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PubMed2001

[Comparative incidence of protrusive atheromatous plaques of the thoracic artery in patients with atrial fluter and atrial fibrillation].

Although it has been demonstrated recently that in patients with atrial fibrillation, protrusive atheromatous plaques of the thoracic aorta (thickness 4 mm) and left atrial abnormalities such as thrombosis, spontaneous contrast and low atrial blood flow velocities carry an additional embolic risk, this has not yet been studied in atrial flutter. Out of 2493 patients undergoing transoesophageal echocardiography between September 1993 and December 1997, 271 consecutive patients in atrial flutter (N = 41) or fibrillation (N = 230) for over 48 hours, underwent transoesophageal echocardiography before cardioversion. Patients with atrial flutter were compared with those with atrial fibrillation. Their characteristics were comparable with respect to age (68 +/- 13 and 67 +/- 12 years respectively, p = 0.628), sex ratio (men 66 and 54% respectively, p = 0.212), previous thromboembolic disease (5 and 15% respectively, p = 0.126). The incidence of protrusive aortic atheroma (12 and 11% respectively, p = 0.919), of spontaneous contrast in the thoracic aorta (15 and 14% respectively, p = 0.847) were identical in both groups. The left atrium was significantly smaller (3.1 +/- 0.7 and 6 +/- 3 cm2 respectively, p = 0.001), spontaneous atrial contrast less frequent (17 and 37% respectively, p = 0.024) and the velocities of atrial emptying higher (47 +/- 10 and 30 +/- 10 cm/s respectively, p = 0.030) in patients with flutter compared with atrial fibrillation. There was no difference in left ventricular fractional shortening (30 +/- 10 and 33 +/- 13% respectively, p = 0.630), the presence of rheumatic valvular disease (5 and 12%, p = 0.301), left atrial diameter (43 +/- 7 and 45 +/- 8, p = 0.134), right atrial surface area (16 +/- 4 and 17 +/- 6 cm2, p = 0.384) or in intraatrial thrombosis (2 and 3%, p = 0.888) respectively. These results show a high prevalence of protrusive atheroma of the thoracic aorta both in atrial flutter and in atrial fibrillation, and fewer left atrial abnormalities in patients with flutter.

Aged↗
PubMed1976

Cor triatriatum: echocardiograhic findings.

The echocardiographic findings in a patient with cor triatriatum are presented. The preoperative echocardiogram demonstrated an unusual structure behind the mitral valve that moved anteriorly during atrial systole. There was also echocardiographic evidence of abnormalities of mitral valve motion, right ventricular and left atrial enlargement, and pulmonary hypertension. Postoperatively, the unusual echo behind the mitral valve had disappeared and the mitral valve appeared more normal. Left atrial and right ventricular dimension had decreased and the pulmonary valve appeared more normal. Fine diastolic mitral valve fluttering, an abnormal echo behind the anterior mitral valve leaflet moving anteriorly with atrial systole, an abnormal pulmonary valve echogram suggesting pulmonary hypertension, and marked right ventricular and left atrial enlargement were the main echocardiographic findings in our patient.

Angiocardiography↗
PubMed1996

Antiarrhythmic and electrophysiologic effects of intravenous ibutilide and sotalol in the canine sterile pericarditis model.

INTRODUCTION: Atrial arrhythmias are a frequent clinical complication following open heart surgery. We compared the Class III agents d,l-so-talol and ibutilide fumarate in an intravenous cross-over study using the canine atrial sterile pericarditis model. METHODS AND RESULTS: We studied pacing-induced sustained atrial flutter over a 7-day post-surgical period in conscious dogs, alternating analysis of ibutilide (1.0 to 30.0 micrograms/kg) and d,l-sotalol (0.1 to 3.0 mg/kg). Ibutilide significantly increased atrial flutter cycle length (AFL CL) 11 +/- 2 msec and atrial effective refractory period (AERP) 13 +/- 2 msec, and terminated atrial flutter in all cases (n = 12) following a mean dose of 6 +/- 2 micrograms/kg. Plasma concentrations of ibutilide were 53 +/- 13 ng/mL. Ventricular effective refractory period (VERP) was not significantly affected (4 +/- 2 msec). Following termination with ibutilide, atrial flutter could be reinitiated in 1 of 12 trials, and was nonsustained (40-sec duration). Sotalol significantly increased AFL CL 23 +/- 3 msec and terminated atrial flutter in 8 of 12 trials following a mean dose of 1.5 +/- 0.4 mg/kg. AERP and VERP were significantly increased 20 +/- 6 and 12 +/- 2 msec, respectively. The incidence of reinduced atrial flutter was 9 of 12 trials (P < or = 0.05 vs ibutilide) (7 nonsustained 57 +/- 7 sec duration, and 2 sustained). Sotalol failed to terminate atrial flutter in two dogs on days 1 and 5, despite increases in AFL CL (21 +/- 8 msec) and AERP (16 +/- 9 msec), whereas on day 3, ibutilide (20 +/- 7 micrograms/kg) terminated atrial flutter in those two dogs while increasing AFL CL and AERP 18 +/- 6 and 15 +/- 0 msec, respectively. CONCLUSION: Both sotalol and ibutilide terminate atrial flutter in this model. Ibutilide converted atrial flutter in dogs in which sotalol was not successful. Following atrial flutter termination, ibutilide had a lower incidence of reinduced arrhythmias compared to sotalol. Ibutilide produced atrial antiarrhythmic effects while having no significant electrophysiologic effects on the ventricle.

