Verapamil in wide complex tachycardia.
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Biomedical subjects
Publications and source records attributed to D E Ward.
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Ablation of AV nodal/His bundle conduction by fulgurative electrical discharges has revolutionized the management of refractory supraventricular tachycardias of any type which requires AV conduction over the normal anatomical pathways. The success and safety of the technique is such that it has eclipsed operative ablation of AV conduction. It is increasingly clear that both anomalous pathway conduction and ventricular tachycardia foci may be destroyed by the technique of fulguration and preliminary evidence suggests that certain types of atrial foci may also be susceptible to this method of ablation. Development of purpose-designed electrodes for delivery of the discharges is likely to reduce maximum energy requirements and increase the safety of fulguration.
The effect of flecainide acetate, a class 1c antiarrhythmic agent, was examined in 15 patients with recurrent ventricular tachycardia. Intravenous flecainide was administered in a dose of 2 mg/kg at the time of intracardiac stimulation and recording studies. Oral flecainide was given to 10/15 patients and retesting was undertaken using an indwelling electrode. Intravenous flecainide terminated sustained stable tachycardia in 8/11 patients and prevented reinitiation of tachycardia in 5/10 patients. Oral therapy prevented induction of tachycardias in only 2/10 patients. Five patients had non-sustained tachycardia and three had slower sustained tachycardia. "New" non-clinical tachycardias could be induced in six patients after flecainide but five of these had had more than one type of induced tachycardia. Four of 10 patients remained free of tachycardias during follow-up. Withdrawal of oral treatment was necessary in three patients, one of whom had severe proarrhythmic effects. Two patients required additional antiarrhythmic therapy. Long-term suppression could not be predicted from the results of oral therapy, but testing after intravenous drug seemed to be a more useful prognostic indicator. In summary, intravenous flecainide is effective for slowing and termination of stable ventricular tachycardia. Oral therapy is also effective but caution should be exerted in patients with multimorphic tachycardias.
Formalin-fixed, paraffin-embedded tissue sections of normal skin, sebaceous hyperplasia, nevus sebaceus, sebaceous adenoma, and sebaceous carcinoma were studied by means of biotinylated and FITC conjugated concanavalin A (Con A) and Lens culinaris agglutinin (LCA). At relatively high concentrations of these lectins, all cutaneous epithelial cells were stained. As the concentration of LCA was lowered, there was a corresponding decrease in the intensity of staining of all epithelial cells. With lowered concentrations of Con A, staining of sebaceous epithelium remained strongly positive, while staining of other epithelia decreased in a manner similar to that seen for LCA. These staining patterns were seen in normal and neoplastic tissues. Both Con A and LCA are known to bind to alpha-D-mannopyranosyl and alpha-D-glucopyranosyl residues of glycoproteins and glycolipids. The difference in staining of sebaceous epithelial cells by Con A and LCA suggests that the binding of these lectins is not determined strictly by the presence of alpha-D-mannopyranosyl or alpha-D-glucopyranosyl residues, but is modified by side-chain substitution on the monosaccharides and/or by the oligosaccharide which contains the particular monosaccharide. Whichever event is operative, a saccharide moiety is present on the surface of mature sebaceous cells which has a strong affinity for Con A.
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Exacerbation of ventricular arrhythmias by antiarrhythmic drugs the lignocaine-type has not been reported previously. In this paper we describe three patients with a variety of ventricular arrhythmias who were treated with tocainide and developed worsening of the ventricular arrhythmias. In one patient, frequent ventricular ectopic beats were converted to sustained ventricular tachycardia (VT) in another, nonsustained VT was converted to sustained VT, and in a third, monomorphic VT was converted to multimorphic VT. These patients illustrate the need for careful supervision of antiarrhythmic therapy for VT, even when lignocaine-like drugs are being used.
A patient with sinuatrial disease and implanted pacemaker was treated with amiodarone (maximum dose 1000 mg, maintenance dose 800 mg daily) for 10 months, for control of supraventricular tachyarrhythmias. He developed pneumonitis, pleural and pericardial effusions, and a predominantly proximal motor neuropathy. Immediate but gradual improvement followed withdrawal of amiodarone and treatment with prednisolone. Review of this and previously reported cases indicates the need for early diagnosis of amiodarone pneumonitis, immediate withdrawal of amiodarone, and prompt but continued steroid therapy to ensure full recovery.
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Three patients with tachycardias associated with the Wolff-Parkinson-White syndrome had failed to respond to antiarrhythmic drugs and underwent transvenous ablation of accessory pathways. Intracardiac studies located the site of accessory pathway to the septum in two patients and mid-posterobasal left atrioventricular junction in one. Ablation was performed by positioning an electrode lead as close as possible to the accessory tract and delivering shocks of 50 to 100J using a conventional defibrillator. In all patients the accessory pathway was abolished after the first three shocks. In two patients followed for four and nine months there was no recurrence of tachycardia or pre-excitation. The other patient developed pre-excitation again three weeks later and repeat ablation was performed. This patient has been followed for six months with no evidence of a recurrence of pre-excitation. This method may provide a valuable alternative to pacemaker and surgical treatment in selected patients with drug resistant arrhythmias associated with accessory atrioventricular connexions.
