6,7 Later human studies left the door open for a focal mechanism. Early studies suggested that flutter had a re-entrant mechanism 3–5 but others attributed flutter to focal discharge. Slower tachycardias displaying discrete P waves, separated by isoelectric baselines, were called ‘atrial tachycardia’. 1,2 On the ECG, flutter was a regular continuous undulation between QRS complexes at a cycle length (CL) of ≤250 ms (≥240 bpm). The term ‘flutter’ was coined to designate the visual and tactile rapid, regular atrial contraction induced by faradic stimulation in animal hearts, in contrast with irregular, vermiform contraction in atrial fibrillation (AF). In patients subjected to cardiac surgery or catheter ablation for the treatment of atrial fibrillation or showing atypical ECG patterns, macro-re-entrant and focal tachycardia mechanisms can be very complex and electrophysiological studies are necessary to guide ablation treatment in poorly tolerated cases. Secondary prevention, based on the treatment of associated atrial fibrillation risk factors, is emerging as a therapeutic option. In patients without a history of heart disease, cardiac surgery or catheter ablation, typical flutter ECG remains predictive of a right atrial re-entry circuit dependent on the inferior vena cava–tricuspid isthmus that can be very effectively treated by ablation, although late incidence of atrial fibrillation remains a problem. Electrophysiological studies have defined multiple mechanisms of tachycardia, both re-entrant and focal, with varying ECG morphologies and rates, authenticated by the results of catheter ablation of the focal triggers or critical isthmuses of re-entry circuits.
Clinical electrophysiology has made the traditional classification of rapid atrial rhythms into flutter and tachycardia of little clinical use.
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