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Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia.

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.

Administration, Oral↗

[Atrial natriuretic factor in acute atrial hyperkinetic arrhythmia and chronic atrial fibrillo-flutter].

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.

Acute Disease↗

Atrial fibrillation and flutter. Immediate control and conversion with intravenously administered verapamil.

The safety and efficacy of the intravenous (IV) calcium channel blocker, verapamil, in controlling the ventricular response or converting to sinus rhythm patients with atrial flutter or atrial fibrillation were assessed. Seventeen patients (nine with atrial flutter and eight with atrial fibrillation) with these arrhythmias that were difficult to control pharmacologically were chosen for the study. All patients at the time of study were receiving digoxin. Either verapamil or placebo was chosen randomly and a bolus of 0.075 mg/kg (up to 5 mg) was administered. Twelve patients had a marked reduction in their ventricular response after IV administration of verapamil (seven with atrial flutter and five with atrial fibrillation). None of these 12 patients converted (nonconverters). The average reduction in heart rate was from 120 +/- 6 beats per minute to a minimum of 83 +/- 13 beats per minute within 20 minutes after drug administration. Verapamil was found to convert five patients with atrial arrhythmias to sinus rhythm (two with atrial flutter and three with atrial fibrillation) (converters). In addition, three patients with atrial arrhythmias of less than one month who did not convert with parenteral drug therapy converted within 24 hours while receiving the oral drug. Converters had their supraventricular arrhythmias of significantly shorter duration (median, three hours v 30 days) and tended to have smaller left atrial size (3.8 +/- 0.7 cm v 4.3 +/- 1.3 cm) compared with the nonconverters. We conclude that verapamil is safe and effective when administered IV to patients with atrial flutter and fibrillation for control of ventricular response. In short duration atrial arrhythmias, conversion to sinus rhythm is likely once the ventricular response is controlled.

Adult↗

Right ventricular pacing to assess transisthmus conduction in patients undergoing isthmus-dependent atrial flutter ablation: a new useful technique?

BACKGROUND: Successful radiofrequency (RF) ablation of typical, isthmus-dependent atrial flutter requires establishment and confirmation of bidirectional conduction block across the cavotricuspid isthmus. Low atrial pacing usually is performed from the bipoles of the 20-pole Halo catheter, septal and lateral to the cavotricuspid isthmus ablation line. However, occasionally this is difficult because of high pacing thresholds and/or saturation of the atrial electrograms recorded near the pacing catheter. OBJECTIVES: The purpose of this study was to assess if right ventricular (RV) pacing and resulting retrograde atrial activation can be used to assess conduction block from the septum to the lateral wall in a clockwise direction. METHODS: Thirty-five consecutive male patients (mean age 64 +/- 10 years; mean ejection fraction 42 +/- 13%; mean left atrial dimension 44 +/- 6 mm) with typical isthmus-dependent atrial flutter were studied. The following electrophysiology catheters were used: 20-pole catheter along the tricuspid annulus, quadripolar catheters at the His and/or RV apex, and 8-mm ablation catheter. Following RF ablation of the cavotricuspid isthmus, bidirectional conduction block was confirmed in all 35 patients by pacing at a cycle length of 600 ms from bipoles septal and lateral to the cavotricuspid isthmus ablation line. Conduction times from pacing artifact to adjacent bipolar atrial electrograms and reversal of atrial activation pattern were analyzed. RV pacing was performed and retrograde atrial activation pattern assessed. If retrograde AV nodal conduction was absent, isoproterenol was infused intravenously at 2 microg/min, and RV pacing was repeated. The conduction time between the double potentials across the cavotricuspid isthmus ablation line was measured. RESULTS: Mean conduction times across the isthmus during septal (S), lateral (L), and RV pacing were 145 +/- 21 ms, 144 +/- 24 ms, and 129 +/- 20 ms, respectively. Retrograde AV nodal conduction was present in 34 of 35 patients (isoproterenol 8 patients). Evidence of conduction block by a clear change in activation pattern across the isthmus was seen during RV pacing in 33 of 35 patients with bidirectional conduction block. CONCLUSION: RV pacing is a simple and easy maneuver that can be performed to assess isthmus conduction in most patients.