Animals↗
PubMed2006

[Management of atrial flutter in 2006].

Typical or common atrial flutter is a frequent cardiac arrhythmia related to a macroreentrant circuit located entirely within the right atrium. Risks associated with this supraventricular arrhythmia include 1 to 1 conduction with extremely rapid ventricular rates, tachycardia-mediated cardiomyopathy and thromboembolic events. Treatment of choice of atrial flutter is radiofrequency catheter ablation of the cavo-tricuspid isthmus, and this form of treatment may be considered either during the first episode or at the time of the first recurrence of atrial flutter. Anticoagulant therapy is the rule in the presence of atrial flutter because this arrhythmia favors thromboembolic complications and because atrial flutter is frequently associated with atrial fibrillation.

Anticoagulants↗
PubMed1993

Cardiac arrhythmias in Chagas' heart disease.

Chagas' disease is a chronic parasitosis affecting most Latin American countries. Its most important clinical manifestation is a late developing chronic myocarditis and, much less frequently, an early acute myocarditis. Chagasic myocardial damage is microfocal and disseminated throughout the heart. In most cases, the coexistence of areas of myocytic degeneration, inflammatory infiltration, and fibrosis suggests a permanent evolving process. Commonly, chronic chagasic myocarditis resembles a dilated cardiomyopathy, with characteristic ECG abnormalities (atrial and ventricular extrasystoles, intraventricular and/or AV conduction disturbances, and primary ST-T wave changes). Since myocardial damage is scattered throughout the heart, the ECG abnormalities (arrhythmias, conduction disturbances, and repolarization changes) are also representative of the widespread cardiac involvement. Thus, sick sinus syndrome, atrial extrasystoles, intraatrial conduction disturbances, and atrial fibrillation or flutter are common findings in different stages of the disease. At the ventricular level, both conduction disturbances and arrhythmias are conspicuous expressions of the myocardial damage. Right bundle branch block alone or in combination with left anterior hemiblock are the most common conduction defects. Further compromise of the conduction system can lead to different degrees of AV block. Chagas' disease is the main cause of bundle branch block and AV block in endemic areas. In advanced cases of Chagas' heart disease, ventricular premature contractions are extremely frequent, multiform, and repetitive (couplets and runs of ventricular tachycardia), and show R on T phenomenon. These arrhythmias are usually aggravated by increased sympathetic tone, implying an enhanced risk of cardiac sudden death among chagasic patients, which is sometimes the first manifestation of the illness. Chronic chagasic myocarditis is the leading cause of cardiovascular death, mostly as a consequence of heart failure and sudden death, in areas where the disease is endemic.

Arrhythmias, Cardiac↗
PubMed1976

"Torsade de pointes" initiated by electrical ventricular stimulation.

Four cases are described in which electrical stimulation of the right ventricle produced the ventricular arrhythmia known as "torsade de pointes". This arrhythmia has previously been described as classically occurring in the context of the chronic bradycardias, particularly when there is also hypokalemia and a long QT interval, being most frequently initiated by a ventricular extrasystole occurring relatively late during ventricular repolarization. One patient had suffered a recent anterior myocardial infarction and developed the arrhythmia during rapid pacing for atrial flutter, when the electrode catheter had inadvertently entered the right ventricle. In the other three patients the arrhythmia was produced during the ventricular extrastimulus test performed during routine diagnostic electrophysiological investigation.

Adult↗
PubMed1996

[Inadequate therapies with implantable cardioverter-defibrillators--incidence, etiology, predictive factors and preventive strategies].

