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6.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations 7 Atrial Flutter See Figure 17 for a schematic depicting classification of atrial flutter/ATs; Figure 18 for the algorithm for acute treatment of atrial flutter; and Figure 19 for the algorithm for ongoing management of atrial flutter. 7.1 Cavotricuspid Isthmus–Dependent Atrial Flutter Atrial flutter is a macroreentrant atrial arrhythmia characterized by regular atrial rate and constant P-wave morphology. When the atrial flutter circuit involves the cavotricuspid isthmus (CTI), it is labeled CTI-dependent atrial flutter. When CTI-dependent flutter involves a circuit that rotates around the tricuspid valve in a counterclockwise direction (up the septum and down the free wall), it is called “typical”; less commonly, the CTI-dependent flutter circuit rotates in a clockwise direction (sometimes called “reverse typical”).203 Counterclockwise CTI-dependent atrial flutter is characterized electrocardiographically by dominant negative flutter waves in the inferior leads (so-called “sawtooth waves”) and a positive P wave in lead V1 at atrial rates of 250 bpm to 350 bpm (Figure 17). Clockwise isthmus-dependent flutter shows the opposite pattern (ie, positive flutter waves in the inferior leads and wide, negative flutter waves in lead V1) (Figure 17). Although the atrial rates for flutter typically range from 250 bpm to 330 bpm, the rates may be slower in patients with severe atrial disease or in patients taking antiarrhythmic agents or after unsuccessful catheter ablation.310 Atrial flutter can occur in clinical settings similar to those associated with AF, and atrial flutter can be triggered by AT or AF.121,311 It is common for AF and atrial flutter to coexist in the same patient. After CTI ablation, 22% to 50% of patients have been reported to develop AF after a mean follow-up of 14 to 30 months, although 1 study reported a much higher rate of AF development, with 82% of patients treated by catheter ablation for atrial flutter manifesting AF within 5 years.312 Risk factors for the manifesting AF after atrial flutter ablation include prior AF, depressed left ventricular function, structural heart disease or ischemic heart disease, inducible AF, and increased LA size.121,312–316 Atrial flutter may result from antiarrhythmic therapy of AF, particularly when flecainide, propafenone, or amiodarone is used for treatment of AF.317,318 In those patients with atrial flutter resulting from antiarrhythmic therapy of AF, ablation of the CTI-dependent flutter may prevent recurrent flutter while antiarrhythmic therapy for AF is continued.318 Patients with atrial flutter are thought to have the same risk of thromboembolism as patients with AF; therefore, Figure 12. Acute treatment of AVNRT. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. AVNRT indicates atrioventricular nodal reentrant tachycardia; and IV, intravenous. Recommendations for Management of Symptomatic Patients With Manifest Accessory Pathways COR LOE Recommendations I B-NR 1. In symptomatic patients with pre-excitation, the findings of abrupt loss of conduction over the pathway during exercise testing in sinus rhythm294–297 (Level of Evidence: B-NR) or intermittent loss of pre-excitation during ECG or ambulatory monitoring297 (Level of Evidence: C-LD) are useful for identifying patients at low risk of developing rapid conduction over the pathway. C-LD See Online Data Supplements 11–15. An important consideration in the evaluation of patients with pre-excitation is determining risk of developing rapid conduction over the accessory pathway and life-threatening ventricular arrhythmias in response to AF. The noninvasive findings that identify a pathway incapable of maintaining rapid conduction during AF include intermittent loss of conduction over the accessory pathway on the resting ECG or during ambulatory monitoring or abrupt loss of pre-excitation during exercise testing.294–297 The ECG should be evaluated closely to make certain the delta wave is truly absent, as accessory pathways (especially left lateral pathways) may demonstrate varying degrees of pre-excitation because of fusion between conduction over the accessory pathway and through the AV node, which may give the appearance of loss of pre-excitation if the subtle delta wave is not identified. Noninvasive tests have an approximately 90% positive predictive value and 30% negative predictive value for identifying pathways with lifethreatening properties.294,295,297 If noninvasive evaluation suggests that the accessory pathway conducts poorly in the anterograde direction, although risk of life-threatening events is likely lower, the EP study still may be useful because of patient symptoms. I B-NR 2. An EP study is useful in symptomatic patients with pre-excitation to risk-stratify for life-threatening arrhythmic events.254,256,298–300 See Online Data Supplements 11–15. Most symptomatic patients with accessory pathways undergo catheter ablation, but in some instances, EP studies are performed to identify whether the patient is at increased risk of rapid conduction down the accessory pathway during AF and development of life-threatening ventricular arrhythmias. The most useful findings for risk stratification are an R-R interval <250 ms between 2 pre-excited complexes during induced AF; the presence of multiple accessory pathways; the finding of AVRT precipitating pre-excited AF; and an accessory pathway refractory period <240 ms.254,256,298–300 Downloaded from http://ahajournals.org by on October 7, 2026