Hfy

Ablation Site

Ablation Site

Kent Potentials Hbe

25 mm/sec

Fig. 6. (A) Typical successful ablation site (ABL) electrograms of an accessory pathway. Also shown are surface leads 1 and V6 and intracardiac recordings obtained from the high right atrium (RA), right ventricle (RV), His bundle (HBE), and CS ostium. The interval from the His bundle (H) recording to the QRS complex is less than 35 ms, confirming the presence of pre-excitation. At the successful ablation site, the ventricular electrogram (V) occurs early relative to the onset of the QRS complex, and a discreet deflection between the atrial (A) and ventricular electrograms is present, consistent with an accessory pathway (or "Kent") potential. (B) Within 2 s of radiofrequency energy delivery, the temperature recorded from the ablation catheter reaches 66°C. Several seconds after onset of energy delivery, pre-excitation disappears abruptly, as best seen in surface ECG lead V6.

25 mm/sec

Fig. 6. (A) Typical successful ablation site (ABL) electrograms of an accessory pathway. Also shown are surface leads 1 and V6 and intracardiac recordings obtained from the high right atrium (RA), right ventricle (RV), His bundle (HBE), and CS ostium. The interval from the His bundle (H) recording to the QRS complex is less than 35 ms, confirming the presence of pre-excitation. At the successful ablation site, the ventricular electrogram (V) occurs early relative to the onset of the QRS complex, and a discreet deflection between the atrial (A) and ventricular electrograms is present, consistent with an accessory pathway (or "Kent") potential. (B) Within 2 s of radiofrequency energy delivery, the temperature recorded from the ablation catheter reaches 66°C. Several seconds after onset of energy delivery, pre-excitation disappears abruptly, as best seen in surface ECG lead V6.

Patients in whom initial attempts are unsuccessful or whose arrhythmia recurs early after sinus rhythm is restored can be stratified into those in whom a potentially curative approach to catheter ablation exists (focal atrial tachycardia or type 1 atrial flutter) and those in whom curative approaches to catheter ablation do not exist or are currently under investigation (AF or atypical atrial flutter). Patients for whom catheter ablation represents an option for cure may elect to proceed directly to catheter ablation or undergo further trials of antiarrhythmic therapy. Patients for whom catheter ablation does not offer a potential for cure may undergo additional attempts at pharmacologic control. If initial measures are ineffective or poorly tolerated, the alternative therapeutic strategy of ventricular rate control can be employed using beta-blockers, calcium-channel blockers, or digoxin. If control of the ventricular response cannot be achieved with pharmacologic agents, catheter ablation or modification of the AV node can be considered. Under rare circumstances, such as patients with dilated cardiomyopathy resulting from recurring atrial tachycardia or atrial tachycardia presenting with significant hemodynamic compromise, electrophysiology testing and catheter ablation may be recommended as initial therapy. For example, an invasive approach would be recommended for a patient with syncope associated with 1:1 conduction of common atrial flutter.

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