Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ventricular Flutter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources
PubMed1986

Verapamil in arrhythmia.

The antiarrhythmic effects of verapamil were observed before it was appreciated that it was a calcium ion-antagonist. Intravenous verapamil is highly effective in the termination of paroxysmal reciprocating atrioventricular tachycardia, whether associated with preexcitation or involving the atrioventricular node alone. It consistently slows and regularises the ventricular response in atrial fibrillation, and usually increases the degree of AV-nodal block in atrial flutter though it occasionally induces a return to sinus rhythm. Given orally it is useful for the prophylaxis of atrioventricular reentry tachycardia, and also in modulating the atrioventricular nodal response in atrial fibrillation. Favourable response in ventricular tachycardia is exceptional and then seen in specific benign varieties. Verapamil is the agent of choice for the termination of paroxysmal supraventricular tachycardia.

Arrhythmias, Cardiac↗
PubMed1981

Haemodynamic effect of the suppression of ventricular tachycardia by atrio-ventricular captures.

In 10 anaesthetized open chest dogs, blood pressure, electrogram from the left auricular appendage or right atrium, peripheral ECG and cardiac output were recorded. Ventricular tachycardia was produced with aconitine and then suppressed by inducing atrial fibrillation or flutter-fibrillation either with aconitine or with electrical stimulation. After the capture of the ventricles by the supraventricular impulses, a haemodynamic improvement took place. This improvement is attributed to: I) beat to beat changes in the length of the cardiac cycles, whereby intermittent strong beats arise; II) restoration of the normal ventricular activation path and time course; III) the active contribution of properly timed atrial contractions, when present. The improvement was more evident when, after the capture, the ventricular rate was lower than during the ventricular tachycardia, because of a longer period available for the ventricular filling. It is believed that the reduction of the ventricular rate immediately after the capture is due to the suppression of the activity of the ventricular ectopic focus by the concealed conduction of high rate impulses coming from the atria.

Animals↗
PubMed2006

A case of acute ventricular capture threshold rise associated with flecainide acetate.

Antiarrhythmic agents may increase capture threshold, but this is rarely of clinical significance. Flecainide acetate, a class IC agent, is reported to have a significant effect on the myocardial capture threshold. In this presentation, we report the case of a 72-year-old male, with a previously implanted VVI pacemaker due to sick sinus syndrome, who was treated with flecainide acetate for paroxysmal atrial arrhythmia control. During the fifteenth day of treatment, an abrupt rise in the ventricular capture threshold with ventricular pacing failure was noted. The capture threshold decreased two days after discontinuation of flecainide acetate.

Action Potentials↗
PubMed1998

Left ventricular geometry and function are related to electrocardiographic characteristics and diagnoses.

We investigated the relationships between echocardiographic indices of left ventricular geometry and function and major electrocardiographic (ECG) abnormalities in 540 elderly (69-74 years old) male participants of a health survey conducted in Uppsala county, Sweden. Comparing men with major ECG abnormalities that were present or absent in various hierarchic mutually exclusive categories, left ventricular mass indexed to body surface area (LVMI) was significantly increased with major Q-waves (P = 0.0002), ST or T-wave abnormalities (P = 0.005), left bundle-branch block (P = 0.005) and also with atrioventricular block type 1 (P = 0.008) and frequent premature beats (P = 0.02). The left atrial diameter was also significantly increased with most ECG abnormalities. The increased LVMI was in left bundle-branch block mainly due to an increased left ventricular diameter, whereas left ventricular wall thickness was increased with frequent premature beats, atrioventricular block type 1 and ST or T-wave abnormalities. The prevalence of Q-waves was highest in eccentric left ventricular hypertrophy, whereas the prevalence of ST or T-wave abnormalities and atrioventricular block type 1 was highest in concentric left ventricular hypertrophy. Both left ventricular systolic (ejection fraction) and diastolic function (E/A) ratio) were inversely related to Sokolow-Lyon QRS amplitude (r = -0.25, P < 0.02 and r = -0.22, P < 0.03 respectively). In conclusion, LVMI was increased in subjects with ECG signs of coronary artery disease as well as in subjects with several other ECG diagnoses. Furthermore, both left ventricular systolic and diastolic dysfunction were related to increased QRS amplitudes. Thus, the finding of ECG abnormalities in elderly men should raise the suspicion of structural and/or functional left ventricular abnormality.

