Anatomic and Electrophysiological Differences Between Chronic and Paroxysmal Forms of Common Atrial Flutter and Comparison with Controls:

Whether chronic typical atrial flutter differs from paroxysmal atrial flutter regarding electrophysiological properties of reentry pathways and cardiac function remains unknown. If so, can remodeling due to long duration of persistently rapid atrial or ventricular rates explain these changes? The aim of the study was to compare RA local conduction velocities and heart function parameters between three groups: (1) chronic atrial flutter, (2) paroxysmal atrial flutter, and (3) controls. The study evaluated 52 patients undergoing radiofrequency ablation for typical atrial flutter. There were 35 patients with chronic atrial flutter (62.7 +/- 14 years) and 17 patients with paroxysmal atrial flutter (62.7 +/- 10 years). Underlying structural heart disease was present in 20 (57%) of 35 chronic atrial flutter patients and in 7 (41%) of 17 paroxysmal atrial flutter patients (P = 0.1). Chronic atrial flutter duration was 10.9 +/- 17 months and paroxysmal atrial flutter duration was 8.5 +/- 10 (P = 0.06). RA conduction velocity measurements were carried out before ablation during sinus rhythm under pacing (600-ms cycle length) with a 12-pole steerable catheter positioned in the high lateral RA (poles 11-12 H6), mid-lateral RA (poles 9-10 H5), and along the inferior vena caval tricuspid isthmus (poles 7-8 H4; 5-6 H3; 3-4 H2) with its distal electrode pair at the coronary sinus origin (pole 1-2 H1). Counter-clockwise RA conduction velocities were assessed from H6 to H1 and clockwise RA conduction velocities from H1 to H6. After successful ablation, RA and LA areas, LV volumes, LVEF, inferior vena caval tricuspid annulus, and coronary sinus tricuspid annulus (septal isthmus) lengths were measured by two-dimensional echocardiography. The control group included 12 patients without structural heart disease, referred for electrophysiological evaluation of AVN reentry. Counter-clockwise RA conduction velocities at the inferior vena caval tricuspid isthmus were lower in chronic atrial flutter than in paroxysmal atrial flutter (H4, 1.19 +/- 0.4 vs 1.89 +/- 1 m/s, P = 0.0051; H3, 1.14 +/- 0.4 vs 1.6 +/- 0.7 m/s, P = 0.0015; H2, 1.16 +/- 0.4 vs 1.53 +/- 0.5 m/s, P < 0.0056 and H1, 1.2 +/- 0.4 vs 1.5 +/- 0.4 m/s, P = 0.03, respectively). Counter-clockwise RA conduction velocities were identical at the high and mid-lateral RA. Counter-clockwise caval isthmus RA conduction velocities from H3 to H1 were significantly different between chronic atrial flutter and controls (H3, 1.14 +/- 0.4 vs 1.7 +/- 0.3 m/s, P = 0.0014; H2, 1.16 +/- 0.4 vs 1.83 +/- 0.4 m/s, P < 0.0001 and H1, 1.2 +/- 0.4 vs 1.94 +/- 0.4 m/s, P < 0.0001, respectively). A difference was found regarding clockwise isthmus RA conduction velocities between the two groups of atrial flutter and controls but not between chronic atrial flutter and paroxysmal atrial flutter. Respectively, chronic atrial flutter had greater RA and LA areas (24.5 +/- 5 vs 13 +/- 2 cm2; P < 0.0001 and 23 +/- 5 vs 16 +/- 3 cm2, P < 0.0001), LV end-systolic and end-diastolic volumes (50 +/- 25 vs 32 +/- 13 cm3, P = 0.0084 and 112 +/- 40 vs 85 +/- 25 cm3, P = 0.01), septal isthmus length (21 +/- 3 vs 13 +/- 2 mm, P < 0.0001), and inferior vena caval tricuspid isthmus length (39 +/- 6 vs 23 +/- 5 mm; P < 0.0001). Chronic common atrial flutter is characterized by more prolonged counter-clockwise conduction times and larger anatomic conduction pathways than the paroxysmal form, the causal relationship between electrophysiological and anatomic characteristics remains to be demonstrated.