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At least 19 recordsLinked to original sources
PubMed1979

Ventricular tachycardia and ventricular fibrillation in a young population.

In this study, we describe the findings in 18 young patients (age range 4 days to 24 years, mean 16.6 years) who had ventricular tachycardia and/or ventricular fibrillation and were followed for 4--70 months (mean 22.4 months). Patients had a variety of problems associated with their arrhythmia, including mitral valve prolapse, cardiomyopathy, myocarditis, prolonged QT syndrome and hypokalemia. Six patients had no clinically recognizable cardiac abnormality. The ventricular tachycardia showed a left bundle branch block contour in 10 of 17 patients, right bundle branch block in four, was multiform in two and had an indeterminate contour in one. Sustained ventricular tachycardia was initiated and terminated reproducibly by atrial and ventricular stimulation in three of seven patients who did not have spontaneous episodes of ventricular tachycardia during the electrophysiologic study. In one other patient, short bursts of ventricular tachycardia were induced. Patients who had ventricular fibrillation, those who died, and those who are still symptomatic with poorly controlled ventricular arrhythmias had significant heart disease. In one patient, a ventricular tachyarrhythmia that had required more than 100 electrical cardioversions spontaneously disappeared after requiring 1 year of antiarrhythmic therapy.

Adolescent↗
PubMed1978

Effect of procainamide on induced ventricular tachycardia.

Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1-gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (less than 4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post-procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shortened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmic effect. Our data emphasize that antiarrhythmic drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.

Aged↗
PubMed1979

Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes.

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.

Adult↗
PubMed1977

Programmed ventricular stimulation in management of recurrent ventricular tachycardia.

Programmed ventricular stimulation was used effectively in the clinical management of six patients with medically refractory, chronic, recurrent ventricular tachycardia. Critically timed ventricular stimuli reliably terminated episodes of ventricular tachycardia and thus obviated repeated countershocks. Critically timed stimuli also reliably induced reentrant ventricular tachycardia. This provided a "clinical model" allowing immediate determination of optimal suppressive drug regimens. The technique has practical application in selected patients with recurrent ventricular tachycardia and can be safely performed within the intensive-care unit.

Adult↗
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

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↗
PubMed1975

Electral stimulation of the heart in the study of ventricular tachycardias.

Mechanisms of ventricular tachycardia in patients with chronic recurrent tachycardia and patients with acute myocardial infarction were studied by electrical stimulation of the heart. While re-entry was the most likely mechanism in chronic recurrent ventricular tachycardia, focal activity or re-entry in a very small area seemed to be responsible for ventricular tachycardia during acute myocardial infarction.

Adult↗
PubMed1976

Recurrent ventricular tachycardia in hypothyroidism.

Ventricular tachycardia associated with myxoedema is rare. Only two cases have so far been documented. In the report by Hansen, the patient had recurrent chest pain which suggested coexisting coronary heart disease. In the second case, the patient developed recurrent ventricular tachycardia only after intravenous triiodothyronine was given. This paper reports a further case of hypothyroidism with recurrent episodes of ventricular tachycardia and ventricular fibrillation which was not associated with any of the established causes of this arrhythmia.

Female↗
PubMed1978

Termination of ventricular tachycardia with bursts of rapid ventricular pacing.

Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 5 12 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent tachycardia.

Adolescent↗
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↗
PubMed1977

Effect of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia.

The effect of short-term intravenous administration of procainamide (12 patients), propranolol (4 patients) and verapamil (4 patients) was studied in 12 patients with chronic recurrent sustained ventricular tachycardia. In all patients tachycardia could reproducibly be initiated and terminated with programmed electrical stimulation of the heart. Procainamide (1) lengthened the effective refractory period of the right ventricle, (2) affected the tachycardia zone, (3) reduced ventricular rate during tachycardia, and (4) lengthened the interval between the tachycardia-initiating premature ventricular beat and the first QRS complex of tachycardia. No effect on the refractory period of the right ventricle or the mechanism of tachycardia was seen after administration of propranolol or verapamil. Apart from their therapeutic implications these data suggest that it may be possible to use drugs to study mechanisms of ventricular tachycardia in the human heart.

Adult↗
PubMed1978

Recurrent sustained ventricular tachycardia. 2. Endocardial mapping.

Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

Adolescent↗
PubMed1979

Treatment of recurrent ventricular tachycardia by patient-activated radiofrequency ventricular stimulation.

A new pacing technique may benefit selected patients with drug-resistant, chronic, recurrent ventricular tachycardia. This report describes two patients treated effectively with permanently implanted, patient-activated, radiofrequency ventricular stimulators. Both used the device successfully for repeated termination of episodic, sustained ventricular tachycardias. Optimal utilization of this technique requires extensive prior electrophysiologic assessment and drug trials, does not supplant continued drug therapy, and is not without potential hazard.

Adult↗
PubMed1977

Treatment of recurrent ventricular tachycardia and fibrillation with aprindine.

Twenty-three patients with recurrent ventricular tachycardia or ventricular fibrillation, or both, were treated with aprindine, a new antiarrhythmic agent. It was found that: (1) no patient had a recurrence of ventricular fibrillation after aprindine therapy was begun, except as a terminal event subsequent to the development of acute myocardial infarction and cardiogenic shock or refractory congestive heart failure; (2) 6 patients experienced ventricular tachycardia after the loading dose, but with continued aprindine therapy the ventricular tachycardia was suppressed in 3 of these 6 patients, and a fourth patient was asymptomatic during brief paroxysms of ventricular tachycardia; (3) in 2 patients, aprindine was ineffective and was discontinued; (4) electrical cardioversion was not required in any patient receiving aprindine; (5) premature ventricular extrasystoles were decreased in 18 of the 23 patients treated with aprindine; (6) aprindine was discontinued in 1 patient because of intolerable side effects, although ventricular arrhythmias were suppressed in this patient; and (7) 5 patients died from acute myocardial infarction or severe heart failure while receiving aprindine.

Administration, Oral↗
PubMed1979

Recurrent sustained ventricular tachycardia. 4. Pleomorphism.

Two or more morphologically distinct ventricular tachycardias were observed during electrophysiologic study in 14 patients with chronic sustained ventricular tachycardia. Nine of these patients had clinical ventricular tachycardia with multiple morphologies. During the study 13 patients manifested both right bundle branch block (RBBB) and left bundle branch block (LBBB) morphologies. The remaining patient had RBBB with both right and left axis deviation. Changing morphologies were observed spontaneously in four patients and could be produced in all 14 by ventricular stimulation. In 12 patients both RBBB and LBBB originated in the left ventricle, and in 11 of these patients, from within a left ventricular aneurysm. Diastolic fragmented activity representing reentry was unchanged during both morphologies in four patients and during one morphology in five patients. Epicardial mapping confirmed the aneurysm as the site of origin of multiform ventricular tachycardias in two patients. Our data suggest that 1) ventricular tachycardia is frequently pleomorphic; 2) multiple morphologies usually represent variable exit sites and/or ventricular activation during the same tachycardia; and 3) there is a frequent association of pleomorphic ventricular tachycardia with left ventricle aneurysm.

Aneurysm↗