Atrial Flutter↗

Fluttering of the interventricular septum. The result of truncal insufficiency.

We present a child with truncus arteriosus and truncal insufficiency who had diastolic fluttering of the anterior mitral valve leaflet and left ventricular surface of the interventricular septum on echocardiogram. Although the fluttering has been previously described in patients with aortic insufficiency, it has not been reported with truncus arteriosus.

Child↗

Automatic arrhythmia identification using analysis of the atrioventricular association. Application to a new generation of implantable defibrillators. Participating Centers of the Automatic Recognition of Arrhythmia Study Group.

BACKGROUND: Atrioventricular association is a key criterion for arrhythmia diagnosis. Its use in a defibrillator should significantly reduce the incidence of inappropriate shocks. Therefore, we evaluated the diagnostic accuracy of an algorithm that uses dual-chamber sensing and analysis of atrioventricular association to discriminate ventricular from supraventricular arrhythmias in a prototype of an implantable defibrillator. METHODS AND RESULTS: The algorithm performed a stepwise analysis of arrhythmias. The rhythm was first classified on the basis of cycle lengths. Each episode was then classified as supraventricular or ventricular in origin on the basis of the stability of cycle lengths and atrioventricular association. This algorithm was evaluated in 156 episodes of induced sustained tachycardias. Eighty-nine tachycardias were taken from the Ann Arbor electrogram library; the others were recorded in 50 patients during electrophysiological studies. The atrial and ventricular signals were stored on an external recorder and then injected into an external prototype of a defibrillator system. The algorithm correctly diagnosed 96% of ventricular tachycardia episodes, 100% of ventricular fibrillation episodes, and 92% of double-tachycardia episodes. The mean detection time for ventricular tachycardia was 2.6 +/- 0.8 seconds, and for ventricular fibrillation, it was 2.1 +/- 0.4 seconds. The positive predictive values for the diagnoses of atrial fibrillation and atrial flutter were 92% and 86%, respectively. For ventricular tachycardia and ventricular fibrillation, the values were 95% and 100%, respectively. CONCLUSIONS: Analysis of atrioventricular association promotes reliable differentiation between ventricular and supraventricular tachycardias and should enhance the diagnostic capabilities of implantable defibrillators.

Algorithms↗

Role of invasive EP testing in the evaluation and management of hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is an inheritable condition that may cause sudden death in the absence of significant symptoms or adverse morphological features. Therefore, there is a need for identification of those patients at sufficiently high risk to warrant prophylactic treatment. Risk stratification for primary prevention of sudden death has relied upon non-invasively derived markers of risk: syncope; a family history of premature sudden death; nonsustained ventricular tachycardia on Holter; abnormal blood pressure response to exercise; and severe left ventricular hypertrophy. The presence of two or more risk factors is associated with a 6-year sudden death survival rate of 72% (56-88%), justifying the consideration of prophylactic therapy. The 6-year sudden death survival rate in patients with one or no risk factors is 94% (91-98%). In these individuals the context and severity of the risk factor may guide the decision for prophylaxis; for example, a highly malignant family history carries greater justification than a large pedigree with only one sudden death. There is a need, however, for determining risk more accurately in those individuals with only one conventional risk factor. Programmed stimulation has been studied for its predictive value in primary prevention. 'Aggressive' protocols have been used and the most commonly induced arrhythmia is polymorphic ventricular tachycardia. These findings, however, are non-specific and of limited prognostic value. In addition the patients studied have been from selected high-risk populations without a low-risk cohort for comparison. Thus invasive EP studies appear to carry little advantage over non-invasive risk stratification. This is not surprising given that the mechanisms of cardiac arrest in HCM can be varied and may be modified by abnormal vascular responses and ischaemia. The relevance of invasively induced arrhythmias may therefore be limited. Other uses for electrophysiological study include the investigation and treatment of individuals with conduction disease and/or Wolff-Parkinson-White syndrome, atrial flutter and fibrillation and monomorphic ventricular tachycardia. Appropriate management may then involve radiofrequency ablation. A permanent pacemaker will be required if the atrio-ventricular node is ablated.

