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Biomedical subjects

L N Horowitz

Publications and source records attributed to L N Horowitz.

At least 109 records · Page 6Linked to original sources

Role of catheter mapping in the preoperative evaluation of ventricular tachycardia.

Although surgery is an accepted mode of therapy for refractory ventricular tachycardia, routine aneurysmectomy has yielded unpredictable results. This is believed to have occurred because there was no documentation that the arrhythmia actually arose from resected aneurysmal tissue. Catheter endocardial mapping has been used to localize preoperatively the area of origin of the arrhythmia. This technique has established that the arrhythmias arise near the endocardium at the borders of the aneurysm or infarction, or both. These regions, particularly when they occur in the interventricular septum, are not resected by standard aneurysmectomy. Intraoperative endocardial and epicardial mapping have validated the accuracy of this technique. We believe that catheter mapping should be performed before surgery for the following reasons: (1) In some patients ventricular tachycardia is not inducible in the operating room (for example, automatic ventricular tachycardia can be mapped in the catheterization laboratory); (2) in some patients not all morphologic forms of tachycardia can be induced or mapped intraoperatively because of failure of inducibility, time constraints or degeneration of the arrhythmia to ventricular fibrillation; and (3) intraoperative endocardial mapping occasionally cannot be performed because of lack of technical skills, physical factors such as mural thrombosis, or the inability to induce ventricular tachycardia after aneurysmectomy. Other methods currently being evaluated to localize the origin of ventricular tachycardia that do not require induction of arrhythmia are analysis of ventricular electrograms during sinus rhythm and pacemapping.

Cardiac Catheterization↗

Electrophysiologic residua and sequelae of surgery for congenital heart defects.

Postoperative arrhythmias may occur in any patient who undergoes intracardiac surgery for a congenital heart defect. The correction of certain intracardiac heart defects predisposes to a large incidence of cardiac arrhythmias. Ventricular arrhythmias and conduction disturbances are seen after correction of tetralogy of Fallot, ventricular septal defect and atrioventricular canal defect. Supraventricular arrhythmias and sinus nodal dysfunction may be seen after surgery for transposition of the great arteries or atrial septal defect. The identification, evaluation and treatment of these patients are discussed.

Arrhythmias, Cardiac↗

Amiodarone for control of sustained ventricular tachyarrhythmia: clinical and electrophysiologic effects in 51 patients.

We evaluated the electrophysiologic effects of amiodarone and its ability to control ventricular arrhythmia in a selected group of 51 patients with refractory sustained ventricular arrhythmia. Amiodarone in doses of 400 to 800 mg/day prolonged refractoriness in the atria, atrioventricular (AV) node, and ventricle as well as conduction through the AV node and His-Purkinje system. Although it had no effect on measurements of sinus nodal function (sinus nodal recovery time and sinoatrial conduction time), it prolonged the sinus cycle length and 2 patients required a permanent pacemaker for symptomatic sinus bradycardia. Amiodarone did not alter the ease of inducibility in any consistent manner, and only 5 of 43 patients (12%) who had inducible ventricular tachycardia before amiodarone therapy had none induced during amiodarone treatment. The clinical effectiveness of amiodarone could be evaluated in 46 patients followed up for 8.6 +/- 6 months (range 0.5 to 22). It provided effective therapy in 23 patients (50%), partly effective therapy in 13 (28%), and was ineffective in 10 (22%). Adverse effects were noted in 28 of 51 patients (55%), and in 11 of these (22%) the drug had to be discontinued because of adverse effects. We conclude that amiodarone is a useful agent for the treatment of refractory sustained ventricular arrhythmia. Its use should be reserved for patients with life-threatening sustained arrhythmia because of the significant incidence of adverse effects. Furthermore, good clinical response can be observed in patients receiving amiodarone in spite of continued inducibility.

