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[What is your diagnosis? Atrial flutter].
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Electrocardiographic artifacts simulating atrial flutter.
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[Isoptin in the therapy of tachycardiac type of atrial flutter].
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[Wenckebach's period between the electrode of the transesophageal stimulator and left atrium in a patient with recurrent atrial flutter].
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[Cases of pediatric electrocardiography. Atrial flutter].
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[Atrial fibrillation, atrial flutter].
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Ibutilide: a class III rapidly acting antidysrhythmic for atrial fibrillation or atrial flutter.
Ibutilide is an intravenous Class III antidysrhythmic approved for the treatment of recent onset atrial fibrillation or atrial flutter. Pharmacological effect occurs within 30 min, and the efficacy approaches 40%. In contrast to DC electrical cardioversion, which requires anesthesia, pharmacologic cardioversion offers an alternative in which sedation can be avoided. Patients receiving ibutilide should be monitored for at least 4 h after completed drug administration because of a small chance of ventricular dysrhythmia, mainly torsades de pointes. Careful patient selection is the key to avoiding dysrhythmic complications. The purpose of this article is to review the mechanisms, clinical applications, potential complications, and appropriate use of ibutilide.
Left atrial appendage function and abnormal hypercoagulability in patients with atrial flutter.
STUDY OBJECTIVES: The prevalence of thromboembolism might be higher than previously recognized in patients with atrial flutter (AFL) based on findings of transesophageal echocardiography (TEE). To evaluate the potential prothrombotic state in patients with AFL, TEE findings and hemostatic markers were compared among patient groups with AFL, normal sinus rhythm (NSR) and chronic nonvalvular atrial fibrillation (AF). DESIGN AND SETTINGS: Cross-sectional study at a university hospital. METHODS: In 28 patients (mean age, 63 years) with AFL, 58 patients (mean age, 66 years) with AF, and 27 patients (mean age, 61 years) with NSR who underwent TEE, plasma levels of markers for platelet activity (platelet factor 4 and beta-thromboglobulin [beta-TG]), thrombotic status (thrombin-antithrombin III complex and prothrombin fragments 1 and 2) and fibrinolytic status (d-dimer and plasmin-alpha(2)-plasmin inhibitor complex) were determined. RESULTS: Left atrial appendage (LAA) blood flow velocity in patients with AFL was higher (p < 0.05) than that in patients with AF, but was lower (p < 0.05) than that in patients with NSR (AF, 25 +/- 2; AFL, 44 +/- 4; NSR, 60 +/- 4 cm/s). Dense left atrial spontaneous echo contrast (SEC) was found in 4 patients (14%) with AFL and 16 patients (28%) with AF. There was no significant difference in plasma levels of hemostatic markers between the AFL group and the NSR group. AFL patients with impaired LAA function (LAA flow < 30cm/s, dense SEC, or both), however, showed higher level of d-dimer and beta-TG than those without impaired LAA function (d-dimer, 1.9 +/- 0.6 microg/mL vs 0.4 +/- 0.1 microg/mL; beta-TG, 73 +/- 17 ng/mL vs 33 +/- 5 ng/mL, p < 0.05). CONCLUSIONS: Patients with AFL as a whole are not in the prothrombotic state as compared with those with AF. However, patients with AFL and impaired LAA function are at potentially high risk for thromboembolism and might require anticoagulation.
Esmolol versus verapamil in the acute treatment of atrial fibrillation or atrial flutter.
The effects of esmolol, an ultrashort-acting beta blocker, and verapamil were compared in controlling ventricular response in 45 patients with atrial fibrillation or atrial flutter, in a randomized, parallel, open-label study. Patients with either new onset (less than 48 hours, n = 31) or old onset (greater than 48 hours, n = 14) of atrial fibrillation or flutter with rapid ventricular rate were stratified to receive esmolol (n = 21) or verapamil (n = 24). Drug efficacy was measured by ventricular rate reduction and conversion to sinus rhythm. The heart rate declined with esmolol from 139 to 100 beats/min (p less than 0.001) and with verapamil from 142 to 97 beats/min (p less than 0.001). Fifty percent of esmolol-treated patients with new onset of arrhythmias converted to sinus rhythm, whereas only 12% of those who received verapamil converted (p less than 0.03). Mild hypotension was observed in both treatment groups. Esmolol compares favorably with verapamil with respect to both efficacy and safety in acutely decreasing ventricular response during atrial fibrillation or flutter. Moreover, conversion to sinus rhythm is significantly more likely with esmolol.
