Large dose procainamide therapy for ventricular tachyarrhythmia.
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Adult↗
Biomedical subjects
S R Spielman
Publications and source records attributed to S R Spielman.
Incidence and clinical significance of induced ventricular tachycardia.
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Adolescent↗
Strength-interval relation in the human ventricle: effect of procainamide.
The effects of procainamide on strength-interval relations were evaluated in 18 patients. At plasma concentrations of 4.3 to 13.6 micrograms/ml procainamide had minimal effects on threshold current in late diastole, but in early diastole it shifted the strength-interval curve to the right. The basic strength-interval relation (that is, decreasing refractory period as current is increased) was not altered. The control refractory period decreased by a mean of 44 ms as the current was increased from threshold to 10 mA, whereas a mean decrease of 42 ms was observed after procainamide. However, the steep portion of the strength-interval curve(absolute refractory period) was shifted to longer coupling intervals by a mean value of 24 ms. These findings suggest that procainamide may primarily affect active membrane properties, but exert little net effect on passive membrane properties late in diastole.
Action Potentials↗
Comparison of endocardial catheter mapping with intraoperative mapping of ventricular tachycardia.
To validate the accuracy of catheter endocardial mapping to localize the origin of ventricular tachycardia (VT), we compared cathether endocardial mapping with intraoperative epicardial and endocardial mapping of 24 morphologically distinct VTs in 18 patients undergoing surgery. Twelve had VT with left bundle branch block morphology and 12 had VT with right bundle branch block morphology. Catheter endocardial mapping localized 23 VT morphologies to the border of a left ventricular aneurysm or myocardial infarction and one VT to a right ventriculotomy scar. Intraoperative epicardial mapping showed epicardial breakthrough on the right ventricle in 10 VTs with left bundle branch block morphology and on the left ventricle in two. In 12 VTs with right bundle branch block morphology, intraoperative epicardial mapping revealed the earliest site of VT with left bundle branch block morphology (11 patients) and VT with right bundle branch block morphology (12 patients) at the border of a left ventricular aneurysm, and one VT with left bundle branch block morphology in the right ventricle. Catheter endocardial mapping predicted the origin of VT within 4--8 cm2 of that determined by intraoperative endocardial mapping, which always identified the earliest site. These data validate the accuracy of catheter endocardial mapping in localizing the origin of VT.
Adult↗
Mechanism of ventricular fibrillation in man. Observations based on electrode catheter recordings.
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Adolescent↗
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↗
Electrophysiologic study of the left ventricle: indications and safety.
Eighty patients (69 with documented or suspected recurrent ventricular tachycardia or fibrillation, ten with left bundle-branch block, and one with the Wolff-Parkinson-White syndrome) underwent both right ventricular and left ventricular programmed electrical stimulation, including ventricular pacing and the introduction of one or two ventricular extrastimuli or electrode catheter mapping of the left ventricle (or both). Left ventricular catheters were introduced precutaneously via the femoral artery (of 61 patients, one required secondary repair) or via brachial arteriotomy (of 19 patients, two required secondary repair). All patients received an intravenously administered bolus of hep arin (5,000 units) following the insertion of the left ventricular catheter and then 1,000 units/hr after the first hour of study. No patients had cerebrovascular, systemic thromboembolic, or cardiac sequelae. In four (12 percent) of 34 patients with inductible ventricular tachycardia, programmed electrical stimulation of the left ventricle was required for initiation. Extensive left ventricular endocardial mapping was performed in 45 patients. Our experience suggests that (1) electrophysiologic study of the left ventricle can be performed safely, (2) programmed electrical stimulation of the left ventricle is indicated when a suspected ventricular tachyarrhythmia cannot be induced from the right ventricle, and (3) endocardial mapping of the left ventricle is indicated when surgery is being considered to abolish recurrent sustained ventricular tachycardia.
Adolescent↗
Ventricular fibrillation during programmed ventricular stimulation: incidence and clinical implications.
Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.
Adolescent↗
Sustained ventricular tachycardia: evidence for protected localized reentry.
The components of the reentrant circuit were evaluated in 26 patients in whom sustained ventricular tachycardia could be reproducibly initiated or terminated, or both. Observations suggesting that the proximal His-Purkinje system was not a requisite component included (1) lack of requirement for retrograde His-Purkinje delay or bundle branck reentry, or both, for initiation of the tachycardia: (2) anterograde depolarization of the His bundle during ventricular tachycardial without alteration of the QRS configuration or cycle length; and (3) the presence of random retrograde His potentials during the tachycardia. Evidence that the reentrant circuit was localized to a small area of the ventricles included (1) the ability to capture large segments of the ventricles transiently or continuously with occurrence of intermittent or continuous supraventricular capture either spontaneously or with atrial pacing without effect on the tachycardia. These findings suggest that the reentrant circuit must be small, electrocardiographically silent and relatively protected.