Adolescent↗

The incidence and clinical significance of epicardial late potentials in patients with recurrent sustained ventricular tachycardia and coronary artery disease.

Seventy-eight patients with ventricular tachycardia associated with coronary artery disease underwent intraoperative mapping while in sinus rhythm to evaluate the frequency and significant of late potentials. In 30 of these patients, the surface ECG was subjected to signal averaging to correlate the incidence and duration of low-amplitude, delayed electrograms with the presence of late potentials recorded during epicardial mapping. One to four epicardial late potentials were observed in nine patients (11.5%). These nine patients did not differ hemodynamically from patients without late potentials. In four patients, the site of epicardial breakthrough during ventricular tachycardia bore no relationship (i.e., greater than 3 cm away) to the late potential or the site of origin of the tachycardia. In the five other patients with late potentials, epicardial breakthrough and site of origin of ventricular tachycardia were closely related to the free wall of an apical aneurysm. However, three of these patients had additional tachycardias from disparate sites. Twenty-seven of 30 patients in whom signal averaging was used had a low-amplitude signal in the terminal 40 msec of the amplified QRS complex. In 24 of these 27 patients (89%), the low-amplitude tail was demonstrated in the absence of epicardial late potentials. We conclude that epicardial late potentials are found infrequently in patients with ventricular tachycardia associated with coronary artery disease; epicardial late potentials cannot be used to localize ventricular tachycardia; and the specific low-amplitude tail on the signal-averaged electrogram is unrelated to epicardial events.

Adult↗

Relation of the endocardial and epicardial ventricular fibrillation thresholds of the right and left ventricle.

Ventricular fibrillation thresholds were measured on the endocardium and epicardium of the right or left ventricle, or both, in 13 dogs. The electrodes, introduced through a right or left atriotomy to avoid injury to the ventricles, were aligned opposite and parallel to each other on the endocardium and epicardium. The ventricular fibrillation threshold was measured during atrial pacing by delivering a train of impulses to the ventricle during the vulnerable period after every 12th paced complex in 1 milliampere (mA) increments of current until fibrillation ensued. The mean (+/- standard deviation) right ventricular epicardial and endocardial fibrillation thresholds were 18.3 +/- 5.3 and 17.6 +/- 5.3 mA, respectively, (values not significantly different). However, the fibrillation threshold of 36.1 +/- 9.5 mA in the left ventricular epicardium was significantly higher than the value of 20.7 +/- 9.4 mA on the left ventricular endocardium. These data suggest that the proximity of the fibrillating electrodes and Purkinje network may be a factor in the measurement of ventricular vulnerability.

Animals↗

Human ventricular refractoriness: effects of increasing current.

The ventricular effective refractory period is commonly employed as a measurement of ventricular excitability. Because the current strength used to make this determination varies among laboratories, the relation of refractoriness and current was examined over a range of current strengths from 0.1 to 10 mA. Sixty determinations of refractoriness at variable current strengths were made in 40 patients using the extrastimulus technique with a rectangular pulse of 1 ms duration. These data were obtained by measuring the effective refractory period at threshold current and at 0.25 to 0.50 mA increments from threshold up to 10 mA. In these studies the drive stimulus (S1) and extrastimulus (S2) were kept at the same amplitude. In all patients the ventricular effective refractory period decreased as the current increased. The total decrease ranged from 8 to 100 ms (mean +/- standard deviation 36.9 +/- 17.1). The current strength at which the ventricular effective refractory period became fixed (that is, less than 2 ms change in ventricular effective refractory period with further increase in current strength) varied among the patients, but in all instances equaled or exceeded 1.8 mA, which in all but three patients was greater than three times threshold. The curves relating current strength and refractoriness were shifted to the left at shorter cycle lengths with no change in threshold. These data suggest that (1) current strength-effective refractory period curves more completely characterize ventricular excitability than does a ventricular effective refractory period at single current strength; and (2) studies of drug effects, alterations of autonomic tone, or reentrant arrhythmias, which may affect or are affected by ventricular refractoriness, may be enhanced by more complete measurements of refractoriness afforded by the current strength-effective refractoriness curves.

