Patterns of atrioventricular conduction during postexercise recovery in patients with atrial fibrillation and Wolff-Parkinson-White syndrome.

The effects of the postexercise recovery phase on the functional anterograde conduction properties of the accessory pathway (AP) were evaluated. Twenty-nine patients with Wolff-Parkinson-White (WPW) syndrome were submitted to supine maximal bicycle exercise testing. In seven patients (group I), in whom sustained atrial fibrillation (AF) could be induced by transesophageal pacing (TP), mean ventricular rate (MVR), the shortest R-R interval (SRR) between preexcited beats, and the observed percentage of preexcited beats were evaluated at rest, after each step of exercise and 2 minutes after the end of exercise. In 22 patients (group II), in whom sustained AF could not be induced, decremental TP was performed to evaluate the shortest atrial cycle length (SCL) with 1:1 conduction over AP at rest, after each step of exercise, and 2 minutes after the end of exercise. In four patients in group I, the protocol was repeated with atropine injected during the last minute of exercise. In 12 patients (three from group I and nine from group II), catecholamine plasma levels were measured at rest, at peak exercise, and during recovery. MVR was 144 +/- 20 beats/min at rest, 186 +/- 21 beats/min at peak exercise (P less than 0.001 vs rest), and 179 +/- 21 beats/min during recovery (P less than 0.001 vs rest; P less than 0.05 vs peak exercise). SRR was 289 +/- 73 msec at rest, 223 +/- 25 msec at peak exercise (P less than 0.05 vs rest), and 227 +/- 29 msec during recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Transesophageal versus intracardiac atrial stimulation in assessing anterograde conduction properties of the accessory pathway in Wolff-Parkinson-White syndrome.

Electrophysiologic intracardiac and noninvasive transesophageal testing, used to evaluate parameters of anterograde conduction across the accessory pathway, the refractory period and shortest atrial cycle length with 1:1 conduction over the pathway, were compared to assess the reliability of the noninvasive technique in identifying patients with Wolff-Parkinson-White syndrome, at risk of rapid ventricular response during atrial fibrillation when this arrhythmia is not inducible. Sixteen patients with Wolff-Parkinson-White syndrome were submitted both to invasive and transesophageal atrial stimulation. We evaluated both the functional and effective refractory periods of the accessory pathway, using the same drive cycle length, and the shortest cycle length with 1:1 atrioventricular conduction over the accessory pathway. There were no differences between the parameters obtained by intracardiac atrial stimulation and by transesophageal atrial stimulation. The two approaches correlated well: mean functional refractory periods of the accessory pathway were 285 +/- 42 msec and 289 +/- 32 msec, respectively (NS, r = 0.88); mean effective refractory periods of the accessory pathway were 267 +/- 41 msec and 271 +/- 32 msec, respectively (NS, r = 0.89); mean shortest cycle lengths with 1:1 conduction over the accessory pathway were 255 +/- 48 msec and 255 +/- 44 msec, respectively (NS, r = 0.94). These data demonstrate the reliability of transesophageal atrial stimulation in estimating the parameters for anterograde conduction across an accessory pathway. These results, and the already documented ability of transesophageal atrial stimulation to induce atrial fibrillation, suggest this noninvasive technique should be taken as a first approach in screening patients with Wolff-Parkinson-White syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical use of transoesophageal atrial stimulation in terminating ventricular tachycardia.

This study was performed to evaluate whether transoesophageal atrial pacing could also stop ventricular tachycardias with low rates and no haemodynamic impairment. Prior to resorting to ventricular endocardial pacing, seven male patients, aged between 15 and 73 years, were treated by transoesophageal atrial pacing for 10 spontaneous episodes of sustained ventricular tachycardia at rates between 105 and 160 beats per minute, without haemodynamic impairment. When atrial pacing did not allow ventricular capture, atropine sulphate was administered. Transoesophageal atrial pacing led to ventricular capture in seven episodes, which made overdriving possible, and blocked six episodes of ventricular tachycardia. In no case did transoesophageal atrial pacing lead to an acceleration of ventricular tachycardia or to degeneration into ventricular fibrillation. Transoesophageal atrial pacing can block low-rate sustained ventricular tachycardias (less than or equal to 150 beats per minute). For low-rate sustained ventricular tachycardias without haemodynamic impairment, transoesophageal atrial pacing can thus be used as the method of choice thanks to its good ratio of risk to efficiency.

The nature and evolution of ventricular arrhythmias in acute myocardial infarction.

The natural evolution of ventricular arrhythmias complicating a first episode of acute myocardial infarction has been studied in a group of 56 consecutive patients, who were admitted to the Coronary Care Unit within three hours of the onset of symptoms, and in whom drug administration (digitalis, antiarrhythmics, diuretics and heparin) was limited. Ventricular arrhythmias have been evaluated by means of Holter monitoring performed during the first 24 hours, the second 24 hours, the eighth day, the 18th day and two years after discharge when antiarrhythmic drugs has been discontinued for at least five half-lives. The overall incidence and prevalence of ventricular arrhythmias showed a steady and statistically significant reduction from the first to the eighth day, and a not statistically significant increase from the eighth to the 18th day. The latter increase was still present at the two-year follow-up. The one-by-one behaviour analysis of discharged patients delineated three different patterns: patients who presented a steady reduction in ventricular arrhythmias from the first to the 18th day (44%); patients who showed an almost constant incidence of ventricular arrhythmias during all phases of acute myocardial infarction (24%); and patients who presented both a decrease and an increase in their ventricular arrhythmias (31%). The follow-up at two years showed that the majority of patients, especially those discharged in a high Lown class, had the same arrhythmias as at their follow-up on the 18th day. Correlation of ventricular arrhythmias with the extent of the infarcted area demonstrated that only the peak and mean values of lactic dehydrogenase correlated with the severity of ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of transesophageal atrial pacing in hyperkalemia-induced impulse formation and conduction disturbances.

