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This kind of ventricular tachycardia presents a special type of tachycardia and the diagnostics is of particular importance in this case. It was described by French authors in 1970 during bradycardia and especially during complete AV block with low ventricular frequency. Arrhythmia present at tachycardial form of atrial flutter, and its treatment with electro-stimulation and sinus rhythm restoration are described.
A 42-year-old woman was admitted to our hospital because of anterior chest discomfort on exercise. She had already been diagnosed as having a complete form of Behçet's disease. On auscultation, there was a grade 2/6 diastolic regurgitant murmur along the left sternal border. Echocardiogram and pulse doppler led to the diagnosis of aortic regurgitation and mitral fluttering in diastole. Left ventriculography disclosed an enlarged left ventricular chamber, but the ejection fraction was 60% within the normal range. Aortography confirmed the diagnosis of aortic regurgitation (III.) and dilatation of the ascending aorta. The coronary arteriogram was normal. An endomyocardial biopsy of the right ventricular wall revealed mild hypertrophy of the myocardial fibers and interstitial edema. In this report, we discussed a case of Behçet's disease with reference to 28 cases reported in the medical literature in Japan.
Catheter ablation using radiofrequency currents has been established as the safe and effective therapeutic modality of tachyarrhythmias. Most stable results were obtained in the ablation of accessory pathway of any location in WPW syndrome, and in the ablation of slow pathway in atrioventricular nodal reentry. However, in ventricular tachycardia, the efficacy is strongly affected by underlying heart diseases as well as the site of VT origin. Idiopathic VT either from the right ventricular outflow tract or left ventricular septum can be highly ablated. Common type atrial flutter is another candidate for catheter ablation. Using catheter, Maze procedure is mimicked in atrial fibrillation.
BACKGROUND: Late postoperative arrhythmias and right ventricular dysfunction may occur after classic repair of tetralogy of Fallot. METHODS AND RESULTS: During a mean follow-up of 8.9 years (range, 5 to 14 years), 24-hour ambulatory electrocardiographic studies were done in 107 patients after repair of tetralogy of Fallot. Radionuclide angiography was performed in 97, and 78 patients also underwent postoperative heart catheterization. The patients were divided into two groups: group A consisted of 71 patients aged 2 months to 61 years (mean, 6.8 years) in whom the right ventricular approach was used; group B included 36 patients aged 8 months to 39 years (mean, 7.9 years) whose repair was through the right atrium. A transannular patch was employed in 42 (59.2%) patients in group A and in 23 (63.9%) patients in group B. Eighteen patients were adults (> 18 years old) at the time of surgery: 13 (18.3%) in group A and 5 (13.8%) in group B. During a mean follow-up of 9.7 years, 57 (80.3%) group A patients were in New York Heart Association (NYHA) functional class I. Atrial flutter was present in 3 (4.2%) patients, and 28 (39.4%) had significant ventricular arrhythmias (> or = Lown grade 2). Postoperative heart catheterization showed good hemodynamic results in 36 of 54 group A patients studied (12 of whom had ventricular arrhythmias); moderate-to-severe pulmonary regurgitation was present in 14 (25.9%) patients; only 2 (3.7%) patients had right ventricular hypertension. On electrophysiological study, 8 of 28 (28.6%) patients in group A had inducible sustained ventricular tachycardia. Despite antiarrhythmic therapy, 2 of these patients died suddenly, presumably from ventricular arrhythmias. Two other late deaths in group A were caused by heart failure. During a mean follow-up of 7.2 years, 33 of 36 (91.7%) patients in group B were in NYHA functional class I. Atrial flutter was not found in any patient in this group. Only 1 (2.8%) patient, who had moderate-to-severe pulmonary regurgitation, had significant ventricular arrhythmias (> or = Lown grade 2). Postoperative catheterization showed good hemodynamic results in 20 of 24 patients; 3 (12.5%) had moderate-to-severe pulmonary regurgitation, and 1 (4.2%) patient had right ventricular hypertension. Sustained ventricular tachycardia could not be induced in any of the 5 adult patients who underwent electrophysiological studies. One late death (caused by endocarditis) occurred in group B. CONCLUSIONS: The right atrial approach significantly reduced the risk of life-threatening ventricular arrhythmias after repair of tetralogy of Fallot (P < .001) without increasing the incidence of supraventricular arrhythmias. Right ventricular dysfunction and severe pulmonary regurgitation were also more prevalent (P < .01) when the right ventricular approach was used.