Cardiomyopathy, Hypertrophic↗

Safety of oral propafenone in the conversion of recent onset atrial fibrillation to sinus rhythm: a prospective parallel placebo-controlled multicentre study.

AIM: Oral propafenone is effective in restoring sinus rhythm however the proarrhythmic effects are still unknown. The Safety Antiarrhythmic Therapy Evaluation (SATE) trial was a prospective randomized placebo-controlled multicentre study which evaluated the safety of acute oral loading dose of propafenone in patients with recent onset atrial fibrillation. Secondary end-points were to evaluate the effect of digitalis added to propafenone in ventricular rate control and the efficacy of propafenone alone or added to digitalis compared with efficacy of digitalis plus quinidine. METHODS AND RESULTS: 246 patients (126 male; 58+/-11 years) with atrial fibrillation of <48 h duration were randomly allocated to one of four groups: digitalis 0.75-1 mg i.v. plus quinidine 1100 mg (D+Q, 70 patients); propafenone 450-600 mg orally (PNF, 66 patients); propafenone 450-600 mg orally plus digitalis 0.750-1 mg i.v. (PNF+D, 70 patients); placebo (Pl, 40 patients). All patients underwent 24-h ECG Holter monitoring. Safety was assessed by evaluating the appearance of adverse events classified as mild, moderate and severe. No severe adverse events were reported. Short lasting asymptomatic atrial flutter episodes with atrio-ventricular conduction > or =2:1 were observed in 14% of the D+Q group, 21% PNF, 18% PNF+D and in 8% Pl. One patient in the D+Q group and four in the PNF+D group showed asymptomatic runs of 3-4 ventricular ectopic beats. Reversible sinus atrial blocks (<3 s) were detected in two patients of the D+Q group and in two of the PNF group. In patients with persistent atrial fibrillation the ventricular rate was similar in the four study groups. At 3 h the high efficacy of propafenone was confirmed. At the 24th hour no differences were found between active treatment and placebo arms. CONCLUSION: Propafenone in a single oral loading dose is safe and promptly effective in patients with recent onset atrial fibrillation.

Administration, Oral↗

Relationship of antiarrhythmic to inotropic activity and antiarrhythmic qualities of the optical isomers of verapamil.

1. The relationship of antiarrhythmic to inotropic activity of the optical isomers of verapamil was studied by comparing their effects on functional refractory period and force of contraction in the isolated left atrium of the guinea pig and on maximum follow frequency and contractility in the dog heart. To evaluate the antiarrhythmic profile of the optical isomers of verapamil the relationship between threshold voltage and impulse duration in the left atrium of the guinea pig and the antagonistic action against ventricular arrhythmias in the rat were studied. 2. (-)Verapamil is nearly 10 times more effective than (+)verapamil in prolonging the functional refractory period in the isolated left atrium of the guinea pig. 3. In the dog heart (-)verapamil is about 8 times more active in reducing a maximum follow frequency at atrial pacing, as well as spontaneous heart rate and in prolonging PQ-duration. 4. In the guinea pig atrium (+)verapamil shows less negative inotropic activity than its enantiomorph. With (+)verapamil the concentration producing a 25% decrease in contractility is 3.7 times higher than that causing a 25% increase in refractory period. With (-)verapamil these concentrations are identical. 5. In the dog i.v. infusion of the isomers, at a dosage inducing identical reduction of maximum follow frequency, is accompanied by a decrease in left ventricular dp/dtmax with (-)verapamil, whereas with the (+)isomer a significant increase of dp/dtmax is observed at a certain dose level. 6. Because of the higher antiarrhythmic activity of (-)verapamil, the antiarrhythmic profile and the inotropic pattern of the racemic compound are mainly due to this isomer. 7. (+)Verapamil shifts the voltage duration curve of the isolated left atrium of the guinea pig to the right and leads to a significant increase in the chronaxie value. (-)Verapamil has no comparable effects on the excitability of the atrial myocardium. 8. In the intact animal (+)verapamil shows additional antiarrhythmic qualities. Like procainamide, but with higher activity, it antagonizes ventricular arrhythmias (ectopic beats, automaticity and flutter or fibrillation) which can be provoked in the rat by i.v. infusion of aconitine. (-)Verapamil and the racemic compound are ineffective against these ventricular rhythm disorders.

