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Ibutilide-induced long QT syndrome and torsade de pointes.

Ibutilide is a class III antiarrhythmic agent used for the termination of atrial fibrillation and atrial flutter. It mainly affects membrane potassium currents and prolongs the cardiac action potential. This effect is reflected as QT interval prolongation on the surface electrocardiogram. Like other drugs that affect potassium currents, ibutilide is prone to induce a malignant ventricular tachycardia, torsade de pointes. We report four cases of torsade de pointes after administration of ibutilide for pharmacologic cardioversion of atrial fibrillation and atrial flutter; three of these cases required direct current cardioversion for termination of torsade de pointes. All four patients were female. We discuss the risk factors for development of ibutilide-induced torsade de pointes.

Aged↗

[Atrial activity and its effects].

The initiation of cardiac impulse is located in the sinus node, in the upper anterior part of the right atrium. The importance of the atrium is not only linked to the regulation of heart rate, but also to its haemodynamic function. Indeed, atrial depolarization leads to atrial contraction which can be responsible for up to 30% of cardiac output by way of ventricular filling. Supraventricular arrhythmias are related to one of the following mechanisms: abnormal automaticity, triggered activity, and reentry. Most of supraventricular tachycardias are due to a reentrant phenomenon (intranodal reentrant tachycardia, orthodromic circusmovement tachycardia, atrial flutter and atrial fibrillation). At the onset of a supraventricular tachycardia, the loss of efficacious atrial contraction as well as the increased heart rate may abruptly decrease ventricular filling. As a consequence, stroke volume is reduced, leading to a decrease in cardiac output and in arterial blood pressure, explaining that the patient may experience syncope. Usually, blood pressure reduction resumes within 30 seconds after activation of the autonomic adrenergic nervous system. In case of an underlying heart disease, the supraventricular tachycardia may lead to acute cardiac failure. When reentry is concerned, the tachycardia is going around a specific circuit. The existence of such a circuit in most of supraventricular tachycardias has led to the development of ablation therapy, the goal of which is to destroy a critical portion of the circuit hence making the recurrence of reentrant tachycardia impossible.

Arrhythmias, Cardiac↗

Symptomatic atrial arrhythmias in hemodialysis patients.

BACKGROUND/AIMS: Cardiac arrhythmias are frequent in hemodialysis patients and can interrupt treatment. However, the frequency and risk factors have remained unclear because previous reports of arrhythmias in dialysis patients have usually been continuous-monitoring studies that looked at all cardiac ectopy regardless of its seriousness. METHODS: We reviewed retrospectively only symptomatic atrial arrhythmias in a population of 106 maintenance hemodialysis patients over three years, in order to estimate their actual frequency and any risk factors. RESULTS: Ten patients, seven men and three women, required treatment for atrial arrhythmias (9.4%): four for supraventricular tachycardia, three for atrial flutter, and three for atrial fibrillation. Their mean age was 53.7 +/- 6.1 years; five of them were < or = 40 years. Seven arrhythmias were new, three were recurrences. All but one occurred between 3 and 4 hours of hemodialysis, and dialysis had to be stopped in nine instances. There was no pattern of hypotensive episodes preceding the arrhythmias. Mean serum K+ drawn at the time of the arrhythmias was 3.8 +/- 0.2 mEq/L. Mean plasma intact parathormone was 1128 +/- 417 pg/mL, compared to 454 +/- 58 pg/mL for our entire hemodialysis population (p = .0036). Subsequent echocardiograms showed abnormalities in 9/10 patients: five had left ventricular hypertrophy, six had left atrial enlargement, five had valvular lesions (four mitral regurgitation; one aortic incompetence), and three had ejection fractions <50%. There were four deaths in these patients over the next 14 months, but probably only one was cardiac. CONCLUSIONS: Serious atrial arrhythmias are common in a hemodialysis population. Risk factors for symptomatic atrial arrhythmias in hemodialysis patients may include hyperparathyroidism and echocardiographic findings of chamber enlargement, valvular lesions, or ventricular dysfunction.

Atrial Fibrillation↗

[Other antiarrhythmic agents].

Digitalis decreases the ventricular rates of chronic atrial fibrillation (AF), and is useful in the treatment of patients with AF. Furthermore it is used for atrial flutter and paroxysmal supraventricular tachycardia (PSVT). ATP has been used as a drug of first choice for quick termination of PSVT. In V-HeFT II, the lower mortality in the enalapril arm was attributable to reduction in the incidence of sudden death, probably due to ventricular arrhythmias. Besides, enalapril experimentally increases cardiac refractoriness. In this paper, recent advances in these three drugs are described.