Adult↗
PubMed2002

[ECG changes in aortic valve defects].

ECG is nowadays no longer the dominant way of diagnosing aortic valve diseases. The basis of accurate diagnosis of these diseases is clinical examination, ECHO and catheterization of the heart, which is essential in the great majority of valve diseases, in particular to rule out coronary changes. ECG is however important for the primary evaluation of left ventricular hypertrophy, left ventricular overburdening, for detection of enlargement or overloading of the left atrium. It is irreplaceable for evaluation of impaired rhythm, or impaired conduction of the impulse. Thus we can prove atrial fibrillation, or flutter bundle branch block, disorders of AV conduction (block of AV transmission grade one to three), supraventricular and ventricular extrasystoles etc. Changes of the ECG tracing provide also some information which cannot be obtained by other means.

Aortic Valve Insufficiency↗
PubMed2004

Supraventricular tachyarrhythmias in Ebstein anomaly: management and outcome.

OBJECTIVE: This study was undertaken to review the role of electrophysiology testing and to determine the early and late results of medical and surgical management of supraventricular tachyarrhythmias in Ebstein anomaly. METHODS: We reviewed 130 patients between 1990 and 2001 with Ebstein anomaly and history of tachyarrhythmia with a median age of 25 years (mean age 27.5 years); 106 underwent electrophysiologic testing and 24 had documented atrial flutter or fibrillation. We excluded 21 patients: negative results of testing (n = 18), ventricular tachycardia (n = 2), and junctional tachycardia (n = 1). The remaining 109 patients had more than one mechanism: accessory pathway-mediated tachycardia (n = 49), atrioventricular nodal reentrant tachycardia (n = 10), and atrial flutter/fibrillation (n = 70). RESULTS: Eighty-three patients underwent at least one arrhythmia procedure combined with surgery for Ebstein anomaly. Early mortality was 4.8%. Forty-one patients underwent surgical ablation of an accessory pathway without recurrent accessory pathway-mediated tachycardia at a mean follow-up of 48 months. Seven patients underwent surgical perinodal cryoablation for atrioventricular nodal reentrant tachycardia without recurrence at a mean follow-up of 57 months. Forty-eight patients underwent surgical intervention for atrial flutter or fibrillation (right-sided maze procedure, n = 38, and cryoablation of the atrial isthmus, n = 10). Freedom from recurrent atrial flutter or fibrillation was 75% at a mean follow-up of 34 months. CONCLUSION: Concomitant arrhythmia procedures can be performed without increase in early mortality and should be added to Ebstein repairs for all patients who have supraventricular tachyarrhythmias. Surgical procedures for accessory pathway-mediated tachycardia and atrioventricular nodal reentrant tachycardia give excellent (100%) freedom from recurrence of those arrhythmias. Surgical intervention for atrial flutter/fibrillation yields freedom from late recurrence in 75% of cases.

Adolescent↗
PubMed1977

The antiarrhythmic efficacy of intravenous therapy with disopyramide phosphate.

Disopyramide phosphate was administered intravenously to 57 patients with 60 episodes of arrhythmia (21 supraventricular and 39 ventricular) as a 2 mg/kg bolus. Conversion to sinus rhythm was achieved in three (38 percent) of eight patients with atrial flutter, two (20 percent) of ten patients with atrial fibrillation, one (33 percent) of three patients with paroxysmal atrial tachycardia, and two (50 percent) of four patients with sustained ventricular tachycardia. In nine (75 percent) of 12 patients with nonsustained ventricular tachycardia, suppression of the arrhythmia was accomplished following the intravenous bolus of disopyramide. In 18 (78 percent) of 23 patients with frequent ventricular premature contractions, greater than 50 percent suppression of the ventricular premature contractions was achieved. These effects were satisfactorily maintained in six (86 percent) of seven patients with nonsustained ventricular tachycardia and in 14 (88 percent) of 16 patients with frequent ventricular premature contractions in whom therapy with disopyramide phosphate was continued as a 20 mg/hour intravenous drip infusion for up to 24 hours. Side effects were observed in only eight patients (14 percent) and were primarily anticholinergic in nature. Transient hypotension, not necessitating treatment with pressor agents, was observed in three patients (5 percent), in two of whom discontinuance of therapy with disopyramide was deemed necessary. Intravenous therapy with disopyramide in the dosage regimen employed appears to be moderately effective against supraventricular arrhythmia and particularly effective against ventricular arrhythmia with minimal toxicity. It appears to be a suitable alternative to intravenous therapy with lidocaine and has the additional advantage of availability for oral administration.

