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Although transvenous pacing is a safe treatment modality for bradyarrhythmias, serious thrombotic and embolic complications are reported to occur in 0.6-3.5% of cases. We describe 5 cases of pacemaker-associated thrombosis, 3 with a superior vena cava syndrome (SVC), 1 with an axillary vein thrombosis and 1 with a thrombus attached to the pacing lead in the right atrium. All of the patients were initially treated with intravenous heparin which proved successful as the sole treatment in only the least severe case (axillary vein thrombosis). One of the patients with SVC obstruction was successfully treated with intravenous heparin followed by thrombolytic therapy. The remaining 3 cases (2 SVC syndromes and 1 right atrial thrombus) required surgical removal of thrombus and pacing leads. Both of the patients with evidence of infection were in the group for whom failure of medical therapy necessitated surgery., (Copyright 2000 S. Karger AG, Basel)

Ventricular tachycardia may result in retrograde atrial depolarization. In all previous examples studied by intracardiac recording techniques retrograde conduction to the atria has been thought to occur via the normal conduction system. In the patient reported here, 1 : 1 retrograde conduction with atrial preexcitation during ventricular tachycardia indicated the presence of a concealed accessory pathway. This was confirmed by the phenomenon of exact atrial capture. The achievement of atrioventricular dissociation during tachycardia by atrial overdrive pacing excluded a reentrant tachycardia involving such a pathway. The widely variable H--V interval in the presence of a constant V--A interval during tachycardia suggested anterograde His bundle depolarization following atrial activation over the accessory pathway. This hypothesis was supported by the long V--H interval during tachycardia and the relationship of the ventricular, atrial and His bundle electrograms of the first and least beat of the tachycardia. This report illustrates the value of careful electrophysiological investigation in evaluating the relationship of an accessory pathway to the tachycardia mechanism.

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.

The function of both the denervated donor and innervated recipient sinus nodes of 14 asymptomatic cardiac transplant recipients was assessed. Tests of sinoatrial function were performed in 14 donor and 10 recipient atria. The mean spontaneous cycle length of the recipient atria was significantly longer than that of the donor atria (944 +/- 246 versus 663 +/- 158 ms, p less than 0.01). Donor sinus node recovery time was prolonged in four patients (greater than 2,500 ms in two) and recipient recovery time was prolonged in six patients. In those patients with normal sinus node function tests, the recovery time of the recipient sinus node was longer than that of the donor sinus node (1,170 +/- 207 versus 864 +/- 175 ms, p less than 0.02). The pattern of response of recovery times to increasing pacing rate was predictable and organized in the donor but chaotic in the recipient, and the longest sinus node recovery time occurred at the shortest pacing cycle length used in 12 of the 14 donor atria but in only 1 of the 10 recipient atria (p less than 0.001). Secondary pauses occurred in none of the normal donor atria and in all of the abnormal donor atria (p less than 0.001); however, they occurred in both normal and abnormal recipient atria. The recipient and donor atria were paced alone and synchronously in the same patients. Synchronous pacing had no effect on the recovery times of the donor sinus node but significantly lengthened those of the recipient (sinus node recovery time: 1,266 +/- 218 to 1,547 +/- 332 ms, p less than 0.02; corrected recovery time: 322 +/- 102 to 686 +/- 188 ms, p less than 0.01). In the donor atria, abnormal recovery time was invariably associated with abnormal sinoatrial conduction time. There was a strong correlation between sinoatrial conduction time measured by the methods of Strauss and Narula and their coworkers in the donor atria (r = 0.98, p less than 0.001) but not in the recipient atria (r = 0.72). In the absence of autonomic influences, tests of sinus node function of the donor atria produce predictable and consistent results and, therefore, may be more clinically reliable than in intact human subjects. There is a high incidence of recipient sinus node dysfunction in asymptomatic long-term survivors of cardiac transplantation.

It is usual to record independent activity from both the innervated recipient and the denervated donor atria in cardiac transplant recipients except for occasional, short-lived periods of entrainment that may occur during exercise. In this report a case is described in which, following orthotopic cardiac transplantation, the recipient and donor atria remained synchronized during a variety of physiological and non-physiological situations. Under no circumstances did the two sets of atria beat independently. The mechanisms that might be involved in this unique situation are discussed.