Adenosine Triphosphate↗

Mechanism of reciprocating tachycardia initiated during sinus rhythm in concealed Wolff-Parkinson-White syndrome: report of a case.

Reciprocating tachycardia in a patient with a leftsided atrioventricular accessory pathway (AP) (Kent bundle, type A) capable only of ventriculo-atrial (V-A) transmission is described. The V-A AP is established as an essential link of the tachycardia circuit, as evidenced by : 1) retrograde atrial activation of the left atrium (LA) 60 msec or more before the low and high right atrium during reciprocating tachycardia and during V-A conduction; 2) the absence of refractory-dependent delay in V-A conduction time with progressively premature ventricular stimulation, characteristic of retrograde conduction through an AP; and 3) the absence of antegrade conduction through the Kent bundle during sinus rhythm, reciprocating tachycardia, pacing from either atrium, or during induced atrial flutter-fibrillation. The onset of the tachycardia was unique in that it could be initiated and perpetuated during sinus rhythm, without a triggering mechanism of an atrial or ventricular extrasystole. The interplay of the following two events seemed to favor the initiation of the tachycardia: 1) shortening of the atrial cycle length causing a decrease in the refractory period of the LA and/or the AP; and 2) the development of rate-dependent left bundle branch block, delaying impulse arrival at the ventricular end of the AP. These observations described an additional mechansim of reciprocating tachycardia in patients with the Wolff-Parkinson-White syndrome.

Action Potentials↗

Clinical electrophysiologic effects of flecainide acetate.

Flecainide acetate depresses the rate of depolarization of action potential (Vmax), the so-called "membrane stabilizing action." In the intact heart it has a unique profile of substantial effect on conduction with modest effect on refractoriness. After intravenous administration, clinical electrophysiologic studies show that conduction through atrial myocardium, atrioventricular (AV) node, His-Purkinje system, and ventricular myocardium is depressed, the most prominent effect being on the His-Purkinje system. Refractorines of the normal atrial and AV nodal myocardium is not prolonged while that of the ventricular muscle is slightly increased. Atrial fibrillation (60% to 70%), atrial tachycardia (90% to 100%), and nodal and AV tachycardia (80% to 90%) are generally terminated, while flutter is usually slowed, but in a small proportion of patients (10% to 20%) might be terminated by the intravenous use of flecainide acetate. This drug has also been shown to be effective in terminating stable ventricular tachycardia (70%). However, it appears to be slightly less effective in suppressing inducibility of ventricular arrhythmias. Administered orally, flecainide is very effective in decreasing ventricular ectopic activity (80% to 95%) and nonsustained ventricular tachycardia. Thus, flecainide has a wide range of antiarrhythmic properties, making it a useful agent in the management of a variety of supraventricular and ventricular arrhythmias. In a small proportion of patients, however, its use can lead to apparent arrhythmogenic effects, the most dangerous being exacerbation of ventricular tachycardia.

Animals↗

False diagnosis of subpulmonary obstruction by echocardiography in d-transposition of the great arteries.

Twenty-one consecutive children (aged 3 to 14 months) with d-transposition of the great arteries were evaluated with standard M mode echocardiography at the time of hospital admission for routine preoperative cardiac catheterization. At catheterization, 6 of the 21 were found to have a systolic pressure gradient between the body of the left ventricle and the main pulmonary artery. Echocardiographic systolic anterior mitral valve motion was noted in nine patients, including five who did not have a left ventricular to pulmonary arterial systolic pressure gradient. Diastolic approximation of the anterior mitral leaflet to the septum was noted in 14 (9 without a gradient), pulmonary valve flutter was also present in 14 (9 without a gradient) and there was premature systolic pulmonary valve closure in 6 (3 without a gradient). Echographic left heart dimensions were not different in patients with a left ventricular outflow pressure gradient than in those without, but patients wit systolic anterior mitral valve motion and diastolic approximation of the mitral leaflet to the septum did have smaller left ventricular and pulmonary root dimensions than did those without these echocardiographic findings. Echocardiographic findings that have been described as suggesting left ventricular outflow obstruction in patients with d-transposition of the great arteries appear to be more related to size and configuration of the left ventricle than to the presence or absence of obstruction.

Cardiac Catheterization↗

[Supraventricular hyperkinetic arrhythmias in acute myocardial infarct: their prognostic assessment and correlation with the echocardiographic evolution].

