional tachycardia with or without Weckebach block. Such findings may have a bearing on some important electrophysiologic concepts such as the origin of A-V junctional rhythms and the need for atrial participation in A-V nodal re-entry.

Atrioventricular Node↗
PubMedDate not supplied

Supraventricular tachycardia that mimics ventricular tachycardia. Part II.

Concealed WPW is a newly described clinical entity. The existence of this syndrome can be ascertained only through specific electrophysiologic intracardiac studies. From the clinical standpoint, the existence of an accessory unidirectional A-V pathway anatomically located in the general area of the Kent bundle should be suspected in those patients with chronic BBB who have recurrent paroxysmal atrial tachycardias initiated by sinus arrhythmias or premature atrial beats. It should be noted that functional BBB can occur following a premature atrial beat. This will also set the stage for the initiation of a reciprocating tachycardia in concealed WPW. Pharmacological therapy aimed at preventing the recurrent tachycardias is disappointing. Pacemaker implantation appears to be successful by rendering one of the bundle branches refractory through concealed conduction. With chronic block of the remaining bundle branch, the natural pathway of A-V conduction is totally blocked at a critical time during the tachycardias, thus eliminating the reciprocating tachycardia.

Adult↗
PubMed1979

Carotid sinus massage induced elimination of rate related bundle branch block during paroxysmal atrial tachycardia: a simple method of proving bypass tract participation in the tachycardia.

Four cases of paroxysmal atrial tachycardia are described in whom rate related left bundle branch block (LBBB) was often present which persisted indefintely and showed no signs of spontaneous disappearance. Transient slowing of the tachycardia by carotid sinus massage in each case eliminated LBBB and this led to tachycardia acceleration. The tachycardia acceleration was traceable to a shortening in ventriculoatrial conduction. These observations proved the participation of a left sided bypass tract in the tachycardia circuit in each of these cases.

Bundle-Branch Block↗
PubMed1979

Transfer of coupling of premature ventricular contractions to an ectopic ventricular tachycardia: a mechanism for atypical bidirectional tachycardia.

Bidirectional tachycardia was observed on Holter tracings recorded from a dog three days after the production of a small freeze lesion on the wall of the left ventricle. A bigeminal rhythm with fixed coupling of ventricular premature contractions was interrupted by a burst of ventricular tachycardia of different morphology. The ventricular premature contractions, originally coupled to the sinus beats, became coupled to the new ventricular tachycardia with an identical coupling interval. This resulted in a dibirectional tachycardia, created by the "transfer" of coupling of premature ventricular contractions to a separate ectopic ventricular tachycardia.

Animals↗
PubMedDate not supplied

Supraventricular tachycardia that mimics ventricular tachycardia.

A short PR interval, a delta wave, and attacks of paroxysmal tachycardia are the principal features of the WPW syndrome. A grossly irregular rhythm with bizzare QRS complexes at rates exceeding 180 per minute is one of the paroxysmal tachycardias characteristic of the WPW syndrome. This arrhythmia deserves special attention, because it is often misinterpretated as ventricular tachycardia. The interpretation is atrial fibrillation with varying degrees of ventricular fusion and phasic ventricular aberration. Prompt electrical cardioversion is indicated because, at times, ventricular fibrillation may result. Quinidine sulfate used prophylactically because of its negative dromotropic effect on the accessory pathway promotes A-V transmission via the A-V node.

Diagnosis, Differential↗
PubMed1978

An unusual form of the bradycardia-tachycardia syndrome: paroxysmal A-V block and ventricular tachycardia.

An unusual case of alternating bradycardia-tachycardia, paroxysmal Mobitz II A-V block and ventricular tachycardia is described. The patient presented with a normal resting (control) electrocardiogram and intracardiac conduction times (A-H and H-V intervals). The clinical evaluation, electrophysiology, and importance of defining the cause of serious rhythm disturbances prior to therapy are discussed.

Bradycardia↗
PubMed1979

[Double tachycardia (hisian and auricular) in a bradycardia-tachycardia syndrome (author's transl)].

The present case corresponds to a patient with a mitro-aortic valvulopathy of rheumatic origin with syncopal episodes and nauseas, who, in the ECG showed alternatively an extreme sinusal bradycardia and supraventricular tachyarrhythmias. It was interpreted as a typical case of bradycardia-tachycardia syndrome in which the crises of tachyarrhythmias consisted of episodes of double tachycardia with incomplete supra-hisian atrial-ventricular dissociation, documented by obtaining right atrial electrograms and hisian-electrograms during the episodes. Treatment was initiated with verapamil (10 mg intravenously every 8 hours) after an endocavitary pacemaker of demand had been placed. After 3 months the result was very satisfactory with good tolerance to the medical treatment and complete disappearance of the symptomatology.