BACKGROUND: In some patients with papillary muscle rupture, the ruptured head may not prolapse into the left atrium, which makes diagnosis by transthoracic or transesophageal echocardiography difficult. METHODS AND RESULTS: In an attempt to find additional or more definite diagnostic echocardiographic features, we analyzed intraoperative transesophageal echocardiograms of 21 consecutive patients with papillary muscle rupture (20 involved the left ventricle and 1 involved the right ventricle) confirmed at surgery. In 7 (35%) of 20 patients with left ventricular papillary muscle rupture, the ruptured head was not seen to prolapse into the left atrium. In these patients, examination of the left ventricle proved most useful. Abnormal, large-amplitude erratic motion (1 to 5 cm in 17 patients; 0.5 cm in 1 patient) of a large echo density in the left ventricle consistent with the ruptured head was noted in 18 (90%) of these 20 patients. This included all 7 patients with non-prolapse of the ruptured papillary muscle head into the left atrium. Less prominent erratic motion or flutter of the papillary muscle still attached to the left ventricular wall was also noted but was less sensitive in the diagnosis of papillary muscle rupture. The single patient with right ventricular papillary muscle rupture showed erratic motion as well as prolapse of the ruptured head into the right atrium. CONCLUSIONS: Transesophageal echocardiographic examination of the left ventricle is useful in the diagnosis of papillary muscle rupture, especially in those patients in whom the ruptured head does not prolapse into the left atrium. The left ventricle should be scrutinized thoroughly during transesophageal echocardiographic examination for erratic papillary muscle motion in all patients with suspected rupture.
Antiarrhythmic therapy for the suppression of atrial flutter has conventionally entailed the use of a class Ia agent such as quinidine or procainamide. However, atrial flutter often recurs despite the use of these conventional antiarrhythmic regimens. Experimental and clinical evidence suggests that the pharmacologic suppression of atrial flutter may depend on the prolongation of the atrial action potential duration and consequently the voltage-dependent refractoriness. Therefore, the efficacy and tolerance of the class III antiarrhythmic agent N-acetylprocainamide was compared to that of the conventional regimen of the class Ia agent quinidine combined with digoxin (to control ventricular response) in patients with a history of symptomatic sustained atrial flutter. The study was randomized but nonblinded, with a crossover to the alternate regimen if the first failed. Eighteen patients entered the study and were followed for up to 18 months. Of the 12 receiving N-acetylprocainamide (eight randomized and four crossovers), one (8%) failed therapy due to side effects, but none had atrial flutter. Of the 11 receiving quinidine and digoxin (10 randomized and one crossover), three (28%) had a recurrence of atrial flutter, two of whom also had intolerable side effects, and two more (18%) had side effects alone requiring withdrawal of therapy (total 46% failed). The probability of therapeutic success over time was greater (p less than 0.04) for N-acetylprocainamide than for quinidine and digoxin. The data suggest that N-acetylprocainamide may be more effective and better tolerated than the conventional regimen of quinidine plus digoxin. Therefore, large-scale blinded studies of the efficacy of N-acetylprocainamide in the suppression of atrial flutter may be warranted.
Atrial flutter with 1:1 atrioventricular conduction giving rise to a ventricular rhythm of 240/min in an 80 year old man was the first sign of the Wolff-Parkinson-White syndrome; all previous electrocardiogrammes had shown no evidence of pre-excitation. It was only on the fifth day of hospitalisation that the ECG showed a short PR interval with a delta wave. This case illustrates that: --all supraventricular arrhythmias with abnormally high ventricular rates (over 220/min in adults) should alert to the possibility of an accessory atrioventricular pathway; --rapid atrioventricular conduction may be the first sign of an accessory pathway; --the differential diagnosis lies between an accessory atrioventricular pathway and an atriohisian tract; --digitalis, which may shorten the refractory period of the accessory pathway, is contraindicated in patients with a Kent bundle.