To assess the prognostic significance of supraventricular tachyarrhythmias (SVTA) during acute myocardial infarction (AMI), we studied 388 patients with first AMI, without ventricular preexcitation or chronic atrial fibrillation. The prevalence of SVTA was 14% (56/388), including atrial fibrillation (57%), atrial flutter (22%), polyfocal atrial tachycardia (14%), monofocal atrial tachycardia (7%). The arrhythmia appeared within 72 hours from the onset of chest pain in 61% of patients (early SVTA < 72 hours), while in 39% appeared later (late SVTA > 72 hours). Patients with SVTA (Group I n = 56) and without SVTA (Group II n = 232) were similar regarding prevalence of hypertension, dyslipidemia, diabetes, site of infarction and fibrinolysis, but SVTA was associated with a significant increase in death (Group I 18% versus Group II 9%; p < 0.05) and complications as pulmonary oedema and cardiogenic shock (Group I 25% versus Group II 14%; p < 0.05). Left atrial dimensions (LAD), end-diastolic left ventricular volume (EDLVV), end-systolic left ventricular volume (ESLVV) and echo-score, evaluated at admission, were not different between Group I and II (LAD 41.3 +/- 6 mm versus 40.1 +/- 5 mm, NS; EDLVV 181 +/- 34 ml versus 173 +/- 30 ml, NS; ESLVV 80 +/- 21 ml versus 75 +/- 18 ml, NS; echo-score 6.7 +/- 3.1 versus 6 +/- 2.7, NS) while pre-discharge echo-grams in Group I showed a trend towards the increase in volumes and echo-score (EDLVV from 181 +/- 34 ml to 194 +/- 36 ml, p = 0.052; ESLVV from 80 +/- 23 ml to 88 +/- 23 ml, p = 0.051; echo-score from 6.7 +/- 3.1 to 7.8 +/- 3.3, p = 0.070).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Ablation of ventricular tachycardia due to a postinfarct ventricular septal defect: identification and transection of a broad reentry loop.

INTRODUCTION: Ventricular tachycardia (VT) after postinfarct ventricular septal defect (VSD) repair has not been well characterized. METHODS AND RESULTS: A 55-year-old man developed refractory VT after inferior wall infarction and VSD repair. Entrainment demonstrated a broad reentry circuit path (outer loop) between the tricuspid annulus and VSD patch. A series of radiofrequency (RF) lesions transected this path, abolishing VT and producing conduction block between the inferior and superior aspects of the basal right ventricular septum. CONCLUSION: Some VTs have broad reentry loops requiring ablation by a series of RF lesions across the path to create a line of block. This approach is analogous to that for atrial flutter.

Catheter Ablation↗

Tachycardia-dependent right bundle-branch block with supernormal conduction.

This paper reports the case of a 76-year-old man in whom atrial flutter with varying atrioventricular block and intermittent right bundle-branch block was found. This is the first report on tachycardia-dependent right bundle-branch block associated with supernormal conduction in a case of atrial flutter. When an impulse is conducted to the ventricles beyond 0.72 s after a QRS complex of right bundle-branch block configuration, the impulse falls after the abnormally long effective refractor period of the right bundle branch and passes through the right bundle branch. When the conducted impulse occurs within 0.72 s after a QRS complex of right bundle-branch block configuration, the impulse usually falls in the refractory period and is blocked in the right bundle branch; however, only when the impulse occurs 0.48 or 0.49 s after that does it fall in the supernormal period and passes through the right bundle branch. The findings in the present report strengthen our previous suggestion that the presence of supernormal conduction plays an important role in the initiation of reentrant ventricular tachycardia.

Aged↗

Conversion efficacy and safety of repeated doses of ibutilide in patients with atrial flutter and atrial fibrillation. Study Investigators.

BACKGROUND: A study was conducted to determine the efficacy and safety of ibutilide fumarate versus placebo in the acute termination of atrial flutter and fibrillation. METHODS AND RESULTS: Two hundred sixty-two patients aged 28 to 88 years with atrial flutter or fibrillation duration of 3 hours to 90 days were randomly assigned in a 5:1 ratio (ibutilide:placebo) to receive two 10-minute infusions, 10 minutes apart, of ibutilide (1 mg) or placebo. Patients were hospitalized and monitored by telemetry for 24 hours, with follow-up 72 hours later. Seventy-three (34.9%) of 209 evaluable ibutilide recipients had termination of atrial flutter or fibrillation within 1.5 hours compared with 0 (0%) of 41 placebo recipients. Those with atrial flutter had a higher success rate. At hour 24, 86.3% remained in normal or alternative sinus rhythm. Of the patients who received ibutilide, 2.3% experienced drug-related sustained polymorphic or monomorphic ventricular tachycardia and recovered after intervention. Additionally, 7.3% experienced nonsustained polymorphic or monomorphic ventricular tachycardia. Other frequent medical events in ibutilide recipients were generally also noted in the placebo group. CONCLUSIONS: Ibutilide is effective and safe for acute termination of atrial fibrillation or atrial flutter.