Aconitine↗

Life-threatening alterations in heart rate after the use of adenosine in atrial flutter.

Adenosine has become the preferred treatment for common types of supraventricular tachycardia because it is extremely effective and rarely associated with with serious side effects. It has also been advocated as an intervention for diagnostic use to assess uncommon types of tachycardia. Evidence is shown in this report that adenosine was associated with dangerous worsening of arrhythmia in patients with atrial flutter. In two patients, adenosine precipitated acceleration of ventricular response, in one case necessitating emergent cardioversion. Both patients had atrial flutter with 2 to 1 atrioventricular block that evolved into 1 to 1 atrioventricular conduction. In three other patients, adenosine was associated with prolonged bradyasystole and hypotension. In each of the five patients, adenosine was given in a standard fashion (6 or 12 mg). In summary, adenosine should be recognized as a potentially dangerous intervention in patients with atrial flutter. If it is used for diagnostic purposes, resuscitative equipment should be readily available.

Adenosine↗

Mechanisms determining the ventricular rate in wolff-parkinson-white arrhythmias.

In patients with WPW syndrome the maximal ventricular rate attained during ectopic rapid supraventricular thythms depended on the type of arrhythmia as well as on the physiological properties of the AP. During reciprocating tachycardias the impulse is almost invariably conducted to the ventricles through the AV node. Therefore, the maxiaml ventricular rate is a function of the AV nodal ERP. On the other hand, when atrial flutter or atrial fibrillation were present the ventricular rate could be moderately elevated (when the ERP of the AP was longer than that of the AV node) or very rapid where the ERP of the AP was significantly short. Therefore, from the electrophysiological viewpoint, the AP appears to behave as His-Purkinje tissue in some cases and as ordinary artrial muscle in other patients. These assumptions await further documentation.

Adult↗

Electrophysiologic effects and efficacy of cibenzoline on stimulation-induced atrial fibrillation and flutter and implications for treatment of paroxysmal atrial fibrillation.

The effects of intravenous cibenzoline (1.5 mg/kg) on atrial vulnerability and electrophysiology were assessed in 25 patients with documented paroxysmal atrial fibrillation (AF), in whom sustained (greater than 30 seconds) AF was induced by atrial stimulation with up to 2 extrastimuli and paced rates between 100 and 180 beats/min. In 7 patients AF persisted despite the application of cibenzoline, and in 8 patients the induction of sustained AF was prevented by cibenzoline. Intraatrial conduction time, flutter cycle length and shortest ventricular cycle length during AF were increased by cibenzoline (p less than or equal to 0.01). Sinus cycle length was decreased (p less than or equal to 0.05), whereas sinus node recovery time remained unchanged. The effective refractory period of the right atrium was not significantly affected. Eight patients with frequent episodes of paroxysmal AF received oral cibenzoline for control of paroxysmal AF irrespective of the efficacy of intravenous cibenzoline. Prevention of stimulation-induced AF predicted successful treatment of paroxysmal AF (p = 0.018). Cibenzoline could be effective in the treatment of atrial arrhythmias, and selection of an antiarrhythmic therapy for recurrent AF seems to be useful.

Administration, Oral↗

[Effects of verapamil on sinusal function and on atrioventricular conduction along normal and abnormal pathways, in patients with pre-existing troubles of excitation conduction (author's transl)].