Adolescent↗

Idiopathic recurrent sustained ventricular tachycardia in children and adolescents.

The electrophysiologic characteristics of recurrent sustained ventricular tachycardia were studied in seven pediatric patients. The mechanisms of the ventricular tachycardia were evaluated using programmed electrical stimulation. Ventricular tachycardia could be reproducibly initiated in two patients and terminated in one patient in the basal state. It could be initiated in one additional patient and terminated in two additional patients after administration of a type IB drug. In four patients, ventricular tachycardia could not be initiated or terminated by programmed electrical stimulation. The site of origin of the ventricular tachycardia determined by catheter endocardial mapping was the right ventricular outflow tract in four patients, the interventricular septum in two patients and the inferior left ventricle in one patient. The ventricular tachycardia more frequently had an automatic than a reentrant mechanism, and originated more often in the right than in the left ventricle; it was not frequently associated with structural heart disease in this group of patients.

Adolescent↗

Anatomic and electrophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation.

In 108 patients with reproducible initiation of ventricular tachycardia by programmed ventricular stimulation, the ventricular tachycardia was initiated only by left ventricular stimulation in 12 (11 percent). Programmed ventricular stimulation included single and double extrastimuli extrastimuli at three cycle lengths and bursts of rapid pacing to cycle lengths of 250 ms. Clinical, electrocardiographic, angiographic, hemodynamic and electrophysiologic data were available in 74 of 96 patients with ventricular tachycardia initiated by right ventricular stimulation (Group A) and in all 12 patients with ventricular tachycardia initiated only by left ventricular stimulation (Group B). there were no significant differences between Groups A and B in clinical characteristics, hemodynamics or presence and site of infarction or aneurysm. Comparison of electrophysiologic variables revealed no significant differences between Groups A and B mean A-H interval (92 +/- 22 versus 89 +/- 15 ms, respectively), H-V interval (59 +/- 15 versus 59 +/- 15 ms) or right ventricular (241 +/- 38 versus 260 +/- 40 ms) or left ventricular (232 +/- 28 versus 251 +/- 42 ms) effective refractory period. Ventricular tachycardia with right bundle branch block and superior axis was more prevalent in Group B (92 percent versus 31 percent, p less than 0.001) but was observed in 32 patients in Group A. It is concluded that 11 percent of patients with clinically documented sustained ventricular tachycardia will require left ventricular programmed stimulation to reproducibly initiate the tachycardia. No clinical, anatomic, electrocardiographic or electrophysiologic features can predict whether left ventricular programmed stimulation will be required. Because initiation of ventricular tachycardia by programmed ventricular stimulation has important prognostic and therapeutic implications in such patients, stimulation should be performed from the left ventricle when the tachycardia is not initiated by stimulation from the right ventricle.

Adolescent↗

Torsades de pointes: electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities.

Electrophysiologic studies were performed in 21 patients who had torsades de pointes. This ventricular tachyarrhythmia, characterized by rapid (200-250 beats/min) and irregular paroxysms and progressively varying QRS amplitude and polarity, occurred in the absence of electrolyte disturbance, antiarrhythmic drug therapy or acute ischemia. The QTc interval was prolonged in seven of 21 patients. Electrophysiologic study included ventricular pacing with the introduction of one to three extrastimuli and rapid ventricular pacing. The effect of i.v. procainamide or quinidine in these patients was also studied. Torsades de pointes was inducible n 19 of 21 patients. Induced episodes closely resembled spontaneous episodes. Torsades de pointes spontaneously progressed to ventricular tachycardia with a uniform morphology in three patients and to ventricular fibrillation in four. In eight patients, procainamide or quinidine converted torsades de pointes into typical reentrant ventricular tachycardia. Our data suggest that torsades de pointes in this setting may be a rapid reentrant ventricular tachycardia closely related to recurrent sustained ventricular tachycardia and a precursor to ventricular fibrillation and sudden death.