The hemodynamic response to exercise stress was assessed in 17 patients with left ventricular (LV) aneurysm, demonstrated by contrast left ventriculography, and congestive cardiac failure (CCF) before and after sublingual isosorbide dinitrate (ISDN). Radionuclide ventriculography was performed at rest and during exercise in 14 patients. ISDN increased mean exercise LV stroke work index (LVSWI) from 31 to 39 g-m/m2 (p less than 0.001) and reduced mean exercise LV filling pressure from 38 to 25 mm Hg (p less than 0.001). Using the combined criteria of LVSWI and ejection fraction of the contractile section of the left ventricle (EFCS), no patient with rest EFCS of less than 40% achieved a good absolute response to exercise in LV performance with or without ISDN. Of the six patients with rest EFCS greater than or equal to 40% only three achieved a good response. While rest EFCS less than 40% indicates poor LV functional reserve, good LV functional reserve is not always indicated by rest EFCS greater than or equal to 40%.

The relation of global and regional right and left ventricular function during the acute phase after a first myocardial infarction was assessed by first pass radionuclide angiography in 20 patients (10 after anterior and 10 after inferior myocardial infarction). The right ventricular ejection fraction did not differ significantly between the groups, but left ventricular ejection fraction was significantly depressed after anterior myocardial infarction. There was evidence of right ventricular dilatation and impaired transit in the group with inferior infarction. Five patients with anterior infarction and six with inferior infarction had abnormal right ventricular ejection fractions. Right ventricular wall motion abnormalities affected the septal wall in the group with anterior infarction and the free wall in the group with inferior infarction. The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with anterior infarction there was a significant linear relation between right and left ventricular ejection fraction, whereas in the group with inferior infarction there was not. Thus right ventricular dysfunction commonly occurs after both anterior and inferior myocardial infarction. Right and left ventricular impairment are related after anterior myocardial infarction, but are independent after inferior myocardial infarction. Finally, the different effects of anterior and inferior myocardial infarction on right ventricular function may be explained by differences in septal and free wall involvement.

The value of 24-hour ambulatory monitoring of the ECG for the diagnosis of symptoms of dizziness, palpitations and syncope is controversial. In this study results from a hospital-based, clinical service have been analysed. Of 1,000 consecutive dynamic electrocardiograms (DCG), 678 were performed for assessment of dizziness, syncope or palpitations in 405 patients. 36 of the patients had pacemakers. 60 DCGs were technically inadequate. The recordings were classified according to the correspondence between DCG findings and symptoms noted in the patient diary: (I) Completely diagnostic: significant arrhythmias (SA) corresponding to diary symptoms - 99 recordings. (II) Incompletely diagnostic: (a) absence of SA in the presence of diary symptoms - 90 recordings; (b) presence of SA but no diary symptoms - 197 recordings; (c) presence of SA corresponding to symptoms other than that for which the DCG was indicated - 52 recordings. (III) Non-diagnostic: absence of both SA and diary symptoms - 180 recordings. Incompletely diagnostic categories were regarded as clinically valuable in that they either excluded a cardiac arrhythmia as a cause of symptoms (group IIa) or they revealed SA which did not correspond to diary symptoms (group IIc). The absence of symptoms corresponding to SA was ascribed to poor diary keeping in 54 of 197 recordings. These results are discussed in the context of the findings in normal and symptomatic patients. A clinical 24-hour ambulatory ECG monitoring service provided useful diagnostic information in 65% of recordings and 74% of patients.

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.

Twp patients with type B WPW syndrome and reciprocal tachycardias have been studied using intracardiac electrograms and programmed electrical stimulation of the heart. One patient, who had a right-sided accessory pathway giving the surface electrocardiographic appearances of type B WPW syndrome, was shown to have an additional left-sided accessory pathway as occurs in type A WPW syndrome. This concealed left-sided atrioventricular connexion formed the retrograde pathway during reciprocal tachycardia. In the second patient the appearances of type B WPW syndrome were shown to be caused by an accessory pathway between the atrial septum and the right side of the interventricular septum rather than an accessory pathway in the right atrioventricular groove. The significance of these findings when considering surgical interruption of an accessory atrioventricular conduction pathway is discussed.

Seven patients with normal specialized conduction system and three patients with the Wolff-Parkinson-White (WPW) syndrome were studied using programmed stimulation of the heart before and after the administration of intravenous disopyramide. The principal effect of this drug was to prolong the effective refractory period of the atria and ventricles, and to prolong the effective refractory period of the anomalous pathway in the WPW syndrome. In addition, it prolonged the conduction time in the anomalous pathway in the WPW syndrome. These findings suggest that disopyramide would be a useful and safe drug in the management of certain atrial and ventricular arrhythmias and in the management of the Wolff-Parkinson-White syndrome with atrial fibrillation.