35 patients with refractory supraventricular arrhythmias were treated in three centres by high-energy shocks delivered to the atrioventricular conduction system from a conventional transvenous pacing catheter. After a mean interval of ten months, 26 patients (74%) had persistent complete heart block, 2 (6%) had intermittent complete heart block, and 3(9%) had first-degree heart block. 3 patients continued to have conducted atrial fibrillation, but with slower ventricular rates than previously, and 1 had normalisation of dual atrio-His conduction. In 1 patient a septal accessory pathway was ablated. 30 patients (86%) are completely symptom-free without additional therapy. There were no important long-term complications. Transvenous ablation of atrioventricular conduction is a safe and effective technique for treating a wide range of refractory atrial and junctional arrhythmias.
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Forty-four patients with congenital cardiac disease underwent surface averaged electrocardiography using a high resolution purpose built module. Twelve patients had complete transposition of the great vessels, 14 had tetralogy of Fallot, 5 had ventricular septal defects, 6 atrial septal defects, 3 atrioventricular septal defects and 4 patients had miscellaneous non-structural abnormalities. All patients with structural disorders underwent corrective or palliative surgery. The aim of the study was to examine the feasibility of the method and its usefulness in detecting His potentials and delayed potentials in the ST segment. A His potential was recorded in 30 patients (68%) with an amplitude ranging from 1.25 to 8.25 microV. Delayed potentials were recorded in only 1 patient with frequent ventricular premature beats. This technique may be useful in assessing intraventricular conduction times in patients with bundle branch block and/or axis deviation especially those who are at risk from intermittent complete AV block after surgical intervention. Detection of delayed potentials may allow better assessment of post-operative risk of ventricular arrhythmias in patients who have undergone ventricular surgery.
Five patients with recurrent tachycardias exhibiting right bundle branch block with left axis deviation were referred for investigation. In each case, a supraventricular mechanism was suspected. During sinus rhythm the QRS morphology and axis (-10 to +60 degrees) and HV intervals were normal. Tachycardia was initiated by timed ventricular premature stimuli in 4 patients, rapid ventricular pacing in 3 patients and rapid atrial pacing in 2 patients. The tachycardia cycle length varied from 275 to 380 ms with right bundle branch block and a leftward axis change of 30 to 125 degrees at the onset of the tachycardia. The HV interval ranged from +15 to -20 ms. In each patient ventriculoatrial dissociation occurred spontaneously or could be induced. All tachycardia could be terminated or greatly slowed by calcium antagonists. These data are consistent with an unusual reentrant mechanism of tachycardia located in the posterior fascicle of the left bundle branch.
Three patients were referred for urgent investigation and treatment of refractory arrhythmias. Each patient had failed to respond to antiarrhythmic drugs and in two patients direct current cardioversion was also unsuccessful. Transvenous ablation of atrioventricular conduction was therefore thought appropriate. With a temporary ventricular pacing system in situ, a second electrode was used to record His and atrial electrograms. A 270 watt-second shock was delivered through this lead when the His potential was maximized. The tachycardia was controlled in two patients and the procedure was without deleterious effects.
Transvenous ablation of atrioventricular conduction by high energy shock through a pacing wire has been used as a method of controlling the ventricular response to rapid atrial arrhythmias. A patient in whom this technique successfully controlled refractory tachycardia was admitted with severe left ventricular impairment five months after the procedure and died. The heart was examined at necropsy. There was no sign of endocardial damage in the region of the atrioventricular node-His bundle. Histological sections failed to show any scarring, inflammation, or infiltration in the region of the atrioventricular node. On the contrary, there was no evidence of any surviving atrioventricular nodal tissue. The mechanism of this effect is not known. The lack of endocardial or myocardial damage further confirms the safety of this new method of controlling tachycardia.
Over a period of five years 12 patients underwent electrophysiological studies for the investigation of recurrent tachycardias which showed ventricular pre-excitation. Nine patients had a type B pattern and two a type A. One patient had episodes of both types. Dual atrioventricular nodal pathways were found in six of seven patients with atrioventricular nodal re-entrant tachycardia mechanisms. Single direct atrioventricular accessory pathways were present in four patients, single nodoventricular pathways in five, and multiple pathways in three. Twenty one tachycardias were induced, of which 13 showed ventricular pre-excitation. Five patients had nodoventricular pathway conduction during atrioventricular nodal tachycardia and one during atrioventricular re-entrant tachycardia. Only three patients had simple antidromic tachycardia and one additional atrioventricular nodal tachycardia with bystander atrioventricular accessory conduction. Three patients had three different tachycardias, three had two types, and six had one type. Thus junctional tachycardias showing ventricular pre-excitation are often associated with multiple mechanisms and complex anatomical and functional substrates. An accessory pathway was an essential component in only six of 13 tachycardias showing ventricular pre-excitation. Determination of the tachycardia mechanism requires detailed study and analysis.