Transvenous pacing lead-induced thrombosis: a series of cases with a review of the literature.

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.

Global and regional right ventricular function after acute myocardial infarction: dependence upon site of left ventricular infarction.

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.

Pacing techniques in the prophylaxis of junctional reentry tachycardia.

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 adequacy of radioisotope mixing from bolus injections in first-pass radionuclide angiographic assessment of right ventricular function: a study using gold-195m.

The adequacy of radioisotopic mixing in first-pass radionuclide studies of right ventricular function was assessed in 27 patients using multiple injections of gold-195m (half-life 30.5 sec). A theoretical disadvantage of the first-pass technique is inadequate mixing of the injected bolus with blood prior to entry into the right ventricle. Since the calculation of ejection fraction is based on the assumption of complete mixing, this would lead to errors. In order to assess the effects of bolus injection rates and bolus duration on the calculation of right ventricular ejection fraction, multiple, rapid, sequential studies were performed using gold-195m at four bolus injection rates (10, 5, 2 and 1 ml/sec). Slowing the injection rate caused a significant increase in bolus duration, and a significant increase in the number of cardiac cycles available for analysis. Mean ejection fraction, however, was not significantly changed. There was good correlation between right ventricular ejection fraction at all injection rates when compared to 10 ml/sec, and no injection rate led to a consistent over or underestimate of right ventricular ejection fraction. There was no significant relationship between change in bolus duration and variation in ejection fraction. These data indicate that mixing is adequate for first-pass studies of right ventricular function using a rapid bolus.

Detection of pathological tachycardia by analysis of electrogram morphology.

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.

Relation between coronary anatomy and serial changes in left ventricular function on exercise: a study using first pass radionuclide angiography with gold-195m.

Serial changes in left ventricular function on exercise were assessed by first pass radionuclide angiography with gold-195m (half life 30.5 s) in 25 men with known coronary anatomy. In the seven patients with three vessel disease, abnormalities of global left ventricular function and regional wall motion occurred earlier during exercise, were of greater extent at peak exercise, and persisted longer after exercise than in the 11 patients with one and two vessel disease or the seven with normal coronary arteries. Although there were significant differences between the groups in absolute change in ejection fraction and the rate of change in ejection fraction related to exercise duration and heart rate, a considerable overlap of values between groups precluded the accurate prediction of coronary anatomy in individuals. These data suggest that the amount of myocardium at risk from ischaemia in some patients with one and two vessel disease may resemble that in patients with three vessel disease. This study shows that an anatomical classification based solely on the number of diseased vessels will not predict the extent of the impairment of left ventricular function on exercise.

Pulmonary mycotic aneurysms secondary to infective endocarditis in a patient with a persistent ductus arteriosus and partial anomalous pulmonary venous drainage.

Mycotic aneurysms are a rare but recognized complication of infective endocarditis. Aneurysms of the pulmonary artery are usually associated with infected congenital heart lesions and especially with persistent ductus arteriosus. This report deals with a patient with a persistent ductus who developed multiple mycotic aneurysms in the right lung following infective endocarditis, and whose management was complicated by anomalous venous drainage of most of the contralacteral lung. Surgical closure of the ductus to reduce pulmonary blood flow failed to prevent haemoptysis, and further surgery to ligate the feeder arteries to the aneurysms was required.

The proarrhythmic effects of flecainide.

Flecainide acetate, a new potent class I antiarrhythmic agent, was administered to 152 patients (orally to 46, intravenously to 106) 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, of whom only 3 had pre-existing ventricular arrhythmias, developed ventricular tachycardia or ventricular fibrillation. QT and QTc interval prolongation was observed, but was due to QRS complex widening rather than an increase in the JT interval. A patient with Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular tachycardia before flecainide administration, but only an antidromic tachycardia was induced after taking the drug. In 1 patient, flecainide administration resulted in an increase of atrial flutter cycle length, which resulted in the development of 1:1 atrioventricular conduction rate, and, overall, a 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. Other published series are also summarised.

Steps towards the development of a safe and effective tachycardia terminating pacemaker.

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.

Clinical experience with implantable scanning tachycardia reversion pacemakers.

An automatic, fully implantable scanning pacemaker was developed and has been used for tachycardia termination in man. Since January 1982, 22 patients have had this pacemaker implanted at St. Bartholomew's Hospital and over 125 devices have been used throughout the world. Clinical results have been encouraging, especially with the second-generation device.

Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias.

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.

Sinoatrial function after cardiac transplantation.

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.

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate.

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.

The electrophysiologic characteristics of the transplanted human heart.