To evaluate the direct electrophysiologic effects of i.v. disopyramide phosphate and to differentiate these effects from its autonomically mediated actions, we administered the drug (2 mg/kg over 5 minutes) during electrophysiologic study to eight cardiac transplant recipients who had documented functional cardiac denervation. After disopyramide, the cycle length of the denervated donor right atrium increased from 626 +/- 129 to 716 +/- 148 msec (mean +/- SD, p less than 0.001), whereas that of the innervated recipient atrium decreased from 846 +/- 195 to 659 +/- 99 msec (p less than 0.02). There were small increases in both the sinus node recovery time (1128 +/- 616 to 1198 +/- 592 msec, p less than 0.05) and corrected sinus node recovery time (440 +/- 418 to 489 +/- 409 msec, p less than 0.02) of the donor atrium, whereas the recovery times of the recipient atrium shortened (sinus node recovery time, 1298 +/- 218 to 1218 +/- 196 msec; corrected sinus node recovery time, 464 +/- 108 to 410 +/- 115 msec). Disopyramide markedly prolonged all conduction intervals. The PA interval increased from 47 +/- 16 to 54 +/- 17 msec (p less than 0.01), the AH interval from 55 +/- 12 to 78 +/- 12 msec (p less than 0.001), the HV interval from 38 +/- 9 to 58 +/- 13 msec (p less than 0.001), the QRS duration from 93 +/- 18 to 129 +/- 34 msec (p less than 0.001) and the QT interval from 339 +/- 23 to 403 +/- 39 msec (p less than 0.001). There was no significant change in the effective refractory period of the atrium, ventricular or atrioventricular node. The functional refractory period of the atrioventricular node increased from 369 +/- 34 to 395 +/- 31 msec (p less than 0.001). The electrophysiologic effects of disopyramide in the denervated heart are markedly depressant. In the innervated normal heart, the majority of these effects are counteracted by the drug's autonomically mediated anticholinergic actions.

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.

Pacemaker recognition of pathological tachycardia relies on heart rate analysis. This can lead to misdiagnosis when sinus tachycardia exceeds the preset tachycardia response trigger rate. We have explored a method for automatic tachycardia diagnosis by analysis of bipolar endocardial electrogram morphology. Electrograms were recorded from 11 patients (pts) during sinus rhythm and during a total of 20 abnormal rhythms: retrograde atrial depolarization from ventricular pacing in six patients; atrioventricular reentry tachycardia in five patients with intermittent left bundle branch block in one of those; AV nodal reentry tachycardia in five patients and ventricular tachycardia in three patients. Posture and respiration were varied during all rhythms except ventricular tachycardia. The electrograms were then digitized and converted to a form in which the amplitudes were proportional to the rates of change of the original electrogram (equivalent to a first time derivative); the derived signal was then analyzed by a new gradient pattern detection (GPD) program. Analysis of the processed atrial signals by GPD resulted in automatic recognition of abnormal rhythms from sinus rhythm in all cases except for one patient's retrograde atrial depolarization. At the ventricular level, GPD successfully distinguished all abnormal rhythms from sinus rhythm including recognition of left bundle branch block and varying degrees of preexcitation. Respiratory and postural variation did not affect the recognition process. We conclude that electrogram GPD has successfully and automatically detected a variety of arrhythmias which can be treated by implantable pulse generators and may, therefore, be a useful adjunct to heart rate analysis in future generations of such antitachycardia pacemakers.

The electrophysiological effects of flecainide acetate (2 mg/kg as an intravenous infusion over five minutes) were assessed in 47 patients undergoing electrophysiological study. Seven patients had normal electrophysiology, 16 had a direct accessory atrioventricular pathway, 12 had dual atrioventricular nodal (AH) pathways, five had paroxysmal ventricular tachycardia, six had conduction system disease, and one patient had a left atrial tachycardia. No significant change occurred in sinus cycle length. The PA interval, AH interval, and HV interval were all significantly prolonged. The QRS complex duration increased significantly. The QT interval showed slight prolongation due entirely to the increase in QRS duration. Refractoriness of the atrial and ventricular myocardium was slightly prolonged, but was significant only at ventricular level. No significant change occurred in refractoriness of the normal atrioventricular node. Pronounced prolongation of retrograde "fast" AH pathway refractoriness was observed in those patients with dual AH pathways. Anterograde and retrograde accessory pathway refractoriness were both greatly increased. These electrophysiological properties strongly suggest that flecainide will be useful in the management of a wide variety of cardiac arrhythmias. It should be administered, however, with caution to patients with pre-existing conduction system disease. Because repolarization is not delayed flecainide is unlikely to induce ventricular arrhythmias related to prolongation of the QT interval.

