Electrophysiological characteristics of asymptomatic Wolff--Parkinson--White syndrome

Although most asymptomatic patients with the Wolff—Parkinson—Whitesyndrome have a good prognosis, some die suddenly. Electrophysiologicaltesting may identify patients at possible risk of sudden death.The mechanism of sudden death in these patients is believedto result from ventricular fibrillation due to atrial fibrillationwith rapid anterograde conduction over the accessory pathway.Consequently, we performed electrophysiological studies in 40asymptomatic patients with the Wolff—Parkinson—Whitesyndrome. Certain electrophysiological properties clearly identifiedthese patients: (1) in most patients sustained reciprocatingtachycardia could not be induced and this explains the absenceof symptoms of regular fast palpitations; (2) the incidenceof inducible sustained atrial tachyarrhythmias (30%), of shortRR intervals between pre-excited beats (20%) and of risk ofsudden death (12.5%) was similar to the incidence in symptomaticpatients with the Wolff—Parkinson—White syndromeand reciprocating tachycardia. Because of the ease with which transoesophageal study can beperformed we think that the asymptomatic Wolff— Parkinson—Whitesyndrome should be systematically evaluated so as to reassurepatients with the benign form that they can lead a normal lifeand take part in sport and secondly to define the real prognosisof the patients whose characteristics suggests a risk of suddendeath.     

Effect of flecainide on left ventricular ejection fraction

Antiarrhythmic agents may depress cardiac contractility andworsen heart failure. Flecainide is an effective antiarrhythmicdrug, but when administered orally in patients with left ventricular(LV) dysfunction, its effect on LV function is unknown. To assessthe effects of flecainide on cardiac function, LV ejection fraction(LVEF) was measured by radionuclide ventriculography in 36 patientswith LV dysfunction (LVEF 40%), prior to and 7 days after drugtherapy was initiated. To analyse the possibility of a dose-dependenteffect on LVEF, 18 patients received 200 mg day^–1 of flecainideand 18 patients with an identical initial LVEF (27±8vs 27±9) (NS) received 300 mg day^–1. The studywas stopped in 7 patients because of severe cardiac adverseeffects; in these patients the LVEF was significantly lower(15±7) than that of the 29 patients who completed theprotocol (27±8) (P<0.01). In patients who completedthe protocol, there was no significant change in LVEF eitherwith a daily dosage of flecainide of 200 mg day^–1 (27±8vs 27±8) or with 300 mg day^–1 (27±9 vs 28±13).Thus, in the patients with LV dysfunction studied, oral flecainidedid not significantly affect LV function either with a low orwith the ususal daily dosage. However in patients with severeimpairment of LV function (LVEF<30%) flecainide must be usedcarefully owing to a higher incidence of adverse effects oncardiac rhythm.     

Proarrhythmic and antiarrhythmic effects of intravenous prostacyclin in man

Prostacyclin (PGI2) has been shown to reduce the occurrenceof experimental ventricular arrhythmias. To assess potentialbeneficial effects in man, the electrophysiological action ofPG12 was studied in 16 non medicated patients. The protocolused in incremental pacing and programmed stimulation in theright atrium and ventricle. This protocol and measurement ofeffective refractory periods (ERP) were performed before andduring the injection of 2.5, 5 and 10 ng kg^–1 min^–1of PGI2. The atrial functional refractory period decreased significantly(P<0.05); PGI2 had no influence on the occurrence of induciblenon-sustained (NS) atrial tachycardias and was responsible forthe occurrence of 2 non-sustained atrial tachycardias in 8 patientswith inducible atrial echo beats under basal conditions. Thirteenpatients did not have inducible ventricular tachycardia ( VT)under basal conditions. Non-sustained VT was induced after PGI2in 4 of them but in only 1 of them after the administrationof propranolol. Three patients had inducible VT under basalconditions (1 non-sustained, 2 sustained VT). PG12 did not preventthe occurrence of VT (1 non-sustained, 1 sustained VT), exceptin 1 patient with ischaemic-related VT, who had non-sustainedVT after PGI2. In conclusion, PGI2 does not seem to have a cardiacantiarrhythmic effect and may increase the atrial and ventricularrepetitive response. This effect could be related to an increaseof adrenergic tone.     

Correlation between inducibility of sustained ventricular tachycardia and QRS duration

Some studies provide a link between the width of QRS complexesand late potentials occurring at the end of the QRS complexin signal-averaged recordings. The purpose of this study wasto compare three methods of QRS duration measurement: the conventional12 lead ECG. the Frank vectorcardiogram (VCG) and the signal-averagedelectrocardiogram. The recordings were made at a similar timein 121 consecutive patients with the Cardionics PC-based system(ECG and VCG) and the ardionics high resolution ECG, based onmethods described by Simson. Patients with bundle branch blockwere excluded. All patients had presented a myocardial infarctionand were studied either for spontaneous ventricular arrhythmiasor systematically 3 to 6 weeks after an acute myocardial infarction. The signal-averaged ECG and VCG QRS durations were similar in41 patients without inducible ventricular arrhythmias and withnormal signal-averaged ECG but were longer (P<0·001)than the conventional ECG QRS duration. In 36 patients withspontaneous and inducible ventricular tachyarrhythmias, theQRS duration was significantly longer on signal-averaged ECGthan on VCG (P<0·05) and longer on VCG than on conventionalECG (P<0·05). The QRS duration was also significantly(P<0·001) longer with the three techniques in patientswith spontaneous ventricular tachycardia (VT) than in patientswithout spontaneous and inducible VT. A QRS duration on VCG 110 ms and on conventional ECG 100 ms had a sensitivity of93% and 77% and a specificity of 83% and 85% respectively forpredicting an abnormal signal-averaged ECG. In conclusion, the measurement of QRS duration with the conventionalECG, VCG or the signal-averaged ECG could be a simple methodto detect the patients with myocardial infarction prone to VT.     

