Menashe B. Waxman

On-line epicardial mapping of intraoperative ventricular arrhythmias: initial clinical experience

An on-line automatic mapping system was developed for beat by beat display of epicardial activation during ventricular tachycardia induced at the time of cardiac surgery. A sock array of 110 button electrodes was used to record and display local activation on a video monitor at 8.3 ms intervals. On instant replay in slow motion, epicardial pacing sites were accurately localized to the nearest electrode. Local unipolar electrograms were also recorded, first from the sock array, then from an array of 16 transmural needle electrodes. The epicardial display was verified by retrospective manually derived maps using the recorded epicardial electrograms. In four patients with coronary artery disease and recurrent inducible ventricular tachycardia, earliest epicardial activation was located on slow motion replay within 1 minute. Subendocardial sites of early activation were located within 10 minutes by replay of electrograms from the needle array before ventriculotomy. Transmural and endocardial resection of these sites prevented inducibility of the tachycardia on postoperative electrophysiologic study in three of the four patients. There has been no clinical recurrence of ventricular tachycardia after 3 to 14 months of follow-up despite cessation of antiarrhythmic therapy in three of the patients. This technique has unique advantages over existing mapping methods. It provides beat by beat display of activation sequences so that clinical tachycardias that are short in duration or pleomorphic in configuration now become amenable to mapping. In addition, it markedly shortens total time on cardiopulmonary bypass.

Torsade de pointes ventricular tachycardia a complication of disopyramide shared with quinidine

Two cases of documented torsade de pointes ventricular tachycardia in association with the use of disopyramide are described. One patient had previously experienced an episode suggestive of quinidine induced ventricular tachycardia while the other developed ventricular tachycardia during quinidine treatment which was later exacerbated and sustained by the administration of disopyramide. Both patients exhibited a prolonged QTc or QUc interval at the time of the arrhythmia. These cases suggest that a propensity of ventricular arrhythmias induced by quinidine may identify individuals who are likely to develop similar arrhythmias disopyramide treatment as well.

Phenylephrine (Neo-synephrine) Terminated Ventricular Tachycardia

Five cases of recurrent, wide QRS complex tachycardia which could be terminated with phenylephrine are presented. These cases fulfilled all accepted criteria for ventricular tachycardia. Carotid sinus massage with and without edrophonium hydrochloride had no effect on the ventricular activity but selectively slowed the atrial rate in cases of atrioventricular (A-V) dissociation, or blocked retrograde conduction in cases of A-V association. The mechanism of action of phenylephrine remains unclear.These cases have many possible implications. Two of the most important are: 1) phenylephrine may be useful in terminating certain cases of ventricular tachycardia; 2) termination of an unknown, regular, wide QRS complex tachycardia by phenylephrine, and possibly other pressors, can no longer be taken as proof of a supraventricular mechanism.

Effects of posture, Valsalva maneuver and respiration on atrial flutter rate: an effect mediated through cardiac volume.

The effects of passive upright tilting from 0 degrees to +60 degrees (n = 27), Valsalva maneuver (n = 16) and respiration (n = 10) on the rate of atrial flutter were studied in 27 patients. After tilting to +60 degrees, the atrial flutter cycle length shortened in all patients from 247.5 +/- 7 to 236.7 +/- 6.9 ms (range of shortening 1 to 21 ms, p less than 0.001). The Valsalva maneuver (strain of 40 mm Hg) shortened the flutter cycle length during the strain (phase 2) from 242.2 +/- 4.6 to 230.5 +/- 5 ms (range of shortening 2 to 19 ms, p less than 0.001). In 10 patients whose respiration was monitored, the flutter cycle length consistently prolonged during inspiration and shortened during expiration. Combined beta-adrenergic and muscarinic receptor blockade in six patients did not significantly alter the flutter cycle length at rest or the effects of the various maneuvers on the changes in flutter cycle length. This study revealed that the atrial flutter cycle length can be shortened by passive upright tilting, the strain phase of the Valsalva maneuver and expiration. Changes in flutter cycle length were independent of autonomic tone, implying that by decreasing cardiac volume, these maneuvers affect characteristics of the atrial flutter circuit, thereby producing dynamic changes in the rate of atrial flutter.

Depressed Conduction and Unidirectional Block in Purkinje Fibres

Re-entry is a mechanism basic to many of the rhythm disturbances that are clinically encountered. An understanding of such disturbances occurring at the ventricular level is perhaps all the more urgent in view of the potentially lethal consequence of ventricular arrythmias. In order to gain some further insight into conditions necessary for re-entry to occur within the Purkinje system we examined the character of depressed conduction produced within the system by a method of focal cooling. Others have used techniques such as ‘blocking current’ (921), graded pressure (546) and local hyperkalemia (160). Focal cooling had the advantages of allowing fine control of the degree of depressed conduction and could be rapidly and completely reversed to allow repeated observations in the same preparation. Furthermore many of the effects produced were qualitatively similar to those reported using other techniques, suggesting that depressed conduction has certain basic characteristics no matter how it arises.