Adolescent↗
The limitations of epicardial mapping as a guide to the surgical therapy of ventricular tachycardia.
The adequacy of intraoperative epicardial mapping as a guide to surgical procedures performed to terminate ventricular arrhythmias was investigated. Ligation of the anterior septal or left anterior descending coronary artery in 28 dogs produced ventricular arrhythmias that were studied 24-36 hours following occlusion. The sites of origin of 26 tachycardias were determined to be in the subendocardium by using extensive epicardial, endocardial and intramural mapping techniques and were verified by demonstrating unaltered activation sequences during pacing from these earliest sites. Epicardial breakthrough followed earliest directly recordable ventricular activity by as little as 7 msec. Without endocardial mapping many of these tachycardias would have been incorrectly identified as originating in the fascicles or epicardium. The sites of epicardial breakthrough were anatomically distant from the sites of origin by a markedly varying extent (5mm to 6cm). Two rhythms might be close in their sites of earliest epicardial appearance yet distant on the endocardium or vice versa. We conclude that epicardial mapping may not be sufficient to identify or predict the origins of many ventricular tachycardias and that the success of surgery to abolish these arrhythmias may be enhanced by preoperative and intraoperative endocardial mapping.
Animals↗
Recurrent sustained ventricular tachycardia 3. Role of the electrophysiologic study in selection of antiarrhythmic regimens.
Twenty patients with recurrent sustained ventricular tachycardia (VT) underwent serial electrophysiological studies (EPS) 1) to determine the predictive value of the EPS in the selection of antiarrhythmic therapy, and 2) to establish the therapeutic efficacy of available antiarrhythmic agents. In each patient VT could be reproducibly initiated by programmed stimulation. After control EPS, the effects of several drugs (lidocaine, procainamide, quinidine, disopyramide and diphenylhydantoin) on the ability to initiate VT were assessed. An oral regimen was chosen on the basis of acute EPS and its effectiveness was evaluated by repeat EPS in 24--72 hours. Blood levels achieved acutely were used as guidelines to chronic therapy. In 14 patients the initiation of VT was prevented by the acute administration of one or more agents. In 13 of these patients, a chronic oral regimen based on these results prevented recurrence of VT with a three- to 27-month follow-up. In the remaining patient, oral therapy could not achieve blood levels of procainamide shown to be effective intravenously, and VT recurred. In six patients no single drug or drug combination was effective during acute EPS, and VT recurred in all while on therapy with the agent shown to make initiation of VT most difficult. Procainamide prevented VT in nine patients; quinidine in three patients; lidocaine in three patients; diphenylhydantoin in two patients; and disopyramide in one patient. The mean duration of EPS studies was 4.5 days. This study suggests that serial EPS provides rapid identification of successful antiarrhythmic therapy and can predict in which patients conventional therapy would be ineffective, thereby identifying patients requiring more aggressive modes of therapy.
Administration, Oral↗
The origin of ventricular arrhythmias 24 hours following experimental anterior septal coronary artery occlusion.
The anterior septal coronary artery was acutely ligated in 16 open-chest anesthetized dogs to produce an infarct of the septal myocardium. Twenty-four hours following occlusion complete epicardial mapping and extensive plunge electrode recording techniques were used to localize the sites of origin and patterns of activation of the ventricular tachyarrhythmias that developed during recovery. The earliest electrical activity for 13 individual rhythms was recorded from surviving septal subendocardial Purkinje fibers at the margins of the infarct, in the right or left ventricle, directly underlying the sites of earliest epicardial breakthrough. The sites of origin were verified by demonstrating unchanged activation sequences during pacing through the electrode sites which recorded the earliest activity. None of the arrhythmias arose from the His bundle or bundle branches despite the fact that these tissues course directly through the necrotic septum. The data presented supports the hypothesis that ventricular arrhythmias occuring in the 24-36 hour post acute infarction period may originate in the surviving subendocardial Purkinje system. Our experimental model shows that in cases in which a malignant rhythm arises from a focus, whether it is due to enhanced automaticity or local re-entry, epicardial mapping alone may not identify the source of the arrhythmias. Extensive endocardial mapping may provide a more rational basis for surgical interventions designed to abolish these arrhythmias.
Animals↗