Administration, Oral↗
PubMedDate not supplied

Ablative therapy for ventricular arrhythmias.

Radiofrequency catheter ablation techniques have enjoyed successful applications in patients with a wide variety of supraventricular tachycardias, especially the Wolff-Parkinson-White syndrome and atrioventricular nodal reentry. More recent reports have shown successful applications in patients with atrial tachycardias and atrial flutter. In addition to these, there are now reports of success during attempts to use radiofrequency techniques to eliminate ventricular tachycardia (VT), both in patients without structural heart disease (idiopathic VT) and patients with structural heart disease (primarily coronary artery disease). Techniques to map sites for ablation in patients with idiopathic VT usually include identifying early endocardial activation and using pace mapping. Success rates for ablation of idiopathic VT have been very high (over 90%) in patients with VT arising from the right ventricular outflow tract. Success rates have not been quite as high when VTs arising from sites other than the right ventricular outflow tract are targeted in the patient with idiopathic VT. In patients with VT caused by coronary artery disease, early endocardial activation and pace mapping can be unreliable. In these patients, searching for mid-diastolic potentials or showing concealed entrainment have proved more reliable. When these latter techniques are applied, success rates in eliminating a single focus of VT in a patient with coronary artery disease has been reported to be as high as 60% to 80%. Future therapies will include new energy sources, new (larger and/or cooled) electrodes, and multipoint catheter mapping, possibly using body surface mapping techniques.

Adult↗
PubMed2002

[Focal atrial fibrillation. Clinical characteristic and results of radiofrequency ablation].

BACKGROUND: Atrial fibrillation can originate in arrhythmogenic foci coming from the pulmonary veins. Patients with atrial fibrillation, initiated from triggering foci, can be treated with radiofrequency ablation. AIM: To report the results of radiofrequency ablation in patients with focal atrial fibrillation. PATIENTS AND METHODS: Thirteen patients with focal atrial fibrillation (8 male, aged 19 to 60 years old) are reported. Twelve had frequent crises refractory to antiarrhythmic drugs. Two had also flutter and tachycardia. One had a permanent atrial fibrillation lasting five years. Two had ventricular dysfunction and left atrial dilatation. The triggering focus was identified during the electrophysiological study, by the precocity of the potential that initiated the atrial fibrillation. RESULTS: All patients had early atrial extrasystolic beats, isolated or repetitives, that preceded atrial fibrillation. During the electrophysiological study, 18 foci (3 in the right and 15 in the left atrium all in pulmonary veins) were identified. Radiofrequency ablation had immediate success in 11 patients. In 5, a flutter was also ablated. One patient had a sinus dysfunction after the procedure and atrial fibrillation was not eliminated. In this and other patient in whom the procedure failed, a pacemaker was implanted and the atrioventricular node was blocked. In a follow up, ranging from 4 to 31 months, eight patients are asymptomatic and 3 recidivated. No complications have been detected. CONCLUSIONS: Patients with focal atrial fibrillation have common clinical and electrocardiographic features. Radiofrequency ablation of the triggering focus is possible and effective in most cases.

Adult↗
PubMed1981

Antiarrhythmic effects of acute betablockade with atenolol on supraventricular tachycardias at rest and during exercise.