Patients with implantable cardioverter defibrillators (ICD) often suffer inappropriate ICD-therapies. The incidence, causes and risk factors of ICD-therapies for a rhythm other than ventricular tachyarrhythmias (VT) were determined retrospectively in 462 consecutive patients (pts). Inappropriate ICD-therapies were identified based on stored R-R intervals and/or electrograms. Eighty-two pts (18%) had inappropriate ICD-therapies. Actuarial rates for inappropriate ICD-therapies were 13%, 20%, 24% and 29% at 1, 2, 3 and 4 years after ICD-implantation, respectively. Atrial fibrillation with rapid ventricular response was the most common cause (34 pts, 39%). In 26 pts (30%), sinus tachycardia triggered inappropriate ICD-therapies, in 21 pts (24%) overseeing, mostly due to fractures and insulation failures of the leads, in three pts atrial flutter, in two pts non-sustained VT, in one pt supra-ventricular tachycardia and in another pt T-wave double sensing caused inappropriate ICD-therapies. In order to prevent recurrences of inappropriate ICD-therapies due to atrial fibrillation or sinus tachycardia, a rate stability (n = 19) or onset (n = 15) criterion was programmed, 41 pts additionally received beta-blocking agents and/or digoxin. In pts with overseeing an operative revision of lead system was performed. During further follow-up (15 +/- 13 months), 15 pts had recurrences of inappropriate ICD-therapies (eight pts due to atrial fibrillation, three due to sinus tachycardia and four due to overseeing). On multivariate analysis (Cox regression), history of atrial fibrillation, maximum heart rate during exercise and low cut-off rate for VT-detection were predictors of inappropriate ICD-therapies. Thus, inappropriate ICD-therapies are frequent, especially in the first year after implantation. Additional detection criteria, beta-blocking agents and/or digoxin prevent recurrences in most patients. In patients with a history of atrial fibrillation, high heart rate during exercise or a low cut-off rate for VT-detection, activation of additional detection criteria should be considered directly after ICD-implantation.

Adult↗
PubMed1979

The response of regular re-entrant supraventricular tachycardia to right heart stimulation.

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.

Adolescent↗
PubMed1993

[Atrial flutter and tachy-systole].

Atrial flutter and tachysystoles may complicate the course of all heart diseases or may be discovered independently of any detectable cardiopathy. Functional tolerance mainly depends on the presence and severity of the associated heart disease, if any. A regular cardiac rhythm of 150 beats/minutes at rest suggests a 2:1 block flutter. Electrocardiographic identification of the disorder is usually easy and may lead, in certain cases, to vagal manoeuvres to recognize the atriogramme and the atrium-ventricle relationship. In all cases, 2:1 flutters must be reduced with amiodarone, by electrical stimulation or by electric shock. A prophylactic treatment of recurrences is often, but not always, indicated. The treatment of tachysystoles must take into account the cause of the ventricular rate.

Atrial Flutter↗
PubMed1986

Emergency treatment of tachyarrhythmias.

The diagnosis, clinical aspects, and emergency treatment of the most common cardiac arrhythmias, including atrial flutter and fibrillation, paroxysmal supraventricular tachycardia, the Wolff-Parkinson-White syndrome, ventricular tachycardia, and torsades de pointes, are discussed. The use of the antiarrhythmic drugs most frequently utilized in clinical practice is described.

Anti-Arrhythmia Agents↗
PubMed1964

TREATMENT OF CARDIAC ARRHYTHMIAS WITH SYNCHRONIZED ELECTRICAL COUNTERSHOCK.

Synchronized electrical countershock is an intriguing new method for the treatment of ectopic tachycardias. The authors applied this treatment to 20 patients with chronic atrial fibrillation and, in 17 patients, sinus rhythm was restored immediately. An additional four patients with atrial flutter were successfully converted to sinus rhythm. One patient developed a hemiplegia two weeks after cardioversion. No other untoward side effects were observed. In two patients with ventricular fibrillation electrical countershock terminated the arrhythmia. After successful cardioversion of atrial fibrillation, a maintenance dose of quinidine is given to help maintain sinus rhythm. In spite of this precaution, one-half of the patients reverted to atrial fibrillation within a month. The quinidine was administered for two to three days in advance of cardioversion; on this regimen, 10 of 34 patients reverted to sinus rhythm on quinidine alone and did not require countershock. The exact place of this treatment of cardiac arrhythmias has not yet been clearly defined.

Arrhythmias, Cardiac↗
PubMed2003

The use of implantable cardioverter-defibrillators in pediatric patients awaiting heart transplantation.

