To study the dispersion of ventricular repolarization following double and triple programmed stimulation and its correlation with the inducibility of ventricular arrhythmias, monophasic action potentials were simultaneously recorded from the right ventricular apex and outflow tract during programmed stimulation in 12 patients with ventricular arrhythmias and a normal QT interval. The time difference between the ends of the two monophasic action potentials were used as a measure of the dispersion of ventricular repolarization, which consists of the activation time difference and the monophasic action potential duration difference. During double and triple programmed stimulation, the dispersion of ventricular repolarization increased significantly with the shortening of the coupling interval but decreased slightly with the shortening of the preceding interval. The induction of the ventricular arrhythmias in these patients was invariably associated with a marked increase in the dispersion of ventricular repolarization. The maximal dispersion of ventricular repolarization was significantly larger in the seven patients with polymorphic ventricular tachycardia and/or ventricular flutter/fibrillation induced than in the four patients with monomorphic ventricular tachycardia induced. Analysis of the two components of the dispersion of ventricular repolarization revealed that the increased dispersion of ventricular repolarization was mainly caused by an increase in the activation time difference in the monomorphic ventricular tachycardia subgroup, and by increases in both the activation time difference and monophasic action potential duration difference in the polymorphic ventricular tachycardia/fibrillation subgroup. These findings suggest that increased dispersion of ventricular repolarization is one of the underlying mechanisms accounting for the myocardial vulnerability to ventricular arrhythmias and that repolarization disturbance is important for the genesis of polymorphic ventricular tachycardia/fibrillation.

(1) Platinum electrodes can be used for timely recording of MAPs in patients. (2) It is feasible to record MAPs and deliver radiofrequency currents via the same platinum-tip electrode. These findings suggest that MAP-guided catheter ablation is technically possible.

The signed value of monophasic action potential duration difference can specify whether an increased dispersion of ventricular repolarization is caused by inhomogeneous repolarization, inhomogeneous conduction or both, and thereby it is useful in study of the mechanism of ventricular arrhythmias.

BackgroundLocal ventricular refractoriness and its dispersion during ventricular fibrillation (VF) have not been well evaluated, due to methodological difficulties.MethodsIn this study, a non-invasive method was used in evaluation of local ventricular refractoriness and its dispersion during induced VF in 11 patients with VF and/or polymorphic ventricular tachycardia (VT) who have implanted an implantable cardioverter defibrillator (ICD). Bipolar electrograms were simultaneously recorded from the lower oesophagus behind the posterior left ventricle (LV) via an oesophageal electrode and from the right ventricular (RV) apex via telemetry from the implanted ICD. VF intervals were used as an estimate of the ventricular effective refractory period (VERP). In 6 patients, VERP was also measured during sinus rhythm at the RV apex and outflow tract (RVOT) using conventional extra stimulus technique.ResultsElectrograms recorded from the RV apex and the lower esophagus behind the posterior LV manifested distinct differences of the local ventricular activities. The estimated VERPs during induced VF in the RV apex were significantly shorter than that measured during sinus rhythm using extra stimulus technique. The maximal dispersion of the estimated VERPs during induced VF between the RV apex and posterior LV was that of 10 percentile VF interval (40 ± 27 ms), that is markedly greater than the previously reported dispersion of ventricular repolarization without malignant ventricular arrhythmias (30–36 ms). ConclusionsThis study verified the feasibility of recording local ventricular activities via oesophageal electrode and via telemetry from an implanted ICD and the usefulness of VF intervals obtained using this non-invasive technique in evaluation of the dispersion of refractoriness in patients with ICD implantation.

Severe throat infection is not usually associated with a higher risk of paroxysmal attacks of torsade de pointes tachycardia. A patient is reported in whom epiglottitis was associated with the sudden development of cardiac syncope caused by an acquired adrenergicdependent long QT syndrome and the development of ventricular arrhythmias. (Br Heart Y 1994;72:205-208) Case report A 70 year old man with a history of essential hypertension was admitted to the emergency ward with fever, dyspnoea, and severe throat pain. He had been treated with propranolol (80 mg daily), polythiazide (1 mg daily), and hydralazine (50 mg three times a day), during which time his electrocardiogram was normal (fig 1). Epiglottitis was diagnosed. In view of his severe respiratory distress, endotracheal intubation was performed and the patient was treated with mechanical ventilation for 10 days. A parapharyngeal abscess developed on aVL VI a ,1 i, III the right side of his neck. Computed tomography localised the abscess, surrounded by a severe inflammatory reaction, near the carotid artery and the sympathetic nerves on this side (fig 2). On the third day the abscess was drained through an incision along the sternocloidomastoid muscle, beneath the omohyoid muscle, and medial to the vessels. A digital dissection towards the abscess was performed. The patient was discharged from hospital after four weeks. Seven weeks later he was readmitted because of repeated transient sudden attacks of unconsciousness. During these attacks he had no signs of tonic or clonic movements or faecal or urinary incontinence. After each episode he felt exhausted and found it difficult to get up off the floor.No abnormalities were found on physical examination. Routine laboratory tests were normal with serum digoxin concentration of 1-9 nmol/l. A consultant neurologist found no signs of neurological deficits or neurological disease. Apart from a slightly enlarged heart, the chest x ray showed no other changes. Treatment with digitalis and propranolol was stopped.