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L N Horowitz

Publications and source records attributed to L N Horowitz.

156 records · Page 9Linked to original sources
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↗
PubMed1978

Continuous local electrical activity. A mechanism of recurrent ventricular tachycardia.

Although the mechanism of most episodes of recurrent ventricular tachycardia (VT) is believed to be re-entry, definitive proof of this hypothesis has heretofore been unavailable in man. Using programmed stimulation and ventricular endocardial mapping we studied three patients in whom the initiation of VT was dependent upon developing a critical degree of fractionation and delay in local left ventricular electrograms. When electrical activity spanned diastole, VT ensued. Maintenance of VT was associated with continuous electrical activity resembling "local fibrillation" while termination of VT required cessation of this continuous activity. During sinus rhythm the electrogram recorded from the areas which subsequently developed continuous activity showed markedly fractionated and prolonged electrical activity exceeding 100 msec in duration. We feel these observations of the temporal relationship of continuous activity with the development of VT represent the first documentation of the re-entrant nature of this arrhythmia in man.

Electrocardiography↗
PubMed1978

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↗
PubMed1978

Limitations of routine long-term electrocardiographic monitoring to assess ventricular ectopic frequency.

Variations in the frequency of ventricular premature depolarizations (VPDs) were evaluated with three consecutive 24-hour long-term electrocardiography monitor recordings from 15 clinically stable patients with various cardiac disorders. Mean hourly VPD frequencies ranged from 37--1,801 per hour. Data were subjected to 4 and 5 factor nested analyses of variance. The extent of spontaneous variation in arrhythmia frequency that occurred in individual patients from day to day was 23%, between 8-hour periods within days was 29%, and from hour to hour was 48%. In addition, the variability between repeated three-day monitoring periods over time was quantified in five patients and found to be 37%. This analysis determined that to distinguish a reduction in VPD frequency attributable to therapeutic intervention rather than biologic or spontaneous variation alone required a greater than 83% reduction in VPD frequency if only two-24-hour monitoring periods were compared, and greater than 65% reduction if two 72-hour periods were compared. The limitations of routine 24-hour electrocardiographic monitoring must be considered in diagnostic and therapeutic decision-making.

Adult↗
PubMed1978

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↗
PubMed1976

Subendocardial origin of ventricular arrhythmias in 24-hour-old experimental myocardial infarction.

In 12 anesthetized open-chest dogs, ventricular epicardial activation maps were constructed and electrograms were recorded from the bundle of His, left bundle branch, and subendocardial Purkinje fibers 24 hours following Harris 2-stage ligation of the left anterior descending coronary artery. All animals developed ectopic ventricular depolarizations and/or ventricular tachycardia. The earliest area of epicardial activation was located along the border of the infarct in the left ventricle in all animals. Bipolar recording from various levels of the conduction system and ventricular myocardium revealed that the earliest recorded electrical activity originated in subendocardial Purkinje fibers which had survived the acute myocardial infarction. The origin of these arrhythmias was further studied by pacing through the electrode which had recorded the early Purkinje activity and comparing the surface ECG and activation sequence with that of the spontaneous rhythm. These data tend to support the hypothesis that ventricular arrhythmias occurring 24-72 hours following acute myocardial infarction have their origin in the subendocardial Purkinje network which has survived the infarction.

Animals↗
PubMed1975

Effects of aminophylline on the threshold for initiating ventricular fibrillation during respiratory failure.

Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PC02 70 to 100 mm Hg: P02 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.

Acid-Base Equilibrium↗
PubMedDate not supplied

Efficacy and toxicity of amiodarone for the treatment of supraventricular tachyarrhythmias.

Amiodarone is an effective agent for all types of supraventricular tachyarrhythmias regardless of mechanism and may, in fact, control a high percentage of supraventricular tachyarrhythmias refractory to conventional antiarrhythmic agents. However, its toxicity should temper enthusiasm for the use of the medication in non-life-threatening arrhythmias. As always, when recommending specific therapies the potential benefit should be weighed in light of the related risk. In patients with life disordering, drug-refractory atrial fibrillation, it seems reasonable to attempt control with amiodarone. Likewise in patients with ectopic atrial tachycardias refractory to conventional agents, this seems reasonable as well. Other and better therapies are available for patients with life-threatening arrhythmias associated with the Wolff-Parkinson-White syndrome. While amiodarone is moderately effective in these patients, the advent of improved surgical techniques and the relatively low risk of an operation make surgery the treatment of choice. The role of IV amiodarone, acutely, in the treatment of supraventricular tachyarrhythmias remains to be defined.

Amiodarone↗
PubMedDate not supplied

Improved pacemaker fixation and performance using a modified finned porous surfaced tip lead.

A simple method was used to modify the tip of a porous surfaced finned pacemaker lead. Comparison between the modified and the unmodified pacemaker electrodes was carried out in experimental animals and in humans. The incidence of early lead dislodgement, acute trapping and pacing thresholds was recorded. The study revealed improved overall performance with the modified pacemaker lead.

Adult↗