This report describes the usefulness of transesophageal atrial pacing in the treatment of five patients with hyperkalemia-induced bradycardias. Three patients had marked sinus bradycardia while the other two had a regular rhythm with QRS of left bundle branch block morphology, with no P waves visible on the surface electrocardiogram. Four patients were in chronic hemodialysis three times a week, and one had severe post-traumatic hemorrhage. In three patients, hyperkalemia had been precipitated by food intoxication. In one case the cause was unknown while, in the last case, hyperkalemia was due to rapid infusion of stored blood and solutions containing high concentrations of potassium. Transesophageal atrial pacing was performed in all cases utilizing a bipolar catheter introduced into the esophagus and a constant current generator delivering square wave pulses of 10 msec duration and 19-28 mA intensity. Atrial capture, followed by impulse conduction to the ventricles, was constant in all cases, being performed for between 15 and 35 minutes until a normal sinus rhythm was restored. The procedure was well tolerated. The advantages of this procedure as opposed to invasive ventricular pacing are discussed.

High doses of L-carnitine in acute myocardial infarction: metabolic and antiarrhythmic effects.

Fatty acids accumulate in the muscle cells in some carnitine deficiency syndromes due to a variety of genetic defects in intermediary metabolism. L-Carnitine administration may relieve this excess by transporting acyl compounds out of the cell as acylcarnitine. Similar fatty acid accumulation occurs during myocardial ischaemia because of the decreased rate of beta-oxidation, and this has been put forward as a cause of ventricular arrhythmias. This study was carried out to investigate whether administration of high doses of i.v. L-carnitine in patients with acute myocardial infarction could increase urinary excretion of acylcarnitine and reduce early ventricular arrhythmias. Fifty-six patients suffering from acute myocardial infarction, admitted to the Coronary Unit between 3 and 12 h after the onset of symptoms, were included in the study. The design of the study was double blind, parallel and placebo controlled. Allocation of treatment to patients was done randomly after stratification (time from onset of pain and site of infarction). The first group (28 patients) received intravenous L-carnitine at a dose of 100 mg kg-1 b.w. every 12 h for 36 h while the second group (28 patients) received placebo intravenously. Immediately before starting treatment two blood samples were taken (at 5-min intervals) and a further 16 samples were taken at regular intervals over the following 48 h. Patients' urine was collected over the same period of time. Concentrations of free carnitine, short chain acylcarnitine esters and long chain acylcarnitine esters in serum and urine were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence of 'dual A-V nodal pathways' in first- and second-degree type I supra-His A-V block.

The incidence of 'dual A-V nodal pathways', diagnosed on the basis of spontaneous or induced modifications in the PR interval, has been assessed in a group of 168 consecutive patients with first- (77) and second-degree (91) type I supra-His block. 'Dual A-V nodal pathways' were found in 12 cases (16%) with first-degree and in 7 cases (7.7%) with second-degree type I supra-His A-V block. His bundle recording confirmed the hypothesis that PR interval variations observed in these cases are due to modifications in the AH interval and thus to changes in A-V nodal conduction velocity. The electrophysiologic study also showed that the phenomenon was easily reproduced by atrial stimulation. The frequent association between 'dual A-V nodal pathways' and supra-His blocks suggests that the block mechanism should be studied in depth as it could have prognostic and therapeutic implications.

Ventricular fibrillation induced by transesophageal atrial pacing in hypertrophic cardiomyopathy.

Sudden death is a rather frequent occurrence in patients with hypertrophic cardiomyopathy, yet the mechanism is uncertain in most cases. We describe a case of an 18 years old patient with a family history of hypertrophic cardiomyopathy and sudden death in whom ventricular fibrillation could be repeatedly induced by means of transesophageal atrial stimulation with 1:1 AV conduction at a rate of 200 beats min-1 and prevented by pharmacological depression of AV node. The not particularly high ventricular rate at which VF occurred could suggest that in hypertrophic cardiomyopathy a major role in favouring VF induction is played by the electrophysiological properties of the myocardium and that sudden death can occur as a consequence of different atrial tachyarrhythmias.

Role of QT prolongation secondary to a postextrasystolic pause as a possible mechanism for the induction of ventricular fibrillation. Report of two cases.

Two patients developed ventricular fibrillation (VF) while undergoing continuous electrocardiographic monitoring. Analysis showed that VF appeared only when a particular combination of circumstances occurred: a postextrasystolic pause, QT prolongation of the subsequent beat and a premature ventricular beat that did not have a short coupling interval. The relevance of this sequence as a trigger mechanism of VF is discussed.