In a total of 18 patients, 7 females and 11 male patients with ages ranging from 23 to 70 years (mean: 45.5 +/- 14.5) diagnostic His bundle studies incorporating programmed atrial and ventricular pacing for the induction of tachycardias was performed before and after betablockade with the cardioselective betablocking agent atenolol, in a dose of 5 mg given iv. over 3 to 5 minutes. In 7 patients the pacing procedure could be repeated following ergometric exercise in order to evaluate the influence of a raised sympathetic tone on the conditions initiating paroxysmal tachycardias. At rest, atenolol prevented the pacing induced tachycardias (20 dysrhythmias in 18 patients) in 3/5 individuals with Wolff-Parkinson-White (WPW)-syndrome, in 4/6 cases with atrial tachycardias, in 4/6 patients presenting atrial flutter, in 2/2 cases developing AV-nodal tachycardias and in 1/1 individual with ventricular tachycardia. Thus, in 13 out of 19 (68%) supraventricular dysrhythmias patients benefitted from atenolol by preventing or controlling the tachycardia. Ergometric exercise changed the tachycardia or echo zone in 5/8 arrhythmias after betablockade when compared to the controls before administration of atenolol (3/5 improvement by narrowing of the tach- or echo zone, 1/5 prevention of tachycardia, 1/5 impairment due to widening of the tachycardia zone). Considering only the prevention of tachycardias, the antiarrhythmic potency of atenolol was improved in one patient with pacing induced flutter and impaired in one individual with a WPW syndrome, by ergometric exercise. These results suggest that atenolol seems to provide a good antiarrhythmic action, especially in supraventricular tachycardias, and that an increased sympathetic tone during exercise may modify the antidysrhythmic strength of betablockade.

Adult↗
PubMed1976

Clinical efficacy of amiodarone as an antiarrhythmic agent.

Amiodarone, administered orally in doses of 200 to 600 mg/day, was remarkably effective in the treatment and prevention of a wide variety of atrial and ventricular arrhythmias. Total suppression and control was provided in 98 (92.4 percent) of 106 patients with supraventricular arrhythmias and in 119 (82 percent) of 145 patients with ventricular arrhythmias. The rates of total control of the arrhythmia were: 96.6 percent in 30 patients with recurrent atrial flutter or fibrillation, 96.6 percent in 59 patients with repetitive supraventricular tachycardia, 100 percent in 27 patients with Wolff-Parkinson-White syndrome and 77.2 percent in 44 patients with recurrent ventricular tachycardia unsuccessfully treated with other drugs. Excellent results were obtained in 6 to 8 patients with repetitive ventricular tachycardia and ventricular fibrillation related to postinfarction ventricular aneurysm and in 12 of 14 patients with ventricular extrasystoles and ventricular tachycardia related to Chagasic myocarditis. Amiodarone proved safe in patients with severe congestive heart failure and severe myocardial damage. Its clinical efficacy was related to its electrophysiologic properties and to two unique properties: its wide safety margin and its cumulative effect. The latter liberates patients from a rigid hourly schedule and provides for continuous antiarrhythmic control, days and even weeks after treatment is discontinued.

Amiodarone↗
PubMed1992

Termination of tachycardias by transesophageal electrical pacing.

To evaluate the therapeutic significance of noninvasive transesophageal pacing for termination of tachycardias the method of rapid atrial or ventricular transesophageal pacing was used in 233 patients with different tachycardiac arrhythmias. We were able to terminate atrial flutter in 136 of 162 patients by transesophageal rapid atrial stimulation (conversion to sinus rhythm in 75 cases, induction of atrial fibrillation in 61 cases). Atrial tachycardias were interrupted in 17 of 23 patients (sinus rhythm in 11 cases, atrial fibrillation in six cases). AV reciprocating/AV nodal supraventricular reentry tachycardias were terminated in 62 of 63 patients (sinus rhythm in 58 cases, atrial fibrillation in four cases). By transesophageal rapid ventricular pacing ventricular tachycardias could be terminated in ten of 15 patients. The success rate of transesophageal pacing was influenced by the pacing rate, by the type of tachycardiac arrhythmia inclusive by the type of atrial flutter and by the tachycardia's cycle length. Because the success rates are comparable with invasive technique and the procedure is simpler, the noninvasive transesophageal antitachycardiac pacing should be respected as the method of the first choice in patients with supraventricular tachycardias.

Atrial Flutter↗
PubMed1999

Accuracy of the LocaLisa system in catheter ablation procedures.

