Biomedical subjects
Publications and source records attributed to D E Ward.
Stimulation of skeletal muscle is a fairly common complication of permanent cardiac pacing. The usual cause is direct apposition of the anode of a unipolar pacemaker with muscle surrounding the pocket. Other causes include electrode insulation defects and electrode displacement. In this report we describe an unusual cause of muscle stimulation related to direct current leakage from the pacemaker.
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We devised a modified artificial anterior chamber that enables Barraquer microkeratome keratectomies on corneas preserved in McCarey-Kaufman medium. It consists of a hydraulic system, which creates a positive pressure of 60 mm Hg or more. An added rotating ring serves as a base to the microkeratome's tracks and varying diameters of lamellar sections can be obtained. This device allows the surgeon to use readily available corneas with scleral rims preserved in McCarey-Kaufman medium rather than whole eyes to obtain precise lamellar sections.
A 25 year old man had experienced virtually incessant ventricular tachycardia since the age of 16 years, and complained of increasing lethargy and shortness of breath over the past 5 years. Despite medical therapy with numerous conventional antiarrhythmic agents, no single drug or combination of drugs had successfully controlled the tachycardia. Isotope and contrast angiography revealed an enlarged left ventricle with poor function. Electrophysiological studies demonstrate earliest endocardial activation at the left ventricular apex. No electrical procedure terminated tachycardia. Following institution of amiodarone, continuous ECG monitoring revealed periods of sinus rhythm alternating with periods of ventricular bigeminy. Repeat isotope angiography indicated a considerable improvement in L.V. function. There was a corresponding reduction in heart size on the chest radiograph. Clinical improvement was evidenced by disappearance of lethargy and shortness of breath. This report demonstrates that amiodarone, a new antiarrhythmic agent, may suppress long standing incessant ventricular tachycardia resistant to other antiarrhythmic agents. The marked reduction in heart size on amiodarone may suggest that the associated cardiomegaly is secondary to tachycardia.
Five patients aged between 27 and 48 years were referred for investigation of recurrent paroxysmal tachycardias. Electrophysiological studies revealed concealed ventriculoatrial accessory pathways in two patients, possible atrionodal pathways in two patients and dual intranodal pathways in one patient. During electrophysiological study, particular attention was paid to methods of terminating tachycardia by pacing techniques including single or double atrial and ventricular extrastimuli, atrial or ventricular underdrive, atrial overdrive pacing, and in two patients, rapid ventricular pacing. 'Autodecremental' atrial pacing was employed in all five patients and autodecremental ventricular pacing in two patients. This system is controlled by a microprocessor interfaced with a stimulator. When tachycardia of a cycle length less than 375 ms is sensed the system initiates pacing sequences. The initial stimulus is introduced at an interval less than the tachycardia cycle determined by a preset decremental value D. Each subsequent pacing interval is reduced by the value of D resulting in a gradual acceleration of pacing. The total duration of pacing is limited by the value of the pacing period (P). The final pacing rate is determined by P but cannot exceed 275 bpm (cycle length of 218 ms). Both P and D are operator programmable variables. Tachycardias of a cycle length less than 218 ms do not activate the pacemaker. The postpacing sensing deadtime of the system is set at 50 ms. In three patients, double atrial extrastimuli or atrial overdrive initiated atrial flutter or fibrillation. Autodecremental atrial pacing was successful in converting tachycardia to sinus rhythm in all five patients without initiation of other tachyarrhythmias. Autodecremental ventricular pacing was successful in one of the two patients in which it was used. This new modality of pacing has several theoretical advantages over conventional methods: the decremental mode may avoid stimulation in the vulnerable period and minimizes the risk of initiating other tachyarrhythmias; gradual acceleration of pacing over a short period results in stimulation at different phases of the tachycardia cycle length; and the operator variables D and P provide a flexible system which may be adjusted to suit a particular patient and tachycardia. The development of a fully implantable programmable system is made attractive by the simplicity and adaptability of this technique.
Changes in the QT and QTc intervals were studied in 16 patients by atrial pacing at rates of 100, 130, and 150 beats/minute. In all patients the measured QT shortened when the atrial paced rate was increased, but when corrected for heart rate the QTc lengthened. Intravenously administered propranolol produced a bradycardia and a lengthening of the QT interval in 15 of the 16 patients studied. When the QT interval was corrected for heart rate using Bazett's formula the QTc was shortened in 13 patients, unchanged in one, and lengthened in two. However, when the QT interval was measured at identical atrial paced rates the QT of the 15 patients studied was lengthened in 10 and unchanged in five. In none was the QT interval shortened. These results show firstly that Bazett's formula is unsuitable for correction of QT interval changes induced by atrial pacing, and secondly that, though intravenously administered propranolol usally produces a shortening of the QTc, when its effect is assessed directly by using an identical atrial paced rate the QT interval usually lengthens, or may remain unchanged, but never shortens. It is suggested that the formal assessment of drug induced QT interval changes should be made at identical atrial paced rates.
Oral amiodarone, an iodine-containing antiarrhythmic agent, was administered to 72 patients with recurrent paroxysmal tachycardias. Thirty-nine patients had tachycardias associated with the Wolff-Parkinson-White syndrome, 15 patients had paroxysmal atrial fibrillation unassociated with the Wolff-Parkinson-White syndrome, and 18 patients had ventricular tachycardia. In all patients, the frequency of symptomatic attacks had not been reduced by at least three other antiarrhythmic agents alone or in combination. The response to amiodarone treatment was graded according to the patients' subjective response (total suppression, partial suppression, and no effect). Overall, 57 per cent of patients had total abolition of attacks and another 22 per cent had a partial suppression of attacks. Side effects, the most common of which were photosensitivity and gastrointestinal upsets, occurred in 44 per cent and were sufficiently severe to warrant withdrawal of treatment in 15 per cent. These results confirm that amiodarone is of considerable value in the treatment of recurrent paroxysmal arrhythmias resistant to other drugs.
