Atrial flutter is a frequent complication in patients with adult congenital heart disease either during natural history or after surgical repair.1 ,2 The incidence of such an arrhythmia increases postoperatively with time and is usually associated with complex atrial surgery.3 ,4 When it occurs, atrial flutter compromises haemodynamics, reduces exercise tolerance, and is often resistant to medical treatment. The P wave has been found to change its electrical characteristics before atrial fibrillation supervenes in patients with coronary artery disease.5 We sought to study the same hypothesis in 39 adult congenital heart disease patients, 31% of them with Mustard or Fontan surgery, who developed atrial flutter long after surgical repair, and compare them with 30 diagnosis matched controls who had never developed atrial arrhythmias. All the patients studied had undergone at least three consecutive annual ECG recordings before the onset of flutter, which were compared with those recorded similarly over three years in controls. P wave amplitude and duration were measured using an electronic “digimetric” caliper (Mitutoga) and a magnifier to confirm reproducibility.

In the control group there was no change in P wave duration or voltage over the three year study period. Although there was no difference in P wave duration in the first ECG recording between patients and controls, in those who subsequently developed flutter, it was significantly longer in the second (115 (24) ms v 104 (16) ms, p < 0.01) and the third (126 (24) msv 106 (15) ms, p < 0.001) recordings before the onset of flutter. In the patient group, P wave duration increased by 11 ms annually for the two years before development of flutter. Thirty five of 39 (90%) patients had a P wave duration over 120 ms on the third ECG compared to 10/30 (33%) controls; this difference in incidence was significant (p < 0.001). P wave voltage was significantly higher in patients on the first ECG compared to the controls (1.9 (0.9) mV v 1.5 (0.5) mV, p < 0.05), but was not different in the second or the third recordings.

Patients with complex congenital heart disease often require multiple atrial reparative surgery. Even those who do not need such corrective surgery early in life are known to develop significant degree of tricuspid regurgitation over the years. A number of possible mechanisms can thus contribute to the occurrence of flutter in these patients. Atrial disease resulting from multiple sutures, chronic tricuspid valve regurgitation, or atrial remodelling may all constitute the substrate for flutter.6-8 Progressive ventricular disease, and increasing end diastolic pressure, may result in increased atrial volume and pressure, and hence atrial myocardial stretch is similar to the ventricle when it becomes arrhythmogenic. These mechanisms have been proposed in patients with complex surgical repair particularly after Mustard and Fontan operations. Regardless of the underlying anomaly, and possible mechanism, it seems that progressive broadening of P wave duration and a fall in its voltage commonly precede the occurrence of flutter in such patients, in a fashion similar to that of the QRS duration in patients with dilated cardiomyopathy. Since atrial flutter in adult congenital heart disease is clinically deleterious and may eventually resist medical or electrical cardioversion, identifying P wave disturbances during follow up in these patients may alter their conventional management policy and raise the possibility that this significant complication may be delayed or prevented.