Value of oesophageal pacing in evaluation of atrial arrhythmias

The study of ‘atrial vulnerability’ is often clinicallyindicated but it requires the use of invasive intracardiac stimulation.The purpose of the study was to assess the use of oesophagealpacing in the evaluation of atrial tachyarrhythmias (ATA). Fifty-fivepatients with documented ATA (group I) and 60 without (groupII) were studied. The protocol of oesophageal pacing consistedof atrial pacing up to the second-degree AV block and programmedstimulation in the control state and after isoproterenol infusion.ATA was induced in 47 group I patients (85%) either in the controlstate (n=27) or during isoproterenol infusion (n=20) and inthree group II patients (5%). There was no other electrophysiologicalabnormality. The presence of underlying heart disease did notprecipitate ATA in group II. In conclusion, because of its good sensitivity (85%) and specificity(95%) transoesophageal pacing could be used to evaluate atrialarrhythmias.     

Effect of isoproterenol on serum potassium and magnesium

Some ventricular arrhythmias can be related to a decrease inthe level of potassium (K) and/or magnesium (Mg). Because adrenergicstimulation decreases serum K⁺ and Mg⁺⁺, we decided to investigatethe effects of a beta-receptor agonist, isoproterenol, on serumK⁺ and Mg⁺⁺, and their consequences on the induction of tachycardia.Programmed atrial and ventricular stimulation was performedin 95 patients before and during infusion of 1.6µg . ml^–1of isoproterenol. During isoproterenol infusion, 61 patientshad no inducible tachycardias (group I) and 34 had induciblesustained tachycardias (group II): 16 of them (group IIA) hadinducible sustained supraventricular tachyarrhythmias and 18(group IIB) had inducible sustained ventricular tachycardia.Serum K⁺ and Mg⁺⁺ were measured at the end of stimulation inthe control state and during isoproterenol infusion. The basalvalues in groups I and II did not differ (3.8 + 0.38 vs 3.86+ 0.39 mEq . 1^–1 for K⁺, and 20.18 + 2.68 vs 19.83+1.63mg l^–1 for Mg⁺⁺). Isoproterenol infusion induced a significant(P<0.001) hypokalaemia in all groups and a decrease in serumMg in group II: there was a significant decrease in serum Mg⁺⁺(P<0.05) in group IIA (19.55±1.7 vs 20.4 + 4.6). Thedecrease in serum Mg⁺⁺ in group IIB (18.9+1.55 vs 19.32 + 1.63)was not significant. However the serum Mg⁺⁺ level during isoproterenolinfusion was significantly lower in group IIB than in groupI. In conclusion, the infusion of isoproterenol was responsiblefor a significant hypokalaemia, which did not explain the inductionof tachycardia. On the other hand, it also induced a decreasein serum Mg⁺⁺, which might facilitate the induction of supraventricularand ventricular tachycardia.     

The Tall R Wave in Lead V1 in Posterior Myocardial Infarction: A Reciprocal Sign or a His-Purkinje Conduction Disturbance?

The significance of the tall R wave in lead V1 with an R/S ratio greater than or equal to 1 in posterior myocardial infarction (PMI) was investigated in 28 patients during programmed electrical stimulation. The patients had been admitted with acute PMI documented by electrocardiogram and proven by enzymatic increase. Electrophysiological study was performed 3 weeks after acute PMI. In 17 of the 28 patients (group 1), the tall R wave in V1 disappeared during stimulation: In 13 of them a premature atrial extrastimulus was responsible for an abrupt normalization of QRS complex in V1 related to an increase in AH or HV interval. In the 4 remaining patients the disappearance of the tall R wave in V1 was related to a sinus pause. In 14 patients of group 1, a different prematurity in atrial stimulation induced a right or left bundle branch block (BBB). In 11 of the 28 patients (group 2) the tall R wave in V1 was unchanged but a premature atrial extrastimulus induced a right BBB in 5 patients and a left BBB in 6. In conclusion, the normalization of QRS complex in lead V1 during atrial stimulation or alterations in cycle length suggests that the tall R wave in V1 in PMI is not a simple reciprocal sign of leads V8 V9. Its association with different varieties of BBB and changes in AH or HV intervals could suggest a relationship with a His-Purkinje conduction disturbance in some patients.     

Initiation of ventricular fibrillation by atrial fibrillation

We report the case of a patient who developed spontaneouslya ventricular fibrillation during atrial fibrillation, 8 minafter a perfusion of isoproterenol was stopped Two mechanismscould explain the ventricular arrhythmia: silent ischaemia anda long-short cycle sequence just before ventricular fibrillation.     

Loss of efficacy of flecainide in the Wolff--Parkinson--White syndrome after isoproterenol administration

Although anterograde conduction through a Kent bundle with ashort refractory period was suppressed by 300 mg of flecainideacetate, the infusion of small amounts of isoproterenol causedthe reappearance of WPW and permitted the induction of an atrialtachycardia with I/I conduction through the accessory pathwayat a rate of 260 beats min^–1. This case shows that the effect of isoproterenol may be maintainedafter apparently successful flecainide therapy.