BACKGROUND: This multicenter study evaluated experience with implantable cardioverter defibrillators (ICD) as a bridge to orthotopic heart transplantation (OHT) in children. METHODS: The application of ICD therapy continues to expand in pediatric populations, due in part to improved technology and new indications, including the prevention of sudden death while awaiting OHT. METHODS: We performed a retrospective review of ICD databases at 9 pediatric transplant centers. RESULTS: Twenty-eight patients (16 males) underwent implantation or had a preexisting ICD while awaiting OHT between 1990 and 2002. The median age at implant was 14.3 years (11 months to 21 years) with a median weight of 49 kg (11.7-88 kg). Diagnoses included cardiomyopathy (n=22), and congenital heart disease (n=6). Indications for ICD implantation included ventricular tachycardia/fibrillation (n=23), syncope (n=5), aborted sudden death with no documentation of rhythm disturbance (n=5), ventricular ectopy (n=1), and poor function (n=5). Of the 28 ICDs, 23 were implanted by a transvenous approach and 5 by epicardial route. There were 55 defibrillator discharges in 17 patients, 47 (85%) of which (in 13 patients) were appropriate. The 8 inappropriate discharges (in 6 patients) were triggered by sinus tachycardia, inappropriate sensing, and atrial flutter. The mean time from implantation to first appropriate shock was 6.9 months (1 day to 2.6 years). Twenty-one patients underwent transplantation during the study period, whereas 2 died while awaiting a donor. Morbidity included a lead fracture, 3 episodes of electromechanical dissociation, and 1 episode of electrical storm. CONCLUSIONS: ICD implantation represents an effective bridge to transplantation in pediatric patients. The complication rate is low, with inappropriate device discharge due primarily to sinus tachycardia or atrial flutter. There is a high incidence of appropriate ICD therapy for malignant ventricular arrhythmias in this highly selected group of patients.

Adolescent↗
PubMed1998

Role of autonomic tone in facilitating spontaneous onset of typical atrial flutter.

OBJECTIVES: This study sought to study the change in autonomic tone that precedes the initiation of paroxysmal atrial flutter. BACKGROUND: An abrupt change in the autonomic tone of the heart is an important initiating factor in the pathogenesis of ventricular tachyarrhythmias and paroxysmal atrial fibrillation. Whether the autonomic tone has a role in the initiation of paroxysmal atrial flutter has not been reported. METHODS: Holter electrocardiographic recording was used to investigate the changes in heart rate variability before the onset of paroxysmal atrial flutter. RESULTS: A total of 12 patients with paroxysmal atrial flutter were analyzed. An increase in the normalized value of the low frequency (LF) component and the LF/high frequency (HF) ratio and a decrease in the normalized value of the HF component began at 6 min before the onset of episodes of paroxysmal atrial flutter, which indicated that sympathovagal balance had shifted to more sympathetic predominance. CONCLUSIONS: An increase in sympathetic modulation or vagal withdrawal, or both, may facilitate the initiation of atrial flutter.

Aged↗
PubMed1983

Efficacy of i.v. amiodarone in converting rapid atrial fibrillation and flutter to sinus rhythm in intensive care patients.

Twenty-six consecutive patients (14 males, 12 females--mean age 66.6) were admitted to an intensive care unit (ICU) because of a rapid ventricular response to atrial fibrillation (RAF). Fourteen of them had been unsuccessfully treated by drugs (other than amiodarone) and/or DC shock before admission. A loading dose of i.v. amiodarone was administered (repeated boluses of 3 mg/kg in 3 min, or 30 min-infusions of 5 to 7.5 mg/kg), followed by continuous infusion, in order to reach a maximal total dosage of 1500 mg in 24 h. This treatment was considered efficacious if a reversion to stable sinus rhythm (SSR) occurred within 24 h and was maintained for more than 48 h. This was achieved in 21 out of 26 patients (80.8%). The mean time between the administration of therapy and the occurrence of SSR was 171 min. The total dose of amiodarone delivered to effect SSR was 6.9 +/- 2.3 mg/kg. No adverse reactions were encountered during the bolus injection but we recommend that continuous infusion be carried out through a central venous catheter to avoid phlebitis. The administration of 7 mg/kg of intravenous amiodarone delivered in 30 min proved a safe and successful first choice of management in atrial fibrillation with a rapid ventricular response.

Adult↗
PubMedDate not supplied

[The role of adenosine on the anti-arrhythmic action of digitalis glycosides].

UNLABELLED: The action of adenosine on atrial functional refractory period, as well as on its ability to interrupt atrial flutter is similar to that of digitalis. The latter suggests the possible existence of an adenilic component to digitalis action. To test this possibility, we measured the plasma concentrations of adenosine after ouabain infusion in dogs, and we investigated the effect of digitalis on atrial refractory period and on flutter in conditions of cholinergic inhibition and purinergic blockade. Ouabain was administered until ventricular fibrillation was induced. Blood was obtained from both the coronary sinus and the femoral vein, and adenosine was measured by liquid chromatography. The refractory period was measured by applying an extra stimulus at variable intervals following a train of 10 basic beats. Flutter was induced by stimulation of the posterior internodal pathway. RESULTS: The concentration of adenosine in plasma collected from the coronary sinus increased by more than 100%; the effect of digitalis on atrial refractory period was independent of cholinergic blockade, but it was inhibited by aminophylline; the ability of digitalis to interrupt flutter was modified by aminophylline. CONCLUSION: The antiarrhythmic action of digitalis seems to include an adenilic component, that results from the liberation of adenosine in the heart.

Adenosine↗