Paroxysmal Ventricular Tachycardia Research Articles

Paroxysmal ventricular tachycardia in Wolff-Parkinson-White syndrome: Case report and review of the literature

A case with Type A Wolff-Parkinson-White pattern and recurrent sustained ventricular tachycardia is presented. Because of ventricular pre-excitation, electrocardiographic clues suggestive of ventricular tachycardia were ignored and the diagnosis of supraventricular tachycardia with conduction to the ventricles over the accessory pathway was made during each admission to the hospital. Ventricular tachycardia was suspected only when programmed stimulation studies performed twelve years after initial presentation and many hospitalizations failed to induce a tachycardia with a QRS pattern similar to that of spontaneously occurring tachycardia. The diagnosis of ventricular tachycardia was later confirmed by intracardiac recordings made during a spontaneous episode of tachycardia. Tachycardia was unresponsive to all conventional antiarrhythmic agents but was controlled with amiodarone. The differential diagnosis of wide QRS complex tachycardia in patients with Wolff-Parkinson-White syndrome, the implications of correctly diagnosing the tachycardia, and the usefulness of intracardiac electrophysiologic studies in differentiating supraventricular tachycardia with aberrant conduction from ventricular tachycardia are discussed.

Observations with endocardial electrography on ventricular tachycardia by intracoronary saline in dogs.

Selective injection of 1.5 ml of 10% saline into the left circumflex coronary artery (LCX) was carried out during sinus rhythm twice in each of 15 mongrel dogs anesthetized with sodium pentobarbital, and multiple endocardial recordings including His bundle electrogram (HBE) were made. Ventricular tachycardia (VT) was elicited in all of the 15 dogs both in the first and second injections. The cycle length of sinus rhythm before injection was 468 +/- 88 msec (mean +/- S.D.). The coupling interval between the last depolarization of the left ventricle (LV) of sinus origin and the first premature LV depolarization of the VT was 395 +/- 57 msec. Coupling interval between the first and the second LV depolarizations was 348 +/- 78 msec. Significant difference was noted between any pair of these values (p less than 0.01). No bundle branch re-entry in the beginning of VT was observed. The site of origin of the VT was referred to the LV in 13 dogs. Rapid pacing during paroxysm of VT applied at the apex of the LV made no marked influence upon VT after pacing. The calcium channel blocker, diltiazem failed to block the production of VT. The Mechanism for genesis of this VT may not be re-entry but rather enhanced automaticity independent of the calcium inward current.

Coronary hemodynamics in simulated paroxysms of ventricular tachycardia: role of myocardial impairment and of extravascular resistance.

In 6 patients with healthy hearts (controls), 17 with coronary artery disease (CAD) and 6 with left ventricular hypertrophy due to aortic valvular disease, aortic pressure, coronary sinus blood flow (CSF) and lactate extraction were determined before and after the sudden onset of a paced ventricular tachycardia of 170 bpm (VT 170 = simulated paroxysmal ventricular tachycardia). Comparison to parameter changes during dipyridamol vasodilation revealed reduced coronary vascular reserve for CAD and hypertrophy. While VT induced a reduction of aortic pressure (stabilized by an average of 22%, and most excessively for CAD; p less than 0.05) and CSF remained at/or slightly above control levels (by an average of 31%; p greater than 0.05) equally for all groups (p greater than 0.05), lactate production in the groups with CAD and hypertrophy indicated myocardial impairment by ischemia. Excessively greater increases of CSF during dipyridamol vasodilation (vs. VT) for all groups suggested VTs extravascular resistance increase to have limited the extent of the potential of coronary vascular decrease. With one variable being kept constant (i.e. 'clamping' the vascular component of coronary resistance at its limit by dipyridamol), tachycardia during dipyridamol (D) vasodilation (VT 170+D and VT 140+D) in the controls and in the CAD group resulted in a linear decrease of CSF, allowing quantification of impaired coronary reserve for CAD. We concluded from the observations that: (1) paroxysmal VT demands fast therapeutic action foremost in the impaired myocardium, and (2) tachycardia per se acts as limiting factor for coronary blood flow via increase in extravascular resistance (aside from a shortened diastole).

Ventricular tachycardia: Prediction of response to oral aprindine with intravenous aprindine

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 ± 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.

