Supraventricular tachyarrhythmias: atrial flutter and atrial fibrillation

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.     

心房颤动与心房扑动的关系

心房颤动(atrial fibrillation，AF)是临床上最常见的持续性的心律失常。AF患者往往有心房扑动(atrial flutter，AFL)发作，而AFL患者也常伴有AF^[1-3]。在使用抗心律失常药物治疗过程中，AF可能变为AFL^[4-5]，或AFL蜕变为AF^[6-9]。这些现象提示二者在发生和维持机制上可能存在一些共性和相互关联。     

Simultaneous occurrence of atrial fibrillation and atrial flutter

INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.     

Pharmacological therapy of atrial fibrillation and atrial flutter

BACKGROUND: Despite the increasing availability of nonpharmacological treatment options for atrial fibrillation, drug therapy targeted at restoration and maintenance of sinus rhythm, or aimed at symptomatic ventricular rate control remains the mainstay of therapy for the majority of patients. METHOD: Available data suggest that these two treatment approaches yield similar responder rates with regard to symptomatic improvement. RESULTS: Detailed results from major prospective studies investigating the prognostic effects of different atrial fibrillation treatment modalities are expected to become available soon. At present, however, the choice of the primary treatment strategy, i.e. rate control or rhythm control, still remains upon the clinical decision and expertise of the treating physician. Cardioversion by means of external biphasic shock delivery has shown to effectively convert atrial fibrillation to sinus rhythm in more than 90% of patients. Pharmacological cardioversion, in contrast, has a far lower success rate and may be followed by severe complications mandating in-hospital administration with the majority of drug regimens. For the maintenance of sinus rhythm, the proarrhythmic side effects of Class I antiarrhythmic drugs currently limit their use to those patients without any structural heart disease. Clinical investigation of newer "pure" Class III drugs have shown to excite considerable prolongation of ventricular repolarization duration resulting in a significant risk for torsade-de-pointes tachycardia. Betablockers are beneficial in many clinical situations associated with the occurrence of atrial fibrillation, such as heart failure, arterial hypertension and coronary artery disease. These substances, however, do not seem to improve cardioversion rates and their effect in maintaining sinus rhythm is only moderate. Patients with structural heart disease in whom maintenance of sinus rhythm is strongly desired, therefore, are left to amiodarone therapy. The cardiac safety profile as well as the proven effectiveness are unsurpassed by any other available drug at present. This paper reviews major studies published during the last decade implementing recent guidelines regarding pharmacological rate control, cardioversion and maintenance of sinus rhythm and the approach towards patients suffering from paroxysmal atrial fibrillation.     

Prognostic differences between atrial fibrillation and atrial flutter

This report presents the outcome of a cohort of 94 patients with atrial fibrillation from the Canadian Registry of Atrial Fibrillation, in which we paid particular attention to the probability of stroke and death. We also evaluated warfarin use over time and compared left atrial dimensions in patients with atrial flutter with those with atrial fibrillation.     

The interrelationship between atrial fibrillation and atrial flutter

For a long time, it has been known that atrial fibrillation and atrial flutter have a close clinical interrelationship. Recent electrophysiological studies, especially mapping studies, have significantly advanced our understanding of this interrelationship. Regarding the relationship of atrial fibrillation with atrial flutter: Atrial fibrillation of variable duration precedes the onset of atrial flutter in almost all instances. During the atrial fibrillation, the functional components needed to complete the atrial flutter reentrant circuit, principally a line of block between the venae cavae, are formed. If this line of block does not form, classical atrial flutter does not develop. If this line of block shortens or disappears, classical atrial flutter disappears. In fact, it is fair to say that the major determinant of whether atrial fibrillation persists or classical atrial flutter develops is whether a line of block forms between the venae cavae. Regarding the relationship of atrial flutter with atrial fibrillation: Studies in experimental models and now in patients have demonstrated that a driver (a rapidly firing focus or a reentrant circuit of very short cycle length) can cause atrial fibrillation by producing fibrillatory conduction to the rest of the atria. When the driver is a stable reentrant circuit of very short cycle length, it is, in effect, a very fast form of atrial flutter. There probably is a spectrum of reentrant circuits of short cycle length, i.e., "atrial flutter," that depend, in part, on where the reentrant circuit is located. When the cycle length of the reentrant circuit is so short that it will only activate small portions of the atria in a 1:1 manner, the rest of the atria will be activated rapidly but irregularly, i.e., via fibrillatory conduction, resulting in atrial fibrillation. In short, there are probably several mechanisms of atrial fibrillation, one of which is due to a very rapid atrial flutter circuit causing fibrillatory conduction. In sum, atrial fibrillation and atrial flutter have an important interrelationship.     