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.

Thirteen patients with left ventricular aneurysms complicating myocardial infarction were studied by contrast angiography and by first pass radionuclide ventriculography. The ejection fraction of the contractile segment (EFCS) was measured from both studies using a double hemishperoid model, and the values correlated closely. There was a monotonic relation between EFCS and stroke volume index measured from thermodilution cardiac outputs carried out simultaneously with the radionuclide study. When radionuclide ventriculography was performed at submaximal supine exercise, changes in EFCS paralleled changes in the total left ventricular ejection fraction in 10 of the 13 cases. In nine patients, changes in EFCS paralleled changes in stroke volume index and the relation between EFCS and stroke volume index was maintained at exercise. After administration of the vasodilator isosorbide dinitrate to 12 patients, repeat exercise radionuclide ventriculography showed an improvement in left ventricular ejection fraction and in eight patients EFCS improved. First pass radionuclide ventriculography can accurately estimate EFCS, which may be an important factor in predicting the likely response to aneurysmectomy. Changes in EFCS on exercise are reflected in changes in total left ventricular ejection fraction and stroke volume index. Isosorbide dinitrate may improve contractile segment function on exercise.

Permanent pacemakers have been used for the treatment of tachycardias. Four studies have been performed to improve termination algorithms. Permanent extrastimulus pacing was assessed in 19 patients. During follow up of 13 to 36 (mean 27) months, 7 also required additional antiarrhythmic drugs. Pacing was effective in all, but there was one unexplained sudden death. Autodecremental (rate-increasing) atrial pacing was used in 20 patients with junctional arrhythmias. It was effective in all, especially with a burst duration of 5000 ms, and caused no acceleration of tachycardia. In contrast, constant rate overdrive pacing produced atrial flutter or fibrillation in 4 patients. Concertina pacing (up to 7 stimuli) was tried, and was effective, in 19 patients. In three patients, using one or two stimuli of short coupling intervals, atrial arrhythmias were induced. As the number of stimuli were increased, longer pacing cycle lengths became effective. The effect of reset has been suggested as a useful method of searching for the termination zone. Ventricular pacing reliably caused reset, but atrial pacing produced inconsistent results. These studies show that adaptive, limited burst pacing modes are most effective methods, but reset is not useful in the right atrium.

A 41-year-old man presented with dizziness associated with sinus bradycardia and sinus arrest. An attempt to implant a transvenous pacing lead was frustrated by absence of the right superior vena cava. The left superior vena cava persisted and drained via the coronary sinus into the right atrium. Absence of the right superior vena cava may present with symptomatic sinus node dysfunction and may require an epicardial demand pacing system.

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.

In patients with the short PR interval, normal QRS complex syndrome, paroxysmal tachycardias are usually the result of circus movement involving the AV node and a partial or complete AV nodal bypass. We report 2 patients with this syndrome who suffered distressing rapid paroxysms of tachycardia but in whom there was evidence of a concealed direct VA connection. In both patients, tachycardia was initiated with critical AV prolongation distal to the His bundle, in response to programmed atrial premature stimuli. The constancy of the timing of the atrial echo from the onset of the QRS complex in the presence of a varying HV interval is evidence for involvement of the ventricles in the re-entry pathway. In addition, in both patients the appearance of left bundle-branch block during tachycardia was associated with appropriate prolongation of tachycardia cycle length consistent with the presence of a direct VA connection. The short AH interval during tachycardia and the absence of critical AH prolongation suggests the participation of a rapidly conducting pathway in the anterograde limb of the tachycardia circuit.

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.

Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.