Effects of verapamil (5 mg i.v.) on excitation conduction in 20 patients who already had a basic alteration (7 with ventricular pre-excitation syndrome) were studied by His electrogram, during spontaneous sinusal rhythm and atrial electrostimulation in increasing frequencies. In 4 cases, a test crossed with atropine was carried out. The effects of the drug on the effective refractory period of the A-V node and the anomalous tract in 3 patients with W.P.W. syndrome of Kent's bundle were studied. The effects were: no significant modifications in the sinusal frequency; increase in the corrected preautomatic pause only in cases with sick sinus node syndrome and serious basic compromise of the sinus node function; slowing down of A-V conduction in the supra-hisian area and increase of the effective refractory period of the A-V node; no modification of the intra-atrial conduction, or the under-hisian and intraventricular A-V conduction; uneven slowing down of conduction along the anomalous tract of the pre-excitation syndrome of the James bundle; modification of the effective refractory period of the anomalous tract of the Kent bundle type, variable from case to case. On the basis of the electrophysiological properties, the possibilities and limits of use of the drug in sick sinud node syndrome in the common supraventricular paroxymal tachycardias, in atrial fibrillation, atrial flutter and arrhythmias of the ventricular pre-excitation syndrome are emphasized.

Adult↗

Intravenous cibenzoline in the management of acute supraventricular tachyarrhythmias.

Intravenous cibenzoline was evaluated in 37 patients with acute supraventricular tachyarrhythmias and a ventricular rate > 120 beats/min. The presenting arrhythmia was atrial fibrillation in 15 patients, atrial flutter in 5, ectopic atrial tachycardia in 11, and paroxysmal atrioventricular (AV) junctional reentrant tachycardia in 6 patients. Intravenous cibenzoline was administered as a bolus given over 2 minutes, at a dose of 1 mg/kg in the first 26 patients and 1.2 mg/kg in the subsequent 11 patients, 15 minutes following failure of placebo (isotonic glucose). The results were evaluated 15 minutes after the intravenous injection. Restoration of sinus rhythm was obtained in 3 out of 6 patients with paroxysmal AV junctional tachycardia (50%) and in 7 out of 31 patients (23%) with atrial tachyarrhythmias (5 out of 15 patients with atrial fibrillation and 2 out of 16 patients with ectopic atrial tachycardia or atrial flutter). Five additional patients with atrial tachyarrhythmias had slowing of ventricular rate below 100 beats/min. Therefore, a satisfactory result, that is, restoration of sinus rhythm or slowing of ventricular rate, occurred in 15 patients (40.5%). Side effects were transient, including visual disturbance (one patient), asymptomatic widening of QRS complex (three patients), incessant reciprocating tachycardia (one patient), and acceleration of ventricular rate (eight patients), resulting in 1:1 flutter, with poor tolerance in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Echocardiography of the tricuspid valve in congenital left ventricular-riht atrial communication.

Two patients, ages 14 and 18, with congenital left ventricular-right atrial communication through a defect in the tricuspid valve were studied by echocardiography. Proof was obtained by angiocardiography and surgery in one and ultrasonic contrast injection and angiocardiography in the other. Both presented clinically as uncomplicated ventricular septal defects. Echocardiography consistently demonstrated a high frequency, low amplitude flutter of the tricuspid valve in systole and none in diastole. Following surgical correction of the defect in one patient, there was complete disappearance of the systolic flutter. Systolic flutter has not been observed with tricuspid incompetence nor with other forms of ventricular septal defects. Fistulous communication from the aorta to the right atrium just above the tricuspid valve did not demonstrate systolic flutter in one patient studies. Tricuspid valve systolic flutter appears to be caused by the passage of the left ventricular jet blood into the right atrium through a defect in the tricuspid valve. Echocardiographic study of the tricuspid valve is of value in the recognition of the congenital left ventricular-right atrial communication.

Adolescent↗

[Electrocardiographic features and vectorial analysis of cardiac potentials in electric shock-induced ventricular fibrillation (author's transl)].