Estimation of the 3-dimensional (3D) position of ablation electrodes from fluoroscopic images is inadequate in the ablation of complex arrhythmogenic substrates. We developed a new technique for real-time 3D localization of intracardiac electrodes. Regular catheter electrodes are used as sensors for a high-frequency transthoracic electrical field, which is applied via standard skin electrodes. We investigated localization accuracy by comparing measured and true interelectrode distances between the tip and the 10th electrode of a decapolar catheter, and the tip and the 4th electrode of a quadripolar catheter during catheter ablation procedures. Long-term stability was analyzed by localization of the proximal His bundle before and after slow pathway ablation. Accuracy achieved with the 54-mm distance between the two outer electrodes of the decapolar catheters was 101% +/- 15%, 95% +/- 10%, and 97% +/- 8% in the right atrium, right ventricle, and left ventricle, respectively. During catheter ablation procedures, the measured distance between the tip and 4th electrode of the mapping catheter was 100% +/- 15% in atrial flutter, 100% +/- 12% in slow pathway ablation, and 100% +/- 14% in ablations for left ventricular tachycardia. After 2 hours, localization of the proximal His bundle was reproducible within 1.4 +/- 1.1 mm. The LocaLisa technique allows for reproducible, real-time nonfluoroscopic 3D visualization of standard mapping and ablation catheters and is sufficiently accurate for the creation of linear radiofrequency lesions. The freedom of catheter choice makes the LocaLisa system an invaluable tool in catheter mapping and ablation procedures.

Atrial Flutter↗
PubMed1990

Sustained intraatrial reentrant tachycardia: clinical, electrocardiographic and electrophysiologic characteristics and long-term follow-up.

Although intraatrial reentry has been traditionally listed as a mechanism for supraventricular tachycardia, few reports describing the clinical features of this arrhythmia exist. Nineteen patients with a clinical history of sustained supraventricular tachycardia were diagnosed as having intraatrial reentrant tachycardia. Seventeen (89%) patients of the 19 had underlying structural heart disease and 17 had echocardiographic evidence of atrial enlargement; the mean left ventricular ejection fraction was 51 +/- 16%. A history of concomitant atrial fibrillation or flutter was present in 13 patients (68%). The mean atrial cycle length during tachycardia was 326 +/- 57 ms (range 260 to 460). Fourteen patients had 1:1 atrioventricular (AV) conduction during tachycardia, of whom 50% had an RP'/RR' ratio greater than 0.5. Intravenous adenosine (dose range 37.5 to 150 micrograms/kg) and verapamil (dose range 5 to 10 mg) had no effect on atrial tachycardia cycle length in 13 of 14 and 9 of 9 patients, respectively, despite induction of second degree AV block. Type 1a antiarrhythmic drugs achieved long-term suppression of intraatrial reentrant tachycardia in only 6 patients, whereas amiodarone (326 +/- 145 mg/day) was successful in 11 patients during a 32 +/- 20 month follow-up period. The remaining two patients and one patient who later developed amiodarone toxicity either progressed to (n = 1) or had (n = 2) catheter-induced high grade AV block and were treated with long-term ventricular pacing. It is concluded that intraatrial reentrant tachycardia is often associated with structural heart disease, particularly of types that cause atrial abnormalities, but left ventricular dysfunction is not a requisite finding. Other arrhythmias are frequently observed in these patients. This arrhythmia responds poorly to type 1a antiarrhythmic drugs, but is effectively treated with amiodarone. Catheter ablation of the AV junction offers a therapeutic option for patients who are refractory to medical therapy.

Adenosine↗
PubMed2006

Pathogenesis of cardiac conduction disorders in children genetic and histopathologic aspects.

