Biomedical subjects
Publications and source records attributed to E Rowland.
In three patients anterograde conduction across a previously undocumented accessory pathway was exposed by the development of atrial fibrillation. This unusual presentation illustrates the possible unmasking of the Wolff-Parkinson-White syndrome by other factors in patients who have not previously demonstrated the potential for anterograde accessory pathway conduction.
A case of permanent unintentional ablation of an accessory pathway during electrophysiological study is reported. Possible factors predisposing to such ablation include the location and depth below the endocardium of the accessory pathway.
Cryoablation of the accessory pathway was used in the management of 20 patients with pre-excitation syndromes. All patients had presented with paroxysmal atrioventricular reentrant tachycardia; in addition, six had experienced atrial fibrillation. In 16 patients pre-excitation was overt and in four the accessory pathway was concealed. Intraoperative epicardial and endocardial mapping showed 10 left free wall pathways, seven septal pathways, and four right free wall pathways. One patient had two right free wall accessory pathways. There was one postoperative death (from a ruptured cerebral haemangioma) and one patient had transient hemiparesis. There was early recurrence of arrhythmia or pre-excitation in six patients and five of these were among the first ten in the series. Four of the six underwent successful reoperation; 17 patients remain symptom free of all antiarrhythmic treatment. Two patients did not undergo reoperation--one became symptom free on drugs that had previously been ineffective and the other received an antitachycardia pacemaker. The mean period of follow up was six years. Accessory pathway function was not restored and atrioventricular nodal function was preserved in all patients, demonstrating the feasibility of this technique in the long term management of patients with the pre-excitation syndrome.
Atrial fibrillation was identified as the initial arrhythmia complicating the Wolff-Parkinson-White syndrome in ten (9%) of 108 patients. Despite initially rapid ventricular responses in seven, long term survival and control of arrhythmia were excellent on medical treatment. Whereas symptom free patients with the pre-excitation syndrome who have additional underlying disease predisposing to atrial fibrillation may need detailed electrophysiological study, a more conservative approach is suitable for the typical symptom free individual.
Histological investigation of a heart with aneurysmal malformation of the anterior cardiac vein showed atypical accessory atrioventricular pathways that could have been the basis for bypass tracts and ventricular pre-excitation. Review of other cases with coronary sinus or venous aneurysms showed a striking association with sudden death. Such malformations may not be as benign as previously thought.
Adenosine (0.05-0.25 mg/kg intravenously) successfully terminated resistant supraventricular tachycardia (SVT) in three seriously ill newborn infants and one older child. Termination of tachycardia was achieved in each case within 20 s. Adenosine, unlike many other anti-arrhythmic agents, has no substantial negative inotropic effect under these circumstances and may become the drug of choice in haemodynamically compromised children with SVT. However, it has no value in prophylaxis against recurrent SVT.
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We treated 13 children aged 0.2 years to 15.7 years (median 7.1 years) with flecainide acetate for refractory symptomatic supraventricular tachycardia. Six children had direct atrioventricular accessory pathways, of whom four had overt Wolff-Parkinson-White syndrome on the 12 lead electrocardiogram, while in the other two the accessory pathway was concealed. Three children had nodal atrioventricular re-entrant tachycardia, two had a re-entrant tachycardia, the exact mechanism of which was not known, one child had ectopic atrial tachycardia, and one had atrial flutter associated with an atrial septal defect. The remaining 12 children had structurally normal hearts. Flecainide (2 mg/kg intravenously) resulted in termination of the tachycardia in 11 of the 12 children treated during tachycardia. In 11 of the children successful prophylaxis was achieved with oral flecainide. Side effects occurred in two children during intravenous administration, but there were no side effects with oral treatment. This experience indicates that flecainide, which has not been used extensively in children, is an effective and safe antiarrhythmic agent, capable of terminating and controlling supraventricular tachycardia in children. Furthermore, flecainide may be successful where conventional agents fail.
Fourteen patients with established atrial fibrillation (longer than three months) that was refractory to treatment were studied to compare the clinical and electrophysiological effects of amiodarone and bepridil. All patients initially received bepridil for three weeks (200-600 mg/day), followed by amiodarone for two to three months (100-400 mg/day). Bepridil seemed to be slightly more effective than amiodarone in converting the fibrillation to sinus rhythm (nine of fourteen compared with four of ten). The ventricular response in atrial fibrillation was equally well controlled by bepridil and amiodarone, both at rest and during exercise. Bepridil was associated with the development of ventricular arrhythmias in eight of fourteen patients; two had torsade de pointes, which in one degenerated into fatal ventricular fibrillation. These arrhythmias seemed to be associated with bepridil induced prolongation of the QTc interval. No ventricular arrhythmias were seen during amiodarone treatment. Although bepridil seems to be an effective antiarrhythmic agent for the management of atrial fibrillation, its arrhythmogenic actions make it unsuitable for this purpose.
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The current technology in the area of catheter ablation for cardiac arrhythmia is limited by the amount of damage sustained by the ablated area in relationship to the energy used. Thus, a newly designed power source is described in this report in three patients, two with resistant atrial flutter/fibrillation and one with a reentrant AV tachycardia. The delivered energy in all patients was 5.1 joules or less with the exception of a single shock of 37.5 joules, which was required in one patient. We conclude that this effort of low energy ablation using a unique power source represents an advance in the field of ablation that merits further evaluation.