The authors examined the electrocardiographic features of ventricular fibrillation and other ventricular paroxysms induced by electric shock in the guinea pig. The analysis of the electrocardiographic patterns, as well as the vectorial study of the cardiac potentials during repeated episodes of ventricular "anarchy" induced in more than forty animals, showed the following data: 1. following electric shock, ventricular paroxysms appear, featuring paroxysmal tachycardia, typical or impure flutter, tachycardia--either "torsade de pointe" or "spindle" type, and typical ventricular fibrillation. Such different electrocardiographic patterns represent evolutive stages of electric activity disorganization, leading to a complete ventricular "anarchy". Such steps may reverse when reorganization of the electric activity and spontaneous defibrillation occur; 2. an attempt can be made at present to classify ventricualr paroxysms, thus eleminating semeiotic and semantic errors, still present in the literature, and providing a standardization of both nomenclature and electrocardiographic interpretation; 3. during fibrillation, the mean ventricular rate decays, featuring an exponential curve. This phenomenon accounts for a metabolic depletion of the myocardium: the higher the number of fibrillation episodes previously induced and subsided (either spontaneously or not) in the same animal, the faster the course of the phenomenon; 4. the vectorial analysis of the fibrillation potentials and, particularly, the graphic construction of "depolarization" and "repolarization" vectorcardiograms, in the differenttypes or variants of ventricular paroxysms, show that the basic mechanisms leading to ventricular electric activity disgregation are the multiple re-entry and the irregular spreading of the activation front; 5. on the basis of the acquired data, the authors believe that the "circus movement" theory (Wiggers) is still the most suitable for explaining the onset and the evolution of ventricualr fibrillation.

Animals↗

Some cardiovascular problems with disopyramide.

Five patients with apparent adverse cardiovascular effects of disopyramide are reveiwed. Attention is drawn to the following problems. (1) A vagolytic effect may produce a sinus tachycardia with wide QRS complexes due to aberrant conduction or intraventricular block superficially resembling a ventricular tachycardia, or may allow increased transmission of an atrial tachycardia or atrial flutter to the ventricles by improving atrio-ventricular conduction. (2) Although the vagolytic effect is helpful in increasing sinus rate in patients with sinus node disease, disopyramide may lead to bradycardia and asytolic cardiac arrest, and should not be used without a demand pacemaker. (3) Dangerous ventricular arrhythmias may be provoked in susceptible subjects, as with quinidine. (4) Rapid intravenous injection may produce transient toxic effects before the drug is distributed. The rate of injection as a loading dose for prophylaxis should be slower (2 mg/kg in 15 min) than for the urgent conversion of a resistent tachycardia (2 mg/kg in 5 min). Although disopyramide seems less toxic than quinidine, caution is advised, as over-enthusiastic application of disopyramide, particularly with rapid intravenous injection, might tend to bring a useful new agent into disrepute.

Adult↗

Neurological outcome of children who were treated for fetal tachycardia complicated by hydrops.

OBJECTIVE: Fetal tachycardia is a condition associated with congestive heart failure and development of fetal hydrops, which may result in neurological morbidity and mortality. The aim of this study was to investigate the long-term outcome of hydropic fetuses. METHODS: This was a retrospective study on cognitive and neurological functioning of 11 infants, aged 6 months to 12 years, who experienced fetal tachycardia complicated by hydrops. RESULTS: Seven fetuses had supraventricular tachycardia (SVT), three had atrial flutter (AF) and one had ventricular tachycardia (VT). Nine fetuses converted to sinus rhythm within a mean time of 8.2 days of presentation; resolution of hydrops was achieved in six of these patients in a mean time of 8.8 days. Mean gestational age (GA) at birth was 35 + 4 weeks. Neonatal cranial ultrasound was normal in seven infants and all but one of these were normal at follow-up: one infant who initially had no abnormalities developed multiple cerebral lesions as a result of a malignant long QT syndrome (LQTS) and died at the age of 2 years. Three infants had periventricular echogenicity (PVE) on neonatal cranial ultrasound, associated with a pseudocyst in one infant. The remaining infant showed a parenchymal hemorrhage of antenatal onset, seen as a porencephalic cyst at birth. One of these infants was normal at follow-up, one died 2 days after birth and two infants had neurological abnormalities at follow-up, consisting of mild hemiplegia with normal cognitive function in one, and a cognitive developmental delay in the other. CONCLUSIONS: In this study, neurological outcome was good in eight out of 11 infants. Initiation of therapy should not be withheld or delayed on the assumption of poor neurological outcome.

Arrhythmias, Cardiac↗