Prevalence of left atrial chamber and appendage thrombi in patients with atrial flutter and its clinical significance.
OBJECTIVES: The study was done to assess the prevalence of left atrial (LA) chamber and appendage thrombi in patients with atrial flutter (AFl) scheduled for electrophysiologic study (EPS), to evaluate the prevalence of thromboembolic complications after transesophageal echocardiographic (TEE)-guided restoration of sinus rhythm and to evaluate clinical risk factors for a thrombogenic milieu. BACKGROUND: Recent studies showed controversial results on the prevalence of atrial thrombi and the risk of thromboembolism after restoring sinus rhythm in patients with AFl. METHODS: Between 1995 and 1999, patients with AFl who were scheduled for EPS were included in the study. After transesophageal assessment of the left atrial appendage and exclusion of thrombi, an effective anticoagulation was initiated and patients underwent EPS within 24 h. RESULTS: We performed 202 EPSs (radiofrequency catheter ablation, n = 122; overdrive stimulation, n = 64; electrical cardioversion, n = 16) in 139 consecutive patients with AFl. Fifteen patients with a thrombogenic milieu were identified. All of them had paroxysmal atrial fibrillation (AF). Transesophageal echocardiography revealed LA thrombi in two cases (1%). After EPS no thromboembolic complications were observed. Diabetes mellitus, arterial hypertension and a decreased left ventricular ejection fraction were found to be independent risk factors associated with a thrombogenic milieu. CONCLUSIONS: The findings of a low prevalence of LA appendage thrombi (1%) in patients with AFl and a close correlation between a history of previous embolism and paroxysmal AF support the current guidelines that patients with pure AFl do not require anticoagulation therapy, whereas patients with AFl and paroxysmal AF should receive anticoagulation therapy. In addition, the presence of clinical risk factors should alert the physician to an increased likelihood for a thrombogenic milieu.
Fetal supraventricular tachycardia: a case of (intermittent) atrial flutter.
Fetal tachycardia of "supraventricular" origin is uncommon. The authors present a patient with fetal ascites and atrial flutter. A review of the pertinent literature is included.
Left atrial flutter following pulmonary vein antrum isolation with radiofrequency energy: linear lesions or repeat isolation.
INTRODUCTION: Left atrial flutter (LAFL) is a known complication of pulmonary vein isolation. Treatment of this arrhythmia currently involves both linear lesions as well as re-isolation. However, it is unknown if re-isolation alone is sufficient to prevent recurrence. This study reviews the incidence of LAFL following segmental PV antrum isolation (PVAI) in a large patient population and evaluates if re-isolation alone is sufficient to prevent recurrence. METHODS AND RESULTS: Seven hundred thirty-seven patients underwent PVAI. Twenty-three patients (3.1%) developed post-PVAI LAFL. All patients underwent a second procedure in which only repeat PVAI was done. During the second procedure, all flutter circuits were electroanatomically mapped. All patients were followed at 3, 6, and 12 months. All 23 patients demonstrated recovery in one or more PV. After repeat isolation of the PVs, 61% of patients were arrhythmia free off all antiarrhythmic drugs. A relationship between the presence/absence of pre-existing left atrial (LA) scar was observed. Of the 11 patients with pre-existing LA scar, 36% remained arrhythmia free off antiarrhythmic drugs. In contrast, of the 12 patients without pre-existing LA scar, 83% remained arrhythmia free off antiarrhythmic drugs (P = 0.03). CONCLUSION: Among patients with LAFL following PVAI, re-isolation alone is sufficient in preventing recurrence in patients without pre-existing LA scar. Patients with pre-existing LA scar tend to have recurrence requiring further ablation including linear lesions, and continue to need antiarrhythmic medications.
Sinus tachycardia and J wave masquerading as atrial flutter.