Adult↗

Surgical treatment of ventricular arrhythmias in coronary artery disease.

Serious ventricular arrhythmias, a common complication of coronary artery disease, frequently respond to medical management. When pharmacologic and pacemaker therapy fail to control them, however, surgical therapy must be considered. In this review we assess the efficacy of surgical treatment of these arrhythmias. Coronary revascularization fails to reduce the frequency and complexity of ventricular ectopic activity and may exacerbate them. Recurrent ventricular fibrillation due to acute, reversible ischemic events may respond favorably to coronary revascularization. Recurrent ventricular fibrillation associated with recent myocardial infarction when unresponsive to medical therapy can be managed with coronary revascularization and infarctectomy with comparatively good results. Recurrent sustained ventricular tachycardia is not optimally treated with coronary artery bypass grafting and myocardial resection. Operations guided by activation mapping that isolate or destroy the site of origin of the ventricular tachycardia show promise.

Arrhythmias, Cardiac↗

Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest.

Fifty-two patients resuscitated from cardiac arrest underwent electrophysiologic studies. The earliest documented arrhythmia at the time of initial or recurrent (18 patients) cardiac arrest was ventricular fibrillation (30 patients) or ventricular tachycardia (20 patients); in 2 patients no arrhythmia was documented before defibrillation. Programmed ventricular stimulation revealed inducible arrhythmias in 33 patients (63 percent). Of the 30 patients with ventricular fibrillation as the initial arrhythmia, 13 had inducible arrhythmias--ventricular fibrillation (4 patients), sustained ventricular tachycardia (6 patients) and nonsustained ventricular tachycardia (3 patients). In the 20 patients with ventricular tachycardia as the initial arrhythmia, sustained ventricular tachycardia was initiated in 17 patients and torsade de pointes in 1. Patients with inducible arrhythmias had longer mean A-H and H-V intervals than those without inducible arrhythmias (91.1 versus 76.6 ms and 62.5 versus 50.3 ms, respectively). Prolonged H-V intervals (17 of 33) and intraventricular conduction defects (18 of 33) were more common in patients with than in those without inducible arrhythmias (4 of 19 and 7 of 19, respectively). Mean cardiac index was lower (2.4 versus 3.9 liters/min per m2), left ventricular end-diastolic pressure higher (17.0 versus 9.4 mm Hg), and ejection fraction lower (36.1 versus 57.2 percent) in the group with inducible arrhythmias than in those in whom no arrhythmia could be induced. These data suggest that (1) ventricular tachycardia often precipitates cardiac arrest; and (2) electrophysiologic testing may provide data on which to base therapy in patients resuscitated from cardiac arrest.

Adult↗

Ventricular resection guided by epicardial and endocardial mapping for treatment of recurrent ventricular tachycardia.

Recurrent, medically refractory ventricular tachycardia is usually associated with ventricular aneurysms after myocardial infarction, but aneurysmectomy alone has not been consistently effective in abolishing this dangerous arrhythmia. Therefore, we have used endocardial and epicardial mapping during induced ventricular tachycardia in 30 consecutive patients to identify the probable site where arrhythmia originated in the endocardial tissue. Complete resection of the site was possible in 27 patients, and partial resection in three. In addition aneurysmectomy was performed in 27 patients, and coronary-bypass grafting in 21. There were two operative and three late nonarrhythmic deaths. None of the 25 surviving patients have had ventricular tachycardia during follow-up of four to 28 months; three patients, who had incomplete resections, have required antiarrhythmic drugs. We conclude that surgical therapy of recurrent ventricular tachycardia can be improved through identification of the endocardial origin of the arrhythmia followed by appropriately guided resection.

Adult↗