长短周期现象与心房颤动和心房扑动

为了解心房颤动及心房扑动发生时的长短周期现象的临床意义,观察经动态心电图或监测心电图证实的心房颤动８例和心房扑动６例。结果显示：心房颤动或心房扑动发生前的长周期多见于房性期前收缩后代偿间歇及明显窦性心动过缓等心律失常;长短周期现象对心房颤动,心房扑动的启动作用可经心脏的程度刺激诱发和复制;６例患者经ＤＤＤ起搏治疗,陈发性心房颤动及心房扑动的发生率明显下降,部分病例还需服用抗心律失常药物。认为长短周     

Momentary atrial electrical axes: II. Atrial flutter,atrial fibrillation,and paroxysmal tachycardia

Curves representing the consecutive atrial electrical axes for each 0.01 second have been derived for the frontal, horizontal, and sagittal planes from patients with atrial flutter, atrial fibrillation, and paroxysmal tachycardia, and three-dimensional models have been constructed.The clinical experimental results of Lewis, Drury, and Iliescu have been reproduced and extended in flutter and fibrillation.The same procedure has been applied in eight cases of paroxysmal tachycardia. The type of curve in this disturbance of atrial mechanism has been found to resemble that obtained during sinus rhythm; it differs only in direction. The characteristic features of flutter and fibrillation are not present. This fails to support the idea that a circus movement is present in paroxysmal tachycardia, and although the possibility of a circus involving the S-A node is not finally excluded, we believe that the weight of the evidence points to the existence of an ectopic site of impulse generation.The available information on the physiology and pharmacology of the atrial musculature and nodal tissues has been reconsidered insofar as it bears on the behavior of paroxysmal tachycardia, and the view that in it an ectopic pacemaker may be operative.     

The alternation between atrial flutter and atrial fibrillation.

Atrial fibrillation and atrial flutter share a common reentrant mechanism. However, the relationship between these arrhythmias has not been systemically studied to date. To evaluate the degree to which these arrhythmias may alternate, consecutive Holter monitor recordings which showed fibrillation or flutter in 96 patients were reviewed. One half of the patients were studied after open-heart surgery and the other half for varying indications. One quarter of the patients had atrial flutter in addition to fibrillation, and this alternation with flutter was significantly associated with the use of a type 1A antiarrhythmic drug (p = 0.007), but not with the use of digoxin or beta blockers (p = NS for both). Furthermore, this alternation with flutter was more common in the postoperative group (p = 0.01). A history of embolization was less common in patients who were in the postoperative group (p = 0.003) and patients who had flutter in addition to fibrillation (p = 0.05).     

Anticoagulation in atrial fibrillation and flutter.

Atrial fibrillation and atrial flutter are important risk factors for stroke. Based on a literature search, pathogenesis of thromboembolism, risk assessment in patients, efficacy of anticoagulation therapy and its alternatives are discussed. Special emphasis is put on issues like paroxysmal atrial fibrillation, atrial flutter and anticoagulation surrounding catheter ablation and cardioversion. A strategy for anticoagulation around the time of pulmonary vein ablation is suggested.     

