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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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

A study was undertaken to evaluate the role of positive infarct scintigraphy in the diagnosis of acute myocardial infarction (AMI), using Technetium99m stannous pyrophosphate (Tc-PYP) and a portable gamma camera. Sixty-one patients admitted to the Coronary Care Unit (CCU) with a presumptive diagnosis of AMI or ischaemic cardiac pain were studied. Positive scans were present in 24/25 (96%) patients with AMI and new Q waves, and in 10/12 (83%) patients with AMI and no Q waves. Nine of eleven (82%) patients with chest pain and no infarction had negative scans. Of thirteen patients with unstable angina, ten (77%) had positive scans. A further eight patients undergoing coronary artery bypass surgery for angina pectoris were studied pre- and postoperatively. Two patients had strongly positive postoperative scans. The Tc-PYP scan is valuable in the detection of peri-operative infarction following coronary artery surgery, and in patients with unstable angina the technique may detect small amounts of myocardial necrosis undetectable by more conventional means. When the diagnosis of infarction is obvious from the ECG, enzymes, or a combination of the two, the Tc-PYP scan provides no extra information helpful in patient management.

A fully implantable automatic scanning pacemaker designed for tachycardia termination has been used in three patients with regular paroxysmal supraventricular tachycardia. The pacemaker recognizes tachycardia and delivers one or two extrastimuli which automatically scan inwards if tachycardia continues. A memory is incorporated to retain and immediately reuse a successful pacing sequence if tachycardia recurs. Ventricular pacing has been used in two patients and atrial stimulation in one. Although all had suffered frequent attacks of tachycardia after implantation no sustained episodes of tachycardia have been appreciated. No unwanted arrhythmias have been induced and drug treatment has been stopped in all three patients. Fully implantable scanning pacemakers which automatically recognize and revert tachycardia offer an effective and versatile form of treatment of recurrent paroxysmal tachycardias.

Eighteen patients with a history of previous anterior myocardial infarction and suspected left ventricular aneurysms were studied both by contrast left ventriculography and by first pass radionuclide ventriculography using Technetium99m and a computerised multicrystal gamma camera. The radionuclide study successfully identified all 14 patients with aneurysms and all 4 with diffusely hypo-kinetic ventricles. Ejection fraction calculated from the change in radioactive counts in the left ventricle correlated well with that calculated from the area-length method from the contrast angiogram (r = 0.83). Ventricular volumes calculated from the area-length formula for both contrast and radionuclide angiograms correlated closely (r = 0.85 and r = 0.89 for end-systolic and end-diastolic volumes, respectively). In the patients with aneurysms, there was a close correlation between the extent of akinesis, as assessed by the two methods (r = 0.94). The ability of the radionuclide ventriculogram to provide accurate information on global and segmental ventricular function, and to differentiate between segmental and diffuse ventricular dysfunction, enables the method to act as a screening procedure in the investigation of patients with suspected left ventricular aneurysms.

Traditional measurement and recording methods are inadequate for continuous monitoring of ambulatory pulmonary artery pressure. Therefore a new miniaturised solid state system has been developed and assessed. A manometer tipped catheter, inserted via a subclavian or cephalic vein, was used together with an isolated amplifier and peak detectors to determine systolic and diastolic pressures. Pressures were averaged over 30 seconds and stored in digital memory. After a 24 hour recording period data were rapidly transferred to a microcomputer for numerical or graphical display. Thirteen patients had continuous ambulatory monitoring performed for between 24 and 96 hours, in seven to evaluate symptoms of dyspnoea in subjects with valvular or coronary disease (group 1), and in six to achieve optimal oral treatment for left heart failure (group 2). The catheter was calibrated before insertion and was rechecked after removal. There was less than 1% zero level drift and similar gain stability. Systolic pressures ranged from 10 to 97 (mean 39.5) mmHg, and diastolic from 1 to 46 (mean 15.3) mmHg. Four patients in group 1 had symptoms of dyspnoea associated with normal pressures, while three had raised pressures. Four of the six patients monitored in group 2 had major alterations in their treatment based on data obtained during monitoring. There were no complications. This system, which allows safe, reliable, and prolonged recording of ambulatory pulmonary artery pressure, represents a considerable advance in the ability to assess the cause of dyspnoea and to manage left heart failure.

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.

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.

Two patients with intractable life-threatening ventricular tachycardias have been studied using intracardiac electrograms and programmed electrical stimulation of the heart. Both patients have shown to have an underlying re-entry mechanism in the ventricles as the basis for the tachycardias. Both patients underwent epicardial mapping studies at cardiac surgery, and the site of re-entry was established. In one patient the re-entry front was found to start in the posterobasal region of the left ventricle and in the other patient the re-entry front was found in the anterobasal region of the right ventricle. In both patients surgical interruption of the re-entry front was carried out. Both patients are alive and free from tachycardias at the time of writing.

The distribution of 201thallium (Tl) in the myocardium has been studied by the new technique of emission tomography, and compared with standard gamma camera images in 5 patients. Tomographic imaging was carried out using a dual-detector scanner operated under the single-photon technique. Initial results have been promising, with visualisation of resting perfusion defects in patients with recent infarction and those with ventricular aneurysms. Emission tomography has also been performed at exercise, and has shown tracer deficits in the distribution of significant coronary stenoses. This new approach to myocardial perfusion scintigraphy may lead to improved sensitivity for detecting apical and inferior wall abnormalities by providing depth information not available from a conventional two-dimensional image.

The effect of digoxin on A-V conduction in 19 patients with known disease of their conduction tissue was studied while a demand pacing system was in position. Fifteen had transient complete heart block after myocardial infarction and four had chronic intermittent complete heart block. The patients were studied on return to sinus rhythm.In no instance was a return to either second- or third-degree heart block precipitated in these patients despite therapeutic levels and, in some cases, high serum level of digoxin for a period of seven days.The duration of complete heart block after myocardial infarction was 4.3 days in those taking digoxin while in heart block and 3.3 days in those who started digoxin only after return to sinus rhythm.