Aortic Valve Insufficiency↗
PubMed1978

Modern concepts of ventricular tachycardia. The value of electrocardiological investigations and delayed potentials in ventricular tachycardia of ischemic and nonischemic etiology (31 operated cases).

Concepts on ventricular tachycardia (VT) have markedly changed in the last 10 yr, with the help of sophisticated electrophysiological methods of study. The importance of the reentry phenomenon in the mechanism of the arrhythmias has been pointed out by stimulation procedures. Epicardial mapping allowed the localization of the abnormal zone where delayed impulses could allow reentry. Surgical techniques have been developed from these observations, to prevent reentrant VT in some refractory cases.

Action Potentials↗
PubMed1976

[Epicardial scintigraphy in 4 cases of ventricular tachycardia caused by reentry of blood after myocardial infarct. Origin of the tachycardia and surgical approach].

110 point cartography was carried out over the ventricular pericardium during sinus rhythm (SR) and during ventricular tachycardia (VT) in four patients whose infarctions were 15 days, 4 months, 4 years and 7 years previously, and in whom electrocardiographic investigation had suggested a ventricular reentry phenomenon. The macroscopical appearances of the heart at operation suggested that the infarct was situated along the left side in two cases, and in or along the septum in two others. Cartography in sinus rhythm showed that the onset of ventricular activity was compatable with a site of origin in the node/bundle of His. Cartography during VT showed up the epicentre of the abnormal impulses which were always situated outside the exit points and dependent upon the node/bundle of His system as demonstrated by cartography in sinus rhythm. Moreover, in at least two cases this was found to lie outside the infarcted area, in portions of the myocardium which could be considered as healthy. In one case it was found to lie along the anterior interventricular groove, facing the septal infarct. In two cases the arrhythmia will not recur, one having achieved this status bu simple ventriculotomy. The failures are reported in relation to the extent of the lesion anatomically, which may cause disorientation of the surgical approach, and make the results difficult to interpret.

Aged↗
PubMed1976

[Epicardial scintigraphy in 4 cases of ventricular tachycardia caused by reentry of blood after myocardial infarct. Study of intra-ventricular conduction disorders in sinus rhythm and in tachycardia, and their relations to anatomical data].

Ventricular pericardial cartography in sinus rhythm (SR) and during ventricular tachycardia (VT) in four cases of myocardial infarction has yielded additional information in the study of conduction disorders in myocardial ischaemia: 1. The significant slowing of activity in SR as well as in VT is demonstrated by this direct method. It is associated with a diminution in amplitude of the pericardial potentials in the zones affected by the ischaemia; 2. Cartography during VT accentuates or reveals disorders of conduction which are slight or latent in SR; 3. Disorders of intra-ventricular conduction are found to be related either to segmental blocks on the branches of the bundle of His, or as focal blocks (peri-infarct block) on the left side, whose nature can be shown up even during VT; 4. Secondary activation of the myocardial fiber found to be related either to segmental blocks on the bundle of His during VT is demonstrated.

Arrhythmia, Sinus↗
PubMed1977

Mechanisms of atrioventricular junctional tachycardia. Role of reentry and concealed accessory bypass tracts.

Electrophysiologic investigations with programmed stimulation of the human heart have clearly established the participation of the atrioventricular (A-V) junction in three different types of junctional reciprocating tachycardia: (1) paroxysmal supraventricular tachycardia in the Wolff-Parkinson-White syndrome: (2) the vast proportion of "paroxysmal atrial tachycardia" without evidence of preexcitation during sinus rhythm with antegrade conduction; and (3) the permanent or almost permanent (chronic relapsing) form of supraventricular tachycardia with its characteristic rate-dependent initiating mechanism. The obvious presence of the Wolff-Parkinson-White syndrome during sinus rhythm does not necessarily imply that the accessory pathway will be utilized during supraventricular tachycardia. Conversely, in the absence of preexcitation, the mechanism of A-V junctional reciprocating tachycardia has been traditionally attributed to pure intranodal dissociation, often without definite direct proof. Concealed accessory pathways (with unidirectional block) may be more frequent than realized and should be carefully searched for. Proof that supraventricular tachycardia utilizes an accessory pathway for retrograde conduction to the atrium often requires meticulous electrophysiologic studies- Conslucions based on the absence of various findings may be misleading. Emphasis must be placed on positive viagnostic features. One or more of the following observations may prove or disprove participation of a Kent bundle during supraventricular tachycardia: (1) induction of A-V block during tachycardia: (2) influence of electrically induced ventricular premature beats upon tachycardia; (3) patterns of retrograde atrial activation during tachycardia; or (4) influence of functional bundle branch block on the rate of the tachycardia. Analysis of events at the onset of rather than during the tachycardia is probably less important but may also provide suggestive clues about the mechanism of reentry. Observation of the following variables may be helpful: (1) behavior of antegrade conduction at the onset of tachycardia; (2) relation of atrial and ventricular activation at the onset of tachycardia; (3) presence of retrograde ventriculoatrial (V-A) conduction; (4) prolongation of the H-V interval at the onset of tachycardia; and (5) atrial stimulation at various sites. Precise understanding of the pathophysiology of supraventricular tachycardia is important because specific therapy (pharmacologic, pacemaker or surgical) may ultimately depend on accurate knowledge of the underlying mechanisms.