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During the 1st year of operation of a national 24-hour ambulatory ECG-monitoring service, 531 recordings were collected. The information from these recordings and accompanying patient diaries were classified according to the indication for monitoring, the presence or absence of the 'indicated' sympton or other symptom in the diary and the presence or absence of correlating arrhythmias on the tape. On the basis of this categorization 7.5% of recordings were considered completely diagnostic (indicated symptom noted in diary with correlating arrhythmias). An additional 26.6% or recordings, although not completely diagnostic, were considered clinically useful in that they provided information regarding the relationship of symptoms to arrhythmias or the presence or absence of arrhythmias. Major causes of loss of information were poorly completed diaries or no diary, lack of precise definition of the indication for monitoring and technical faults resulting in uninterpretable recordings. Rectification of these deficiences could improve the efficiency of data collection and analysis.
Serial 2-channel 24 h dynamic ECGs in 7 patients who were referred with the "tachy-brady" syndrome for consideration for permanent cardiac pacing revealed: 1. atrial premature beats (APBs) which were conducted to the ventricles normally or aberrantly; 2. intermittent atrial bigeminy with block towards the ventricles (this rhythm mimicked sinus bradycardia with ventricular rates of 38-45 beats/min and the ectopic P waves were visible on only one of the ECG channels); 3. paroxysms of atrial fibrillation initiated by closely coupled APBs. These findings suggested that both the ventricular bradycardia and the atrial fibrillation were caused by frequent APBs and that pacing therapy was unnecessary. Disopyramide was given to 5 patients resulting in suppression of the arrhythmia and relief of symptoms. In one patient there was spontaneous resolution and one patient refused treatment. This variant of the "tachy-brady" syndrome can be successfully treated by suppression of abnormal atrial impulse formation without recourse to pacemaker implantation.
The cardiac electrophysiological effects of sotalol were studied in ten patients (pts) aged 20--65 years undergoing intracardiac stimulation studies for palpitations (7 pts) or dizzy spells (3 pts). The following measurements were made: 1. basic sinus cycle length (SCL): 2. SINUS NODE RECOVERY TIME (SNRT) following overdrive pacing; 3. intra-atrial (PA), atrio-His (AH) and His-ventricular (HV) conduction intervals during regular atrial pacing; 4. effective refractory periods of the atria (AERP), AV node (AVERP) and ventricular myocardium (VERP). AV nodal functional refractoriness (AVFRP) was also determined. All measurements were repeated 10--15 min after i.v. administration of 0.4 mg/kg of sotalol. Results were analysed by the Wilcoxon Signed Rank test. Significant increases in SCL (p less than 0.01), AH (p less than 0.01). SNRT (p less than 0.01), AVERP (p less than 0.02) and AVFRP (p less than 0.01) were observed. These effects are consistent with the beta-blocking action of sotalol. The acute increase in AERP (p less than 0.01) is, however, not a common property of other beta-blockers and may be related to the 'class III' cellular effect of sotalol. These results are discussed in relationship to the electrophysiological effects of other beta-blocking drugs.
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A 13 year old girl with Ebstein's anomaly was investigated for refractory paroxysmal tachycardias and ventricular pre-excitation. Intracardiac electrophysiological studies demonstrated that ventricular pre-excitation was due to conduction in an anomalous nodo-ventricular pathway. Tachycardia occurred as a result of re-entry within the A-V node with pre-excitation during tachycardia due to conduction in the nodo-ventricular pathway. These tachycardias were controlled initially by medical therapy but because of increasing frequency of attacks, occasionally requiring D.C. conversion, further electrophysiological studies and epicardial mapping were undertaken. The epicardial surface of the right ventricle and right atrium were mapped during tachycardia. The results of the studies confirmed that a direct anomalous atrio-ventricular pathway was not present and that re-entrant tachycardia did not involve an accessory pathway of this type. A rapid atrial pacing system was implanted and paroxysmal tachycardias have been successfully controlled.
The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.
A 'concealed' accessory pathway was suspected in 12 patients because of eccentric left atrial activation during tachycardia. Retrograde conduction during ventricular pacing may occur over the atrioventricular node, the accessory pathway, or both. There were 4 patterns of ventriculoatrial conduction in response to ventricular extrastimuli (V2) at various coupling intervals: (1) exclusive accessory pathway conduction throughout the cardiac cycle in 2 patients; (2) exclusive accessory pathway conduction at long coupling intervals and exclusive atrioventricular node conduction at short coupling intervals in 2 patients; (3) variably fused accessory pathway/atrioventricular node conduction at long coupling intervals but exclusive accessory pathway conduction at short coupling intervals in 4 patients; (4) fused accessory pathway/atrioventricular node conduction at long coupling intervals but exclusive atrioventricular node conduction at short coupling intervals in 4 patients. With increased prematurity of V2 the ventricle to right atrial interval prolonged conspicuously in 11 of 12 patients whereas the ventricle to left atrial interval remained constant until the refractory period of the accessory pathway in all but 2 instances where intraventricular delay occurred. This study emphasises the importance of left atrial recordings in these patients.
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Two patients with dystrophia myotonica showed high-grade atrio-ventricular block. Both underwent electrophysiological studies which revealed sinus and A-V nodal disease with normal intraventricular conduction in 1 case and His-Purkinje conduction disease in the other. Dystrophia myotonica may, therfore, involve all parts of the cardiac conduction system and may affect the generation of cardiac impulses. Pacemaker implantation may be necessary especially if drugs such as procainamide, which in addition to controlling myotonic symptoms may aggravate conduction disorders, are to be used.