Lack of effectiveness of bretylium in paroxysmal sustained ventricular tachycardia

Lack of effectiveness of bretylium in paroxysmal sustained ventricular tachycardia

"Nonsustained": A Semantic Snake

Letters and Corrections1 September 1980"Nonsustained": A Semantic SnakeBRENDAN PHIBBS, M.D.BRENDAN PHIBBS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-93-3-513_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The excellent article by Follansbee and colleagues (1) in the June issue of theAnnalsis marred by a semantic reptile that should be scotched before it becomes a full-blown viper. I refer to the use of "nonsustained" to describe brief paroxysms of ventricular tachycardia. Other authors have used this same miserable negative definer in the same context, and, unless strenous measures are taken, it may become a permanent and depressing resident of medical terminology. The word for a brief episode is "transient." Please, fellow workers, come back to the English language and the glories of its...Reference1. FOLLANSBEEMICHELSONMORGANROTH WEJ. Nonsustained ventricular tachycardia in ambulatory patients: characteristics and association with sudden cardiac death. Ann Intern Med. 1980;92:741-7. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: BRENDAN PHIBBS, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1980Volume 93, Issue 3Page: 513-513KeywordsVentricular tachycardia ePublished: 1 December 2008 Issue Published: 1 September 1980 PDF downloadLoading ...

Nonsustained ventricular tachycardia in ambulatory patients: characteristics and association with sudden cardiac death.

Thirty-seven patients with nonsustained ventricular tachycardia (greater than or equal to triplets) were identified retrospectively from a population of 518 consecutive patients referred for 24-hour Holter monitoring and studied to determine the prognostic significance of this finding. Ten of these 37 patients suffered sudden cardiac death during a mean follow-up of 19 +/- 5 months. Nine of 19 patients with a diagnosis of congestive cardiomyopathy or history of congestive heart failure died suddently compared to only one of the other 18 patients. No other patient data were predictive of sudden death. Remarkably, no characterisitc of the ventricular tachycardia including beats per episode, episodes per day, rate, prematurity index (RR1/QT) of the initiating beat, or the occurrence of associated arrhythmias was important prognostically. Thus, patients with congestive cardiomyopathy or congestive heart failure and nonsustained paroxysmal ventricular tachycardia are at a high risk for sudden death and are ideal candidates for prophylactic interventions.

Paroxysmal ventricular tachycardia during repeated 24-hour ambulatory electrocardiographic monitoring of postmyocardial infarction patients.

Paroxysmal ventricular tachycardia during repeated 24-hour ambulatory electrocardiographic monitoring of postmyocardial infarction patients.

Chronic Longterm Electrophysiologic Study of Paroxysmal Ventricular Tachycardia

Nine patients with recurrent paroxysmal ventricular tachycardia underwent chronic electrophysiologic studies to delineate effective drug therapy for prevention of recurrence of this arrhythmia. The frequency of attacks of ventricular tachycardia necessitating hospitalization ranged from 2 to 12 (mean 5 +/- 4) attacks per year. Pacing induction of ventricular tachycardia was performed prior to and following intravenous or oral administration of procainamide (eight patients), disopyramide phosphate (nine patients), aprindine (five patients) and propranolol (four patients). Successful drug response (prevention of ventricular tachycardia induction or induction of nonsustained episodes of tachycardia) was noted in six of nine patients (66 percent). Lack of drug effect on the ability to sustain ventricular tachycardia was noted in three patients (34 percent). In addition, a deleterious drug response, manifested by potentiation of ventricular flutter or fibrillation, was observed in two of the three patients who failed to respond to drugs. Chronic drug therapy based on successful response in six patients resulted in cure of ventricular tachycardia in five of six patients (83 percent), one patient having one attack necessitating hospitalization. Of the three patients who demonstrated lack of drug effect during chronic electrophysiologic studies, one died suddenly and two had recurrent episodes of ventricular tachycardia while receiving a drug that did not prevent induction of ventricular tachycardia.

The management of paroxysmal ventricular tachycardia and fibrillation associated with the long QT syndrome

The management of paroxysmal ventricular tachycardia and fibrillation associated with the long QT syndrome

Infiltrative cardiomyopathy with conduction disease and ventricular arrhythmia: Electrophysiologic and pathologic correlations

Two cases are described, one of cardiac sarcoidosis and another of primary cardiac amyloidosis, in which correlation was made between electrophysiologic and postmortem conduction system studies. In Case 1 the electrocardiogram revealed right bundle branch block with first degree and intermittent third degree atrioventricular (A-V) block and recurrent unifocal paroxysmal ventricular tachycardia. Electrophysiologic studies disclosed normal sinus rhythm with prolonged A-H (175 ms) and H-V (60 ms) intervals and extrastimulus induction of repetitive ventricular firing. Postmortem examination revealed a sarcoid aneurysm of the posterior left ventricle and granulomatous infiltration of the A-V node, His bundle and bundle branches. In Case 2 the electrocardiogram revealed sinus bradycardia, a prolonged S-T interval and recurrent ventricular fibrillation. Electrophysiologic studies demonstrated a prolonged sinus nodal recovery time (6,080 ms) and H-V (85 ms) interval. Postmortem examination revealed marked amyloid infiltration of the sinoatrial node, atria, proximal bundle branches and left and right ventricular myocardium. There was thus excellent correlation between electrophysiologic and pathologic findings. These cases indicate the importance of making a clinical diagnosis of the disease that might in some cases allow specific therapeutic intervention in addition to antiarrhythmic therapy.