Anti-Arrhythmia Agents↗
PubMed1978

Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia.

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined in 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia. In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.

Adolescent↗
PubMed1979

[Medical management of tachycardias (author's transl)].

Guidelines for a step-wise plan of treatment of tachycardias have been compiled based on clinical empirical experience and with the aid of surface electrocardiograms, intracardial electrograms and stimulation techniques. The plan is primarily with the aid of surface electrocardiograms, intracardial electrograms and stimulation techniques. The plan is primarily oriented with respect to the antiarrhythmic efficacy, the adverse reactions and the practicability of the respective agents. Any type of tachycardia, including premature atrial or ventricular contractions, may be regarded as indication for treatment. Treatment is not indicated only in those asymptomatic patients with rare and evanescent tachycardias and in those with less than 300 premature contractions per hour. Beta-adrenergic blockers are the drugs of choice for the persistent sinus tachycardia. Should the latter agents be contraindicated, propafenon, amiodarone or aprindine may be administered. Verapamil and/or digitalis are indicated only for suppression of paroxysmal sinus tachycardias. Atrial premature contractions are best managed with guinidine or disopyramid. An acute reduction of rapid ventricular rates associated with atrial tachycardias, atrial flutter or fibrillation can best be attained through the administration of verapamil prior to digitalis or beta-adrenergic blockers. Re-establishment of sinus rhythm and prophylactic suppression of the latter should be undertaken with quinidine or disopyramid in combination with digitalis and/or either a beta-adrenergic blocker or intravenously-administered verapamil. Verapamil is the drug of choice for initial management of AV-junctional tachycardia for which a combination with digitalis may be considered. An alternative combination is that of a beta-adrenergic blocker and digitalis. For the acute treatment of ventricular tachycardias, lidocain has proved most effective. Although ajmaline and/or propafenon may be given should no response be obtained, electrical cardioversion would be more appropriate. To prevent ventricular tachycardia or when treatment is indicated for ventricular premature beats, ajmaline, propafenon, quinidine, disopyramid or mexiletine, occasionally in combination with a beta-adrenergic blocker should be employed. Verapamil and/or ajmaline, are usually very effective for termination of reciprocal tachycardias. Ajmaline or propafenon in combination with a beta-adrenergic blocker is recommended for the prophylactic treatment of reciprocal tachycardia. In patients who additionally have bradycardia, prolonged QT-intervals or pre-excitation syndromes, the guidelines should be modified accordingly.

Anti-Arrhythmia Agents↗
PubMed1979

The response of regular re-entrant supraventricular tachycardia to right heart stimulation.

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.

Adolescent↗
PubMed1979

Paroxysmal supraventricular tachycardia induction in patients with Wolff-Parkinson-White syndrome.

In 54 patients with pre-excitation, 30 (56%) had inducible A-V re-entrant paroxysmal tachycardia. Of these 30, 20 had spontaneous paroxysmal tachycardia (four also had atrial fibrillation), four had spontaneous paroxysmal atrial fibrillation, five had a history of palpitation without arrhythmia, and one was asymptomatic. In 24 patients (44%), paroxysmal tachycardia was not inducible. Of these 24, none had documented paroxysmal tachycardia, four had atrial fibrillation, none had palpitation without arrhythmia, and 11 were asymptomatic. The incidence of documented paroxysmal tachycardia was higher in the patients with inducible tachycardia (P less than 0.001). Tachycardia induction was noted in 20 of 20 patients with spontaneous paroxysmal tachycardia, eight of 12 patients with paroxysmal atrial fibrillation, five of 14 patients with palpitation and no arrhythmia, and one of 12 asymptomatic patients. The frequency of ability to induce paroxysmal tachycardia was significantly higher in both the patients with documented spontaneous paroxysmal tachycardia and the patients with paroxysmal atrial fibrillation than in the asymptomatic group (P less than 0.01).

Adolescent↗