The admission electrocardiogram (ECG) from a patient with severe heart failure was considered diagnostic of atrial flutter with 2:1 atrioventricular conduction. Slowing of the heart rate revealed sinus tachycardia with prominent 'J' waves that had been previously thought to be 'F' waves.
[Pharmacologic restoration of sinus rhythm in atrial flutter and fibrillation].
Restoration of the sinus rhythm in atrial fibrillation and flutter can be achieved by cardioversion, using an electric discharge, or by medicamentous treatment. Medicamentous treatment is based above all on a combination of antiarrhythmic drugs. By the concurrent administration of quinidine, verapamil and digoxin restoration of the sinus rhythm is achieved in 80% patients, on average after 37 hours at plasma quinidine levels of 2.57 +/- 1.4 (SD) micrograms/ml and digoxin levels of 1.90 +/- 1.3 (SD) nmol/l. Restoration of the sinus rhythm in atrial flutter calls for higher quinidine and digoxin levels than in atrial fibrillation (p less than 0.01). Prolonged persistence of the sinus rhythm during treatment with maintenance doses of quinidine, verapamil and digoxin is not satisfactory so far and after 12 months the sinus rhythm persists only in 30% of the patients where the rhythm was originally restored.
Severe nodal arrhythmia following direct current cardioversion for atrial flutter.
A case of long-lasting nodal arrhythmia and severe hypotension following DC cardioversion for atrial flutter is presented. The patient, treated with the selective serotonin reuptake inhibitor sertraline and with sotalol, thiopental and digoxin, showed no sign of organic disease or drug intoxication. We suggest that drug interaction in combination with the DC shock and an altered sympaticus/parasympaticus balance during anaesthesia provoked the incident.
Correlation of atrial electrocardiographic amplitude with radiofrequency energy required to ablate cavotricuspid isthmus-dependent atrial flutter.
OBJECTIVES: The purpose of this study was to evaluate a possible correlation between atrial ECG amplitude in common atrial flutter (AFL) and radiofrequency (RF) energy required to achieve cavotricuspid isthmus block. BACKGROUND: The amount of RF delivery required for ablation of typical AFL is variable. This variation has been attributed to the cavotricuspid isthmus anatomy. Atrial ECG amplitude can be a marker of atrial anatomic variations and therefore may correlate with RF duration required to achieve cavotricuspid isthmus block. METHODS: Seventy consecutive patients were prospectively studied. Ablation of the cavotricuspid isthmus was performed by creating a line of block between the inferior tricuspid annulus and the inferior caval vein using 8-mm-tip electrode catheters. If more than 20 minutes of RF time was required to achieve conduction block, the catheter was changed to an irrigated-tip catheter. Atrial ECG amplitude was assessed in leads II, III, aVF, and aVL. RESULTS: A total of 14 +/- 11 minutes of RF energy was delivered to achieve block in all patients; 12 patients (8%) required more than 20 minutes. Atrial ECG amplitude showed highly significant correlations with cumulative RF energy (F and P waves in lead II: r = 0.703 and r = 0.737, P < .001). P-wave amplitude <0.2 mV and/or flutter wave amplitude <0.35 mV in lead II have a high negative predictive value to predict <20 min RF delivery (96% and 89% respectively). CONCLUSIONS: A significant correlation exists between atrial ECG amplitude and amount of RF required to ablate typical AFL. Atrial ECG amplitude may be a surrogate marker of characteristics of isthmus anatomy. These findings may influence the choice of catheter used for cavotricuspid isthmus ablation.
[Paroxysmal AV block induced by atrial flutter in acute inferior myocardial infarction].
Conduction disturbances in the acute phase of an inferior myocardial infarction are frequent. Paroxysmal AV block and ventricular standstill is, on the other hand, an unusual event. We describe a case of paroxysmal AV block precipitated by, and dependent on, the presence of atrial flutter. Concealed conduction of atrial impulses to the AV node is the likely cause of this form of AV block. The transient development, ischaemia related, of a longitudinal and transverse dissociation of the AV node, increased the concealed penetration of atrial impulses and its effect on subsequent impulse formation, given rise to a form of paroxysmal AV block.