The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias.

1 Reccurent paroxysmal atrial, atrioventricular and ventricular tachycardias in 50 patients without acute coronary insufficiency, heart failure or metabolic abnormlity were treated with disopyramide phosphate in a dose of 2 mg/kg body weight infused over 5 min. 2 Conversion to sinus rhythm within 10 min of the completed infusion occurred in 10 of 14 (71%) patients with paroxysmal 'lone' atrial fibrillation, 3 of 7 (43%) patients with paroxysmal atrial flutter, 6 of 9 (67%) patients with paroxysmal atrial tachycardia, 5 of 9 (56%) patients with paroxysmal atrioventricular tachycardia associated with the Wolff-Parkinson-White syndrome and 8 of 11 (73%) patients with paroxysmal ventricular tachycardia. 3 Side effects: significant systemic hypotension in 3, high grade AV block in 1, an increased ventricular response producing symptoms in 4, post conversion asystole in 1 land sinus bradycardia in 2. 4 The anti-arrhythmic effect and arrhythmogenic side effects may be related to both the direct membrane stabilizing effect and the anticholinergic effect of disopyramide.

Evaluation of warning arrhythmias before paroxysmal ventricular tachycardia during acute myocardial infarction in man.

In order to determine the relationship of paroxysmal ventricular tachycardia (PVT) to any antecedent (premonitory) ventricular arrhythmias during the early phases of acute myocardial infarctions, 24-hour Holter monitoring was begun on 52 male patients an average of 12.6 hours after the onset of prolonged chest pain that was documented as acute infraction. Twenty-four patients had PVT and 28 did not. We analyzed in detail the incidence of frequency of premature ventricular complexes (PVCs), prematurity and pairing during the 10 minutes immediately preceding PVT from a continuous 10-minute rhythm strip. There was no positive correlation between PVT and the number or complexity of PVCs in the 10 minutes immediately before ventricular tachycardia. These findings suggest that there is no consistent pattern or frequency of ventricular arrhythmia that could be identified as premonitory for PVT during the immediate pre-PVT period, even during the acute phase of myocardial infarction in man.

Pituitary Stones and Associated Hypopituitarism

IN 1975 DiChiro and colleagues¹described two women with pituitary stones. They emphasized the benignity of this process and its rarity. We report two additional cases, both men, one of whom had clinical hypopituitarism. <h3>Report of Cases</h3><h3>Case 1.—</h3> A 73-year-old white, single man was admitted to the hospital in March 1977 because of recurrent episodes of dizziness and confusion. Paroxysmal atrial fibrillation was noted at this time. Subsequent examination also disclosed a ten-second run of paroxysmal ventricular tachycardia on dynamic ECG monitoring in July 1977. A skull x-ray film in March 1977 demonstrated dense intrasellar calcification (Fig 1). Review of the history and physical examination failed to show symptoms or signs of hypopituitarism. He had no known children. Quinidine sulfate and digoxin were prescribed to treat the arrhythmia. Endocrine evaluation showed a thyroxine (T₄) level of 6.0 μg/dL (normal, 3.5 to 11.9 μg/dL) and free thyroxine index of

CLINICAL AND ELECTROCARDIOGRAPHIC FINDINGS IN SUSPECTED VIRAL MYOCARDITIS OF PUPS

Surviving puppies from three separate litters in which deaths had occurred from suspected viral myocarditis were examined clinically and electrocardiographically. Of 11 puppies examined, 5 subsequently died or were euthanised within 11 days of initial examination. ECG changes present in these puppies for 1 to 11 days prior to death were small R waves (less than 0.4 mV in lead II), S-T segment elevation, QRS notching and paroxysmal ventricular tachycardia (PVT). No clinical signs referable to the ECG changes were present before the terminal episodes of apparent sudden death or death following a brief period of dyspnoea. Multifocial subacute myocarditis was present on post-mortem examination. A sixth puppy with small R waves remained clinically normal for a further 4 weeks. It then developed severe dyspnoea which persisted for 24 hours before euthanasia. Extensive fibrosis of the left ventricle was present on post-mortem examination.

Intravenous disopyramide phosphate and ventricular overdrive pacing in the termination of paroxysmal ventricular tachycardia.