Adult↗

A jump in cycle length of orthodromic common atrial flutter during catheter ablation at the isthmus between the inferior vena cava and tricuspid annulus; evidence of dual isthmus conduction directed to dual septal exits.

INTRODUCTION: In orthodromic common atrial flutter (AFL), details of intraseptal propagation of the flutter (FL) wave exiting from the isthmus between the inferior vena cava and tricuspid annulus (IVC-TA isthmus) remain unknown. We hypothesized the existence of dual septal exits of the FL wave from the IVC-TA isthmus to both the anterior, coronary sinus ostium (CSO-TA) isthmus, and the posterior septal (IVC-CSO) isthmus, and that the IVC-TA isthmus might consist of dual muscle bundles directed to both septal isthmuses over the eustachian ridge; therefore, segmental ablation of the IVC-TA isthmus could change intraseptal FL wave propagation. METHODS AND RESULTS: To test the hypothesis, we investigated the influence of segmental ablation of the IVC-TA isthmus on intraseptal FL wave propagation. In seven of 40 (18%) consecutive patients, segmental ablation of the ventricular side of the IVC-TA isthmus during orthodromic common AFL led to sudden prolongation of the flutter cycle length (FCL) (from 266 +/- 33 ms to 291 +/- 45 ms) associated with changes in intraseptal activation sequences. They consisted of prolongation of the interval between the IVC-TA isthmus and the CSO (from 38 +/- 13 ms to 86 +/- 25 ms), shortening of the interval between the CSO and His (from 31 +/- 15 ms to 9 +/- 15 ms), and atrial electrogram polarity change at the His-bundle recording site. Morphological change in the FL wave was also seen on the 12-lead ECG. CONCLUSIONS: In some patients, segmental ablation of the IVC-TA isthmus can lead to a jump in FCL and changes in intraseptal activation sequences of FL waves due to anterior-to-posterior shifting of the septal exit. This indicates that the IVC-TA isthmus may contain dual circumferential muscle bundles as conduction pathways directed to dual septal exits both anterior and posterior to the CSO.

Atrial Flutter↗

Efficacy of intravenous amiodarone in the management of paroxysmal or new atrial fibrillation with fast ventricular response.

We tested the efficacy of intravenous amiodarone (5 mg/kg) in slowing ventricular response and/or restoring sinus rhythm in 26 patients with paroxysmal or new atrial fibrillation with fast ventricular response. There were 16 men and 10 women with ages ranging from 35 to 84 years, mean 63 years. Intravenous amiodarone initially slowed the ventricular response in all patients from 143 +/- 27 to 96 +/- 10 beats/min (P less than 0.001). Twelve patients (46%) reverted to sinus rhythm within the first 30 min (range 5 to 30 min, mean 14 +/- 9 min). One patient reverted to atrial flutter after 10 min and 40 min later to sinus rhythm. Six patients (23%) converted to sinus rhythm after 2 to 8 hr and in these 6 cases, the initial slowing in ventricular response obtained with amiodarone persisted until conversion. Seven patients (27%) did not convert to sinus rhythm following amiodarone administration and they required further medical therapy to slow the ventricular response and/or to convert to sinus rhythm. No serious side effects from drug administration were noted. Intravenous amiodarone appears as a highly effective medication in the conversion or control of new onset atrial fibrillation with fast ventricular response.

Adult↗

Successful long-term ventricular pacing via the coronary sinus after the Fontan operation.

A man with double inlet left ventricle and severe subpulmonary stenosis underwent a Fontan operation at the age of 29 years. Eight years later he developed atrial flutter with complete heart block. To avoid a further thoracotomy, a unipolar carbon tipped electrode was placed into the posterior cardiac vein via the coronary sinus. More than 8 years after implantation of the original lead, and after two generator changes, telemetric thresholds remain between 1.8-2.1 volts. Percutaneous transvenous ventricular pacing via the coronary sinus can produce an excellent long-term result and should be the initial approach of choice after a Fontan-type operation.

Adult↗