房颤与房扑的射频消融治疗研究

目的 探讨房颤与房扑之间的相互关系，寻找房颤的射频治疗方法。方法 对40例阵发性房颤患者进行了电生理标测及射频消融。结果 40例中有6例患者发生房扑，行右房峡部消融，1例行Halo电极标测示峡部双向阻滞，随访12－30个月房颤消失或次数明显减少。结论 房颤与房扑为两种密切相关的心律失常，消融右房峡部可能对部分房颤患者起到治疗作用。     

Canadian Cardiovascular Society atrial fibrillation guidelines 2010: catheter ablation for atrial fibrillation/atrial flutter

Catheter ablation of atrial fibrillation (AF) offers a promising treatment for the maintenance of sinus rhythm in patients for whom a rhythm control strategy is desired. While the precise mechanisms of AF are incompletely understood, there is substantial evidence that in many cases (particularly for paroxysmal AF), ectopic activity most commonly located in and around the pulmonary veins of the left atrium plays a central role in triggering and/or maintaining arrhythmic episodes. Catheter ablation involves electrically disconnecting the pulmonary veins from the rest of the left atrium to prevent AF from being triggered. Further substrate modification may be required in patients with more persistent AF. Successful ablation of AF has never been shown to alter mortality or obviate the need for oral anticoagulation; thus, the primary indication for this procedure should be improvement of symptoms caused by AF. The success rate of catheter ablation for AF is superior to the efficacy of antiarrhythmic drugs, but success is still in the range of 75%-90% after 2 procedures. Ablation is also associated with a complication rate of 2%-3%. Thus, ablation should primarily be used as a second-line therapy after failure of antiarrhythmic drugs. In contrast to AF, catheter ablation of atrial flutter has a higher success rate with a smaller incidence of complications. Thus, catheter ablation for atrial flutter may be considered a first-line alternative to antiarrhythmic drugs.     

Lidocaine-induced cardiac rate changes in atrial fibrillation and atrial flutter

To assess atrial and ventricular rate changes after lidocaine injection, 18 atrial flutter patients and 35 atrial fibrillation patients were given intravenous lidocaine, mean dose 100 mg. Continuous electrocardiographic recording for 5 minutes before and at least 10 minutes after lidocaine injection was used to determine rate changes. The atrial flutter rate decreased after lidocaine in 17 of 18 patients (94 per cent), mean maximal decrease 27 beats/minute. The ventricular rate response in atrial flutter was variable but in three patients increased 21, 27, and 47 beats/minute respectively (P less than 0.001). In atrial fibrillation, the mean ventricular rate after rapid lidocaine injection increased six beats/minute (P less than 0.01). In three of 35 atrial fibrillation patients (9 per cent), the ventricular rate increase was greater than 20 beats/minute (P less than 0.001), and in two patients (6 per cent), the ventricular rate increase was associated with potentially serious clinical events. Lidocaine-induced ventricular rate increases are common in atrial flutter and fibrillation, particularly in patients who are also receiving quinidine.     

Inter-relationships of atrial fibrillation and atrial flutter mechanisms and clinical implications

There is a close interrelationship between atrial fibrillation (AF) and atrial flutter (AFL). Atrial fibrillation of variable duration precedes the onset of AFL in almost all instances; during AF, the functional components needed to complete the AFL re-entrant circuit, principally a line of block (LoB) between the vena cavae, are formed; if this LoB does not form, classical AFL does not develop. In contrast, there seems to be a spectrum of atrial re-entrant circuits (drivers) of short cycle lengths (CLs) (i.e., AFL). When the CL of the AFL re-entrant circuit is so short that it will only activate portions of the atria in a 1:1 manner, the rest of the atria will be activated rapidly but irregularly (i.e., via fibrillatory conduction), resulting in AF. In short, there are probably several mechanisms of AF, 1 of which is due to a very rapid AFL causing fibrillatory conduction. All of these interactions of AF and AFL have important clinical implications.