Both antiarrhythmic drugs and bursts of rapid ventricular pacing provide alternatives to DC cardioversion for the treatment of paroxysmal ventricular tachycardia. This report considers the individual and combined success of burst ventricular pacing and intravenous disopyramide phosphate in the tretment of 11 examples of paroxysmal ventricular tachycardia. Rapid ventricular pacing, at a rate of up to 50 beats/min faster than the tachycardia rate terminated 7 of the tachycardias. Intravenous disopyramide resulted in increased tachycardiac cycle length (342 +/- 34 ms-385 +/- 56 ms), increased QRS complex width (147 +/- 42 ms-180 +/- 41 ms) and termination of 8 the tachycardias. The remaining 3 tachycardias could be terminated by bursts of ventricular pacing following the infusion of disopyramide. Of these, 2 could not be terminated prior to disopyramide. The use of both techniques allowed the extinction of all 11 tachycardias and prevented the need to proceed to DC conversion.

Effect of Postural Changes on Pulsus Alternans: An Echocardiographic Study

We describe a patient who had severe left ventricular dysfunction and pulsus alternans following an episode of severe viral myocarditis. Pulsus alternans was mild with the patient in the supine and squatting positions but increased dramatically on standing. Echocardiograms were used to study changes in left ventricular dimension and function with changes in posture. On standing, there was a decrease in the left ventricular diameter and an increase in the absolute and relative shortening fraction and the velocity of shortening on the strong beats, and there was a decrease in end-diastolic dimension and the measurements of ventricular contractility on the weak beats. The marked increase in pulsus alternans during standing may have been induced by increased sympathetic stimulation following the decrease in ventricular loading conditions, while the great beat-to-beat differences in end-diastolic dimension suggest, in addition, the importance of Starling's mechanism. We describe a patient who had severe left ventricular dysfunction and pulsus alternans following an episode of severe viral myocarditis. Pulsus alternans was mild with the patient in the supine and squatting positions but increased dramatically on standing. Echocardiograms were used to study changes in left ventricular dimension and function with changes in posture. On standing, there was a decrease in the left ventricular diameter and an increase in the absolute and relative shortening fraction and the velocity of shortening on the strong beats, and there was a decrease in end-diastolic dimension and the measurements of ventricular contractility on the weak beats. The marked increase in pulsus alternans during standing may have been induced by increased sympathetic stimulation following the decrease in ventricular loading conditions, while the great beat-to-beat differences in end-diastolic dimension suggest, in addition, the importance of Starling's mechanism. The Successful Cryosurgical Treatment of Paroxysmal Ventricular TachycardiaCHESTVol. 75Issue 5PreviewCryotherapy has been successfully applied to the destruction of conduction tissue and accessory pathways. In this report, its successful application to the ablation of a focus of paroxysmal ventricular tachycardia is described. Full-Text PDF

The Successful Cryosurgical Treatment of Paroxysmal Ventricular Tachycardia

Cryotherapy has been successfully applied to the destruction of conduction tissue and accessory pathways. In this report, its successful application to the ablation of a focus of paroxysmal ventricular tachycardia is described. Cryotherapy has been successfully applied to the destruction of conduction tissue and accessory pathways. In this report, its successful application to the ablation of a focus of paroxysmal ventricular tachycardia is described. Direct Surgical Treatment of Arrhythmias: The Last Frontier in Surgical CardiologyCHESTVol. 75Issue 5PreviewCamm and colleagues have described in this issue (see page 621 ) their interesting experience with the identification and ablation of an area of ventricular myocardium that was the origin of a malignant ventricular arrhythmia (MVA). This is the direct approach to the surgical treatment of arrhythmias in contrast to an indirect one as exemplified by coronary artery bypass and dorsal sympathectomy. The underlying disease in their patient was not known; although the patient's QRS was prolonged, and there was a structural defect in the aorta. Full-Text PDF

Asynchronous Breathing: A Possible Etiology for Dyspnea in a Patient with Normal Lungs

Asynchronous breathing has been frequently noted in patients with respiratory failure or severe parenchymal pulmonary disease but only rarely in relatively healthy patients. We describe a patient with relatively normal lungs whose dyspnea, we believe, is a consequence of asynchronous breathing. Asynchronous breathing has been frequently noted in patients with respiratory failure or severe parenchymal pulmonary disease but only rarely in relatively healthy patients. We describe a patient with relatively normal lungs whose dyspnea, we believe, is a consequence of asynchronous breathing. The Successful Cryosurgical Treatment of Paroxysmal Ventricular TachycardiaCHESTVol. 75Issue 5PreviewCryotherapy has been successfully applied to the destruction of conduction tissue and accessory pathways. In this report, its successful application to the ablation of a focus of paroxysmal ventricular tachycardia is described. Full-Text PDF

Spontaneous Resolution of Mediastinal Pancreatic Pseudocyst

We report the findings in a 39-year-old man with alcoholic pancreatitis and a lower posterior mediastinal mass. Endoscopic retrograde pancreatographic and ultrasonographic studies permitted an unequivocal diagnosis of mediastinal pancreatic pseudocyst. The pseudocyst resolved spontaneously five weeks after diagnosis, without specific therapy.