Demand Pacemaker Malfunction Due to Abnormal Sensing Report of Two Cases

Two cases with external demand pacemakers are presented because of abnormal prolongation in the pacing interval. In both cases, pacemaker inhibition was caused by signals which were not recorded by the conventional surface electrocardiograms. In one case, inhibition was related to a partial lead fracture which generated a voltage transient in the region of the T wave. In the other case, inhibition was caused by current emitted from a faulty pacemaker unit. In both cases precise localization of the problem was possible by simple bedside recordings and measurements.

The reflex effects of tachycardias on autonomic tone.

Tachycardias, irrespective of their origin, mechanism, or cause, alter cardiovascular function because they affect cardiac filling and stroke volume.’-3 Blood pressure and pulse pressure decline in direct relationship to the rate, atrioventricular synchrony, and cardiac function.334 This reduces stretch on the pressure-sensitive baroreceptors which are located mainly in the carotid The reduced pressure decreases the afferent nerve traffic from the baroreceptors to the vasomotor centers. This in turn augments sympathetic efferent tone and withdraws vagal efferent tone. These changes affect the ongoing tachycardia rate, the blood pressure recovery, as well as the overshoot of the blood pressure following termination of the tachycardia.’ The overshoot of the blood pressure activates vagal tone which in turn slows the heart rate for a period of time after the tachycardia ends.’ and thus the peak stimulus for sympathetic compensation and vagal withdrawal occurs at this time.’ While autonomic tone may not play a significant role in the initiation of a given tachycardia, once the arrhythmia is established, changes in neural tone can exert significant effects on the arrhythmia depending on its location, innervation, and responsiveness to autonomic As well, changes in autonomic tone are vital in restoring cardiac output and blood pressure during the tachycardia. While the fall in blood pressure leads to a reflex increase in sympathetic tone through extracardiac barorecept~rs ,~’~ signals from ventricular and atrial mechanoreceptors may result in an opposite effect.”.’* During supraventricular and ventricular tachycardias, atrial pressure and ventricular diastolic pressure rise d r a m a t i ~ a l l y ~ * ~ ~ ’ ~ ’ ~ (FIGURE 1 ) . The increased filling pressure can activate cardiac mechanoreceptors leading to a reflex withdrawal of sympathetic tone and an enhancement of vagal tone.”.’2 Thus, during paroxysmal tachycardia, the cardiac”.I2 and extracardiac baroreceptorss,6 may result in opposite types of reflex changes in sympathetic tone. It is also pertinent to point out that stretch receptors in the atrium and possibly in the ventricles cause release of atrial natriuretic factor (ANF) which not only promotes a Tachycardias generally cause a maximum blood pressure fall a t their

Recurrent paroxysmal supraventricular tachycardia: A complication of ventricular pacing in a patient with occult Wolff-Parkinson-White syndrome

A 60 year old man suffering from syncope believed to be due to the sick sinus syndrome was treated with a permanent demand ventricular pacemaker. This led to almost continous bouts of paroxysmal supraventricular tachycardia (SVT) over the ensuing two years, mistakenly believed to be part of the sick sinus syndrome. Careful study showed that this man had a type A Wolff-Parkinson-White accessory atrioventricular connection which consistently conducted retrogradely, but only rarely antegradely, during applications of carotid sinus massage. Episodes of SVT were repeatedly induced whenever ventricular-paced impulses captured the atria retrogradely. All episodes of SVT stopped when the ventricular pacemaker was removed. Following insertion of an atrial pacemaker, the patient had no episodes of SVT or syncope over a nineteen month follow-up period. This case illustrates the care required in selecting a proper site for protective pacing in patients who suffer from paroxysmal SVT.

Slowing of the Atrial Flutter Rate During 1:1 Atrioventricular Conduction in Humans and Dogs: An Effect Mediated Through Atrial Pressure and Volume

Atrial Flutter Rate and Atrial Pressure. Introduction: During atrial flutter the effects of 1:1 atrioventricular (AV) conduction on the rate of atrial flutter was studied in 12 patients and 14 dogs.

Effects of Autonomic Tone on Tachycardias

The pioneering work of Bernard [70B], Gaskell [40G], Langley [12L], Cannon [12C], Herring [76H], and Heymans and Neil [84H, 85H] established that the autonomic nervous system plays a major role in regulating cardiac function, arterial and venous tone, blood pressure, and heart rate [127S]. In the last 30 years, beginning with a classification of adrenergic receptors by Alquist in 1948 [38A], there has been intense research into every facet of autonomic control of cardiovascular function [1A, 118B, 89K, 44V]. This has included exacting anatomic descriptions of afferent and efferent pathways [4A, 91H], central interconnections [87K], cardiac localization of receptors and nerves [3J, 39K], physiologic description and measurement of diverse reflexes [99C, 106D, 47F, 88K, 58L, 92L], measurement of neurotransmitters [30], the development of selective alpha- and beta-receptor agonists and antagonists [22D, 182W], characterization of the mechanisms of modulation of the release and reuptake of neurotransmitters [241, 10L, 12V, 5Y), and elucidation of the mechanisms of binding and action of agonists and antagonists on cell receptors [33L, 34L, 35R, 172S, 228S, 36W, 37W].