The electrophysiologic characteristics of the denervated human heart were assessed in 14 cardiac transplant recipients. Conduction intervals and refractory periods were measured at pacing cycle lengths of 500 msec and 400 msec. The faster pacing rate caused lengthening of the AH interval (83 +/- 23 msec to 116 +/- 41 msec, p less than 0.01) and shortening of the QT (338 +/- 27 msec to 313 +/- 22 msec, p less than 0.001) and JT (249 +/- 21 msec to 229 +/- 19 msec, p less than 0.001) intervals. There was no change in the SA, HV, or QRS durations. Wenckebach periodicity occurred at a longer cycle length in the retrograde than in the anterograde direction (409 +/- 96 msec vs 318 +/- 46 msec, p less than 0.01) and anterograde conduction was better than retrograde conduction in 13 of the 14 patients (93%). Increasing pacing cycle length resulted in shortening of the atrial effective (203 +/- 28 msec to 190 +/- 25 msec, p less than 0.001), ventricular effective (224 +/- 18 msec to 211 +/- 17 msec, p less than 0.01), and AV nodal functional (367 +/- 38 msec to 357 +/- 36 msec, NS) refractory periods. The AV nodal effective refractory period lengthened (294 +/- 31 msec to 314 +/- 52 msec, p less than 0.05). There was a close correlation between AV Wenckebach cycle length and the functional refractory period of the AV node (r = 0.853, p less than 0.001). These results are qualitatively and quantitatively similar to those reported in the innervated heart. The autonomic nervous system appears to have little influence on the resting electrophysiologic characteristics of the atrioventricular conduction system in the innervated heart.

Electrophysiological abnormalities in the transplanted human heart.

Fourteen relatively long term survivors of cardiac transplantation underwent systematic electrophysiological evaluation and ambulatory electrocardiographic monitoring. Six patients had prolonged conduction intervals during sinus rhythm. Sinus node function could be assessed in all donor atria and in 10 recipient atria. Sinus node recovery times were prolonged in four of the donor atria and in six recipient atria. In the donor atria abnormalities of sinus node automaticity were invariably associated with abnormalities of sinoatrial conduction. Four patients showed functional duality of atrioventricular nodal conduction during programmed extrastimulation, but no patient developed re-entrant arrhythmia. During ambulatory electrocardiographic monitoring no pronounced tachyarrhythmias were recorded. Three patients showed abnormalities of sinus node impulse formation. All three patients had abnormal sinus node recovery times during their electrophysiological study. Long term survivors of cardiac transplantation have a high incidence of electrophysiological abnormalities. Abnormalities of donor sinus node function are probably of clinical significance. The clinical significance of abnormalities detected within the atrioventricular conduction system of the denervated heart remains to be elucidated.

Unusual atrial potentials in a cardiac transplant recipient. Possible synchronization between donor and recipient atria.

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.

Cardiac electrophysiologic effects of flecainide acetate for paroxysmal reentrant junctional tachycardias.

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.

A comparison of the antiarrhythmic effects on AV junctional re-entrant tachycardia of oral and intravenous flecainide acetate.

Both the electrophysiological and antiarrhythmic effects of some antiarrhythmic agents may differ markedly depending on their route of administration. Flecainide acetate, a new class 1 agent, was therefore administered both intravenously and orally to 13 patients with recurrent paroxysmal tachycardia to assess whether the acute response to intravenous flecainide accurately predicts the response to oral therapy. Eight patients had atrioventricular re-entrant tachycardia (AVRT) and five patients intra AV nodal re-entrant tachycardia (AVNRT). When administered by either route, flecainide markedly prolonged both the anterograde and retrograde conduction intervals during constant rate pacing and the anterograde and retrograde Wenckebach cycle lengths during incremental pacing. Five of the 13 patients developed complete retrograde block after both routes of administration of the drug. All 13 patients received intravenous flecainide during tachycardia with successful reversion to sinus rhythm in all cases. Tachycardia could be reinitiated in five of the patients with AVRT after intravenous flecainide and in one further patient after oral administration. It was not possible to reinitiate tachycardia in any of the five patients with AVNRT after either intravenous or oral flecainide. The size of the tachycardia initiation windows, by either atrial or ventricular premature stimuli, were significantly reduced by both intravenous and oral flecainide. In those patients in whom tachycardia could be reinitiated, tachycardia cycle length was significantly increased, and to a similar degree, by both routes of administration of the drug. This increase in cycle length was predominantly due to prolongation in retrograde conduction. It is concluded that flecainide acetate is a potent antiarrhythmic agent for use in patients with junctional tachycardia. The intravenous administration of flecainide reliably predicts the subsequent response to oral therapy.