In studies of the right ventricle the complexities of chamber shape may be overcome by use of multiple tomographic imaging planes. An established protocol for the echocardiographic description of the heart was used to examine the right ventricle in an ordered series of transducer locations and orientations. Diastolic measurements were made of the right ventricular inflow tract, outflow tract, and right ventricular body, and the range and reproducibility of normal values for cavity size and right ventricular free wall thickness were established. These measurements of cavity size in 41 normal subjects were highly reproducible and the views that were used correctly described the truncated and ellipsoidal shape of the right ventricular inflow tract and body with a separately aligned outflow tract. Cavity trabeculation prevented measurement of the free wall thickness in some areas; however, values of nearly twice the previously reported upper limit of normal for anterior regions were measured from the apex or lateral right ventricular wall. These normal data provide a basis for future echocardiographic studies of the right ventricle.
The belief that there is total irregularity of the pulse in atrial fibrillation has been re-examined. In a computerised analysis of R-R intervals and pulse volumes, 100-500 (mean 237) consecutive cycles were examined in 74 patients with atrial fibrillation, of whom 36 were on digoxin and 38 were not taking any antiarrhythmic treatment. A Doppler ultrasound technique was used to assess pulse volumes, against which R-R intervals were correlated. Although the sequence of consecutive R-R intervals was random in 52 (70%), patients there was a significant correlation between consecutive intervals in 22 (30%), the correlation coefficient being negative in 11 and positive in 11. In 43 (58%) cases the sequence of consecutive pulse volumes was significantly non-random; 34 (46%) showed pulsus alternans, indicated by a negative correlation between consecutive volumes. The proportion of patients with a non-random sequence of R-R intervals or pulse volumes was the same whether or not they were taking digoxin. Thus patients with atrial fibrillation often have patterns of regularity of the pulse, with the ventricular rhythm being non-random in almost one third and the sequence of pulse volumes being non-random in over a half. Contrary to classic teaching, in many patients with atrial fibrillation the pulse is not irregularly irregular.
Patients with right ventricular tachycardia may have adverse electrophysiological abnormalities linked to disturbed right ventricular structure. Seventeen patients who presented with right ventricular tachycardia without coronary artery disease or gross abnormalities of left ventricular function were studied. Patients had the ventricular tachycardia characterised at electrophysiological study and most underwent radionuclide and contrast angiography. At echocardiography specific attention was paid to the right ventricular chamber size. Two groups were identified at echocardiographic study. In group 1, nine patients had normal left ventricular dimensions and relatively normal features at electrophysiological study. Mean right ventricular ejection fraction was 0.45 by krypton-81 measurement. Group 2 comprised eight patients who had dilatation of right ventricular inflow tract, outflow tract, and right ventricular body. This group had more severe features at presentation and at electrophysiological study. In this group all available echocardiographic measurements of right ventricular chamber size were greater than those of group 1 and outside the normal range. Four of the eight patients in group 2 showed regional right ventricular dyskinesia at echocardiography. Mean right ventricular ejection fraction (0.23) in group 2 was significantly lower than in group 1. One patient in group 2 subsequently died. In patients with right ventricular tachycardia, those with less favourable prognostic features at electrophysiological study may have distinct abnormalities of right ventricular structure that can be identified at echocardiographic study. Echocardiography may be of value in the recognition of potentially malignant clinical and electrophysiological features in this group.
Patients with acute congestive cardiac failure had elevated plasma concentrations of atrial natriuretic peptide (ANP) which fell towards normal levels with successful diuretic therapy. The plasma ANP concentration was closely correlated with the clinical condition of the patients as assessed by serial clinical measurement of the jugular venous pressure and body weight. Plasma ANP concentrations were also raised in patients with a spontaneous acute onset of supraventricular tachycardia but to a lesser extent in patients with chronic tachycardia. Again, successful treatment with d.c. cardioversion returned plasma ANP concentrations towards normal. Induction of atrioventricular re-entrant tachycardia produced an acute and marked rise in plasma ANP concentrations, which rapidly returned to normal when the sinus rhythm was restored. This acute ANP rise probably mediates the known acute natriuretic effect of paroxysmal tachycardia. All the data are consistent with the hypothesis that atrial distension, whatever the cause, releases ANP into plasma.
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Bepridil (2 mg/kg intravenously) was given to 20 patients with atrioventricular (AV) reentrant tachycardia and its effects were compared with those of verapamil (0.15 mg/kg intravenously) in 8 patients and ajmaline (0.75 mg/kg intravenously) in 12. After baseline electrophysiologic measurements, the drugs were given during sustained AV reentrant tachycardia (8 patients had dual AV nodal pathways and 12 had an accessory AV pathway). Verapamil terminated AV reentrant tachycardia in 7 patients and bepridil terminated it in 6. In 8 of the patients who received ajmaline, AV reentrant tachycardia was terminated and in 6 of this group bepridil did so. Bepridil was more successful in terminating AV reentrant tachycardia in those with dual AV nodal pathways than in those with an accessory AV pathway. Bepridil slowed sinus rate by 10% (p less than 0.0001), whereas verapamil did not change it significantly. Both verapamil and bepridil administration prolonged AV nodal conduction (39% and 44%, respectively), lengthened AV nodal effective refractory period (18% and 17% respectively) and increased the Wenckebach cycle length of the AV node (24% and 25%, respectively) to a significant degree (p less than 0.05). Bepridil also lengthened atrial and ventricular effective refractory periods (p less than 0.01) and QT interval (p less than 0.0001) in the group as a whole; in those receiving ajmaline and bepridil only atrial refractoriness was significantly altered (p less than 0.05). After treatment for 3 to 5 days with oral bepridil, 19 patients underwent repeat study.(ABSTRACT TRUNCATED AT 250 WORDS)