Of 8 patients with the short PR interval, normal QRS complex syndrome studied recently, 3 reported here displayed gaps in anterograde conduction. Atrial premature beats at decreasing coupling intervals conducted with minimal AH prolongation until a zone within the cardiac cycle was reached where conduction failed at a supra-Hisian level. Conduction resumed at earlier atrial coupling intervals and was associated with a sudden increase in the AH interval and the appearance of atrial echo beats with earliest atrial activation on the proximal coronary sinus electrogram. It is suggested that the failure of anterograde conduction at relatively late atrial coupling intervals was caused by a short AH functional refractoriness produced by the pre-excitation of the lower AV junction by a partial AV nodal bypass. Conduction resumed only when early atrial premature beats found the extranodal pathway refractory and were transmitted with decremental delay through the AV node.

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.

Atrial premature beats (APBs) which encounter sufficient AV delay may initiate junctional reentry tachycardia (JRT). This form of initiation may be prevented by rendering part of the reentry circuit refractory by artificial stimulation following an APB which would otherwise initiate JRT. Two such approaches have been suggested: preexcitation pacing, that is, ventricular stimulation with a short AV delay triggered by atrial depolarization; and preemptive pacing, which consists of early atrial stimulation coupled to the initiating APB. We compared these approaches and describe them as follows. Ten patients with JRT (six with atrioventricular reentry and four with AV nodal reentry) were studied. Against a background of regular atrial drive, the range of coupling intervals over which a stimulated APB initiated JRT (tachycardia initiation window) was determined (control). The tachycardia initiation window was also measured when a second atrial stimulus followed the initiating APB 20 ms after atrial recovery (preemptive pacing) or when a ventricular stimulus closely followed the initiating APB with an AV delay of 65 ms (preexcitation pacing). The tachycardia initiation window in response to an isolated APB was also assessed following regular AV pacing with a short (65 ms) AV delay (preconditioning pacing) and the effect of preexcitation pacing following the initiating APB was also assessed after a similar drive (combined preconditioning and preexcitation pacing). All protocols were performed at two basic drive cycle lengths. The results are arranged for the slow and fast drives, respectively, and were as follows: control initiating windows--49.5, 28.5 ms; preemptive pacing initiation windows--151, 38 ms; preexcitation pacing initiation windows--26, 23.5 ms; preconditioning pacing initiation windows--45.5, 35 ms; combined preconditioning and preexcitation pacing initiation windows--10.0, 2.5 ms. Whereas preemptive pacing tended to widen the tachycardia initiation windows (a proarrhythmic effect) the combination of preconditioning and preexcitation pacing considerably reduced the possibility of JRT initiation by an atrial premature beat.

The electrophysiological effects of intravenous sotalol hydrochloride (0.4 mg/kg) were assessed in 24 patients, including 13 with the Wolff-Parkinson-White syndrome, undergoing routine electrophysiological study. Fifteen to 30 minutes after sotalol administration there was a significant increase in sinus cycle length and in sinus node recovery time. There was a small increase in the AH interval, but the HV interval was unchanged. The QT and JT intervals, measured during sinus rhythm, were both increased. The atrial, ventricular, and atrioventricular nodal effective refractory periods were all prolonged, as was the atrioventricular nodal functional refractory period. In 13 patients with ventricular pre-excitation there was an increase of the accessory pathway anterograde and retrograde effective refractory periods. In 12 of these 13 sotalol was given during atrioventricular re-entrant tachycardia, resulting in termination in five. Tachycardia cycle length increased in all patients, with the major effect being in the atrioventricular direction. Though some of the effects seen in these patients are consistent with the beta adrenergic antagonist properties of sotalol, the effect on atrial, ventricular, and accessory pathway effective refractory periods and on ventricular repolarisation is not typical of that observed with other beta blockers but may be the result of lengthening of the action potential duration. These findings suggest that sotalol may be a more versatile antiarrhythmic agent than other beta receptor antagonists.

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QTc interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.