Fetal dysrhythmias are usually transient. Abnormal fetal rates and rhythms during labor are "functional." Fetal dysrhythmias may be associated with congenital heart disease and fetal hydrops. Bradycardia is usually related to fetal distress; supraventricular tachycardia, atrial flutter, and atrial fibrillation may be associated with severe congestive heart failure. Ventricular fibrillation is rare in the fetus and infant and is usually associated with myocardial necrosis with perimembranous septal defect; the nonbranching atrioventricular (AV) bundle may have an aberrant position and result in cardiac arrhythmia. Wolff-Parkinson-White syndrome with conduction abnormalities and left ventricular hypertrophy (LVH) is due to an accessory pathway that bypasses the AV sulcus and results in faster conduction. Carnitine deficiency may be primary or secondary and may result in cardiac arrhythmia. Histiocytoid cardiomyopathy is characterized by cardiomegaly, incessant ventricular tachycardia, and frequently sudden death. Arrhythmogenic right ventricular dysplasia (ARVD) results in ventricular tachycardia and left bundle branch block. Noncompaction of the left ventricle predisposes to potentially fatal arrhythmias. Long Q-T syndromes (LQTS) are a heterogeneous group of disorders with many genetic mutations. Brugada syndrome is an autosomal dominant trait with right bundle branch block and ST elevation. Barth syndrome is an X-linked disorder with dilated cardiomyopathy, cyclic neutropenia and skeletal myopathy. Hypertrophic cardiomyopathy in infancy may be related to metabolic diseases, particularly glycogen storage diseases; the familial form predisposes to sudden death. Arrhythmias following cardiac surgery may occur after closure of a ventricular septal defect (VSD) or damage to the conduction system.

Arrhythmias, Cardiac↗
PubMed1985

Arrhythmias induced during termination of supraventricular tachycardia.

Pacing is being used frequently for the treatment of drug-resistant, paroxysmal supraventricular tachycardias (SVT). SVT can usually be terminated by pacing, but arrhythmias may be induced which interfere with the safety of antitachycardia pacing. To quantify these pacing-induced arrhythmias, 453 attempts to terminate SVT in 111 patients were analyzed. The patients were 6 to 73 years old (mean 41); 62 were male. Seventy-six patients had SVT using an accessory atrioventricular bypass, and 35 patients had intranodal SVT. Single and then, if required, multiple ventricular and atrial premature beats and overdrive pacing were delivered from the atrium and ventricle. A pacing-induced arrhythmia occurred in 9% of all attempts (34% of patients). Atrial flutter or fibrillation (AF) was the most frequent arrhythmia (in 8% of all attempts and sustained in 75%). Atrial vs ventricular pacing resulted in a 12% vs 2% incidence of AF. AF was unrelated to age, sex, atrial size and SVT type, and was predominantly induced by multiple premature beats. In 6 patients a different SVT and in 2 patients a nonsustained ventricular tachycardia was induced. In 6 patients SVT could only be terminated by initiating another arrhythmia. Thus, AF is frequently induced during attempted pacing termination of SVT. To limit the risk of AF, a single premature beat should preferentially be used to terminate SVT. In 6% of patients, SVT can only be terminated by inducing another arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Determinants of anterior mitral leaflet fluttering in pure aortic regurgitation from pulsed Doppler study of the early diastolic interaction between the regurgitant jet and mitral inflow.

Fluttering of the anterior mitral leaflet may be absent in patients with moderate to severe aortic regurgitation (AR), suggesting that the volumetric severity of AR alone does not determine the presence or absence of abnormal diastolic mitral valve motion. Fifteen patients with moderate to severe AR and normal mitral valves, 9 of whom demonstrated anterior mitral leaflet fluttering, were studied to elucidate the determinants of abnormal anterior mitral leaflet motion in these patients. Pulsed Doppler mapping of the flow-velocity disturbance of AR demonstrated its presence in the third of the left ventricular outflow tract adjacent to the anterior mitral leaflet in 8 of 9 patients with anterior mitral leaflet fluttering and none of the 6 patients without anterior mitral leaflet fluttering (p less than 0.02). The impact of this regurgitant jet on early diastolic transmitral inflow was examined with pulsed Doppler in these 2 groups of patients with AR and in age-matched control subjects. Deceleration of early diastolic transmitral filling was slower in patients with AR and anterior mitral leaflet fluttering than in age-matched control subjects (283 +/- 107 vs 457 +/- 176 cm/s2, p less than 0.02), whereas it was not significantly different from controls in AR patients without anterior mitral leaflet fluttering. This resulted in significant prolongation of the duration of early diastolic transmitral filling in patients with AR and anterior mitral leaflet fluttering (297 +/- 93 vs 203 +/- 44 ms for age-matched control subjects, p less than 0.02), which was not observed in patients with AR who did not have anterior mitral leaflet fluttering.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