INTRODUCTION: Coronary sinus (CS) recordings are routinely used during electrophysiologic studies for various supraventricular and ventricular arrhythmias with the understanding that they represent left atrial (LA) activity. However, the behavior of CS electrical activity during atrial arrhythmias has not drawn any special attention beyond standard considerations. METHODS AND RESULTS: The study population consisted of 9 patients (3 women; mean age 59 +/- 11 years) with atrial fibrillation (AF) and atrial flutter (AFL) who developed dissociation of conduction between the CS and posterior LA during spontaneous AF and AFL. In all patients, the LA and the CS were mapped using a 64-electrode basket catheter and a multipolar electrode catheter, respectively. The right atrium (RA) was mapped simultaneously using a 24-polar electrode catheter (7 patients) or a 64-electrode basket catheter (2 patients). Eight patients showed stable double potentials in CS recordings during AF (9 episodes) and AFL (3 episodes). During ongoing arrhythmias, the first row of potentials maintained a constant relationship with the RA activity, whereas the second row of potentials was discordant with the posterior wall of the LA in 7 patients and concordant in 2 patients. In 1 patient with counterclockwise AFL, CS activation was isolated from the posterior wall of the RA until it reached the distal portion of the CS, after which it entered the lateral region of the LA. In 1 patient, a macroreentrant LA tachycardia involving CS muscle was observed. Rapid atrial pacing from the proximal CS and extrastimuli produced longitudinal dissociation of CS activation in all patients. CONCLUSION: Conduction between the CS and posterior LA can be dissociated during spontaneous atrial arrhythmias and provocative proximal CS pacing.
We assessed the safety and efficacy of intravenous propafenone in the treatment of atrial fibrillation and flutter of recent onset (1-10 days). The drug was administered, at a dosage of 2 mg/kg, to 46 consecutive patients (with age variable from 35 to 86 years), 36 with atrial fibrillation, 10 with atrial flutter. The efficacy of propafenone was influenced by the interval from the onset of the arrhythmia and the start of therapy. All patients underwent echocardiographic control: mean left atrial dimensions were non significantly different in responders and non responders. Serious hypotension developed in two patients, regressed with appropriate therapy. Non responders showed a significant reduction of ventricular rate. By synthesis, propafenone is a safe and effective drug for treatment of atrial fibrillation or flutter of recent onset, in refractory patients it allows however an adequate control of ventricular rate.
Implantable defibrillators either monitor heart rate or use a probability density function to detect ventricular fibrillation/tachycardia. As a result, they are unable to discriminate sinus tachycardia and atrial arrhythmias from malignant ventricular rhythms. We have assessed high fidelity fiber-optic pressure recordings in the right atrium during cardiac arrhythmias in 23 patients (mean age 44 years, 11 females) undergoing electrophysiological study. The unfiltered pressure signal was amplified and recorded on paper. During sinus rhythm, a constant amplitude deflection occurred during atrial systole (a wave). A characteristic waveform pattern was observed during each of the studied tachyarrhythmias, which included atrial flutter and fibrillation, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and ventricular tachycardia with and without ventriculoatrial conduction. The waveform pattern allowed clear visual discrimination of the underlying arrhythmia. Mean atrial pressure was increased during all arrhythmias and did not allow discrimination of the nature of the tachycardia. High fidelity pressure recordings produced characteristic appearances for pattern recognition of each arrhythmia studied. They allowed determination of the temporal relation between electrical and mechanical cardiac events and may have potential in the detection and recognition of cardiac arrhythmias.
Over a 5-year period, 110 cardioverter-defibrillators (109 epicardial, 1 transvenous) were implanted consecutively in selected patients with ventricular tachyarrhythmias. The perioperative course of this patient population was examined to determine the associated morbidity and mortality of the procedure. Patients were predominantly male, with coronary artery disease and a decreased left ventricular ejection fraction. Most underwent median sternotomy for implantable cardioverter defibrillator implantation. The incidence of perioperative mortality was found to be 2.7%. New-onset atrial fibrillation or flutter occurred in 17.3% of the patients during the postoperative period and aggravation of ventricular tachyarrhythmias in 19.1%. The ICD system became infected in 2.7% of the patients and the mediastinal incision site infected in 2.4%. Pneumonia developed in 4.5%. Other complications included significant blood loss, ICD pocket hematomas, and lead dislodgement. There is an appreciable incidence of morbidity and mortality associated with ICD implantation.
A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.