Intravenous flecainide acetate was administered to 33 patients undergoing routine electrophysiologic study: 18 patients had a direct accessory atrioventricular (AV) pathway and 15 patients had functional longitudinal A-H dissociation (dual A-H pathways). Flecainide was given to 14 patients during sustained AV reentrant tachycardia and to 9 patients during sustained intra-AV nodal reentrant tachycardia. AV reentrant tachycardia was successfully terminated in 12 of 14 patients. Tachycardia termination was due to retrograde accessory pathway block in 11 patients and AV nodal block in 1. During flecainide administration, tachycardia cycle lengths increased (327 +/- 55 to 426 +/- 84 ms) principally because of retrograde conduction delay in the accessory pathway (127 +/- 34 to 197 +/- 67 ms). After flecainide administration, tachycardia reinitiation was not possible in 6 patients. In all 18 patients with accessory AV pathway conduction, flecainide significantly increased both anterograde and retrograde accessory pathway effective refractory periods, with anterograde accessory pathway block in 3 patients and retrograde accessory pathway block in 8. Intra-AV nodal reentrant tachycardia was successfully terminated in 8 of 9 patients. Tachycardia termination was due to retrograde "fast" A-H pathway block in 7 patients and anterograde "slow" A-H pathway block in 1 patient. During flecainide administration, tachycardia cycle lengths increased (326 +/- 50 to 433 +/- 64 ms) due to both anterograde, A-H and H-V (AV 242 +/- 97 to 343 +/- 75 ms), and retrograde, earliest ventricular to earliest atrial (51 +/- 14 to 70 +/- 23 ms) conduction delay. After flecainide administration, reinitiation of intra-AV nodal reentrant tachycardia was not possible in 4 patients. In all 15 patients with dual A-H pathways, flecainide selectively prolonged the retrograde effective refractory period of the fast A-H pathway, having little effect on anterograde fast A-H pathway refractoriness or on anterograde and retrograde slow A-H pathway refractoriness. Anterograde fast A-H pathway block occurred in 1 patient and retrograde fast A-H pathway block occurred in 6 patients. No serious adverse effects were encountered during the study. Flecainide acetate is an effective agent for the acute termination of both orthodromic AV and intra-AV nodal reentrant tachycardias. This antiarrhythmic action appears to be mediated through a predominant effect on either accessory AV pathway or retrograde fast A-H pathway refractoriness.

Four patients, two with congenital QT prolongation (Romano-Ward syndrome) and two with acquired idiopathic QT prolongation not related to bradycardia, drug toxicity, electrolyte imbalance, or neurological disorder were investigated for the onset of recurrent palpitations and/or syncope. The effects on the measured QT interval of intravenously administered propranolol (QTp), an infusion of isoproterenol (QTi) and left stellate ganglion block (QTs) were assessed at identical atrial paced rates and during sinus rhythm, corrected for rate change (QTc). Propranolol shortened the QTc in all patients. The QTp shortened only in those with congenital QT prolongation. Isoproterenol lengthened the QTc in the three patients studied. However, the QTi lengthened in the congenital syndrome whereas it shortened in the acquired syndrome. The QTs was uninfluenced by left stellate ganglion block in all patients. It is suggested that the congenital and acquired forms can be differentiated by pharmacological interventions and that the efficacy of propranolol in the former may result from its ability not only to increase the threshold for ventricular fibrillation, but also its ability to shorten the QT interval.

A microprocessor-based system is described which employs the autodecremental mode of atrial pacing. Preliminary experience suggests that this modality of pacing retains the advantages of rapid asynchronous atrial pacing but reduces the risk of provoking resistant atrial tachyarrhythmias. If the technique continues to prove successful it is suitable for incorportation into a fully implantable pacemaker.

To examine possible augmentation of the effects of isosorbide dinitrate by salbutamol, haemodynamic measurements were made in 10 patients with severe chronic congestive cardiac failure who received isosorbide dinitrate 2.5 to 25 mg sublingually and salbutamol 4 to 12 mg orally, alone and in combination. Isosorbide dinitrate reduced mean left ventricular filling pressure from 29 to 18 mmHg and increased mean cardiac index from 1.7 to 2.0 1/min per m2, with no significant change in mean heart rate. Systemic arterial mean pressure fell from 85 to 72 mmHg. Salbutamol increased cardiac index from 1.8 to 2.2 1/min per m2. There was no significant change in left ventricular filling pressure, heart rate, or systemic arterial pressure. Compared with control, combined isosorbide dinitrate and salbutamol reduced left ventricular filling pressure from 27 to 19 mmHg and increased cardiac index from 1.8 to 2.7 1/min per m2, with no significant change in heart rate. Systemic arterial pressure fell from 82 to 75 mmHg. The reduction in left ventricular filling pressure by combined treatment was similar to that produced by isosorbide dinitrate alone, but the increase in cardiac index was significantly greater than that produced either by isosorbide dinitrate alone or salbutamol alone. Combined sublingual isosorbide dinitrate and oral salbutamol have an additive effect in improving left ventricular performance in patients with severe chronic congestive cardiac failure.

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.