Procainamide remains one of the most widely used antiarrhythmic agents in clinical practice. Currently, it is widely used alone or in combination with class I agents (eg, mexiletine or tocainide) to prevent recurrent ventricular tachycardia or symptomatic nonsustained ventricular tachycardia. Procainamide is also used for short-term treatment of ventricular tachycardia and a variety of supraventricular tachycardias, primarily atrial flutter and atrial fibrillation. Long-term procainamide therapy is limited by a number of systemic side effects, primarily lupus-like syndrome, gastrointestinal disturbances, and autoimmune blood dyscrasias. Procainamide levels can be useful in initial dose titrations; however, QRS and QT interval measurements help prevent drug toxicity. It is recommended that patients being started on antiarrhythmic therapy with procainamide be admitted to the hospital for monitoring to ensure that their QT interval is not excessively prolonged.
The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of ibutilide are reviewed. Ibutilide is the first class III antiarrhythmic agent to rely on activation of a slow inward sodium current to prolong the action potential and effective refractory period of atrial and ventricular tissue. The drug is indicated for the rapid restoration of normal sinus rhythm in patients with atrial fibrillation or atrial flutter of recent onset who are hemodynamically stable. The effects of ibutilide are concentration dependent. The drug undergoes rapid and extensive hepatic metabolism. The pharmacokinetics of ibutilide fumarate are linear well above the maximum proposed therapeutic dose of 2 mg. The elimination half-life averages six hours. Clinical trials have established ibutilide's efficacy in converting sustained atrial flutter and atrial fibrillation to normal sinus rhythm. It has been shown that patients with atrial flutter respond at a greater rate than patients with atrial fibrillation, but that atrial fibrillation is converted more rapidly than atrial flutter. In one study, atrial flutter and atrial fibrillation were successfully converted in significantly more patients receiving ibutilide than those receiving sotalol. Ventricular tachycardia is the adverse event of primary concern, occurring in 4.3% of patients in clinical trials. The recommended initial dose is 0.01 mg/kg for patients weighing less than 60 kg and 1 mg for patients weighing 60 kg or more, infused over 10 minutes. About 70% of patients will require a second dose. The list price is $119.75 per dose. Ibutilide appears to be an effective alternative to other antiarrhythmic agents for rapid conversion of arrhythmias to normal sinus rhythm in hemodynamically stable patients.
Electrophysiologic properties of various conduction pathways responsible for preexcitation syndrome are illdefined; they explain the incidence of arrhythmias : supraventricular tachycardia, atrial fibrillation and, in much rarer cases, flutter. The site of Verapamil activity is chiefly the atrioventricular junction, while its action on the refractory period of atrio-ventricular bypass is small and unforeseable. In a patient with type B. W.P.W. syndrome, complicated with atrial flutter Verapamil induced a preferential stimulation through the anomalous pathway. Right BBB which was obvious during the attack of atrial flutter, was hidden by the type B W.P.W. syndrome, the right branch being shunted by the anomalous pathway. The infrequency of atrial flutter in type B W.P.W. syndrome is emphasized.
The antiarrhythmic effect of oral propafenone was evaluated in 10 patients with Wolff-Parkinson-White syndrome presenting with non-ventricular arrhythmias (paroxysmal supraventricular tachycardia n = 7, atrial fibrillation or flutter n = 3). The mean age was 38 +/- 13 years, the dose varied from 300 to 900 mg three times a day (mean 450 +/- 188) and the mean follow-up period was 7 +/- 3.5 months. All patients' drug responses were assessed on 12-lead electrocardiograms and 24-hour ambulatory Holter monitoring. Electrophysiologic studies were performed in cases of sustained tachycardia while echocardiography identified 2 cases with mitral valve prolapse. Four of 10 (40%) patients became asymptomatic on a starting propafenone dose of 300 mg, while 6 (60%) had recurrences necessitating an increase in dose for the complete control of the symptoms. We observed a slight slowing of the heart rate and an increase of the mean Q-T interval (P less than 0.001). Three patients reported minor side effects including nausea, dizziness and constipation that were tolerable and dosage dependent. It is concluded that propafenone is an effective and well tolerated drug for the treatment of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome.
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Symptoms range from mild palpitations to overt cardiac failure and cardiogenic shock, depending on the ventricular rate and the patient's underlying cardiac status. Drug therapy is the mainstay treatment. In atrial fibrillation, digoxin is used to control the ventricular response and therefore improve cardiac function. Verapamil may also be used for this purpose.