Double lines of block were frequently observed in patients with AFL, and both lines may form the posterior boundaries of the AFL circuit. Block was fixed in the lower part of the CT and was functional in the upper part of the CT.

The cavotricuspid isthmus (CTI) is a slow conduction area in the circuit of typical atrial flutter. However, conventional methods are limited by the inaccuracy of measurements of distance on the surface of the heart. The aim of the study was to define the conduction properties of the atrial flutter circuit along the tricuspid annulus by using a three-dimensional noncontact mapping system. In 34 atrial flutter patients (30 men, 4 women; mean age 54 +/- 14; 27 counter-clockwise, 4 clockwise, and 3 both), a noncontact multielectrode array was used to reconstruct electrograms in the right atrium. Isochronal and isopotential propagation mapping was performed during atrial flutter. The conduction velocity was calculated by dividing conduction time by surface distance. The right atrium along the tricuspid annulus was divided into five regions: lateral wall, superior right atrium, septum, septal CTI, and lateral CTI. Conduction velocities were 0.99 +/- 0.85, 1.67 +/- 1.21, 1.58 +/- 1.05, 0.82 +/- 0.72, and 1.68 +/- 1.00 m/s in counter-clockwise and 0.81 +/- 0.71, 2.61 +/- 1.90, 1.52 +/- 0.91, 0.91 +/- 0.80 and 1.91 +/- 0.83 m/s in clockwise, respectively. Conduction velocities were significantly slower in the septal CTI and lateral wall than in the lateral CTI, the septum, and the superior right atrium (P < 0.05). No significant difference was found between the septal CTI and the lateral wall. Conduction within the septal CTI was slower in patients treated with antiarrhythmic agents than in untreated patients (P < 0.05). The septal part of the CTI (but not the lateral CTI) and the lateral wall are slow conduction zones in the atrial flutter circuit, and both may, therefore, be mechanically important for the development of atrial flutter.

The sinus venosa and not the crista terminalis results in a rate-dependent line of block during transverse right atrial activation. The morphologic characteristics of the sinus venosa appear to facilitate block in this region.

1 Adenosine-5'-triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P 2 receptor activation or by A 2A -adenosine receptor activation. 2 E ects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea-pig isolated hearts perfused at a constant¯ow of 10 ml min 71 . 3 ATP and adenosine both caused sustained, concentration-dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD 2 (+s.e.mean) for ATP and adenosine were 6.68+0.04 and 7.06+0.05, respectively. Adenosine was signi®cantly more potent than ATP (P50.0001, n=10).4 The values of pIC 50 for the selective A 2A -adenosine receptor antagonist SCH58261 to antagonize equivalent responses to ATP and adenosine were 8.28+0.08 and 8.28+0.06 (P=0.99, n=6), respectively. 5 The non-selective adenosine receptor antagonists xanthine amine congener (XAC) and CGS15943 antagonized similarly the equivalent vasodilations caused by ATP (pIC 50 values 7.48+0.04 and 7.45+0.06, respectively) and adenosine (pIC 50 values 7.37+0.13 and 7.56+0.11). 6 In contrast to ATP and adenosine, the two P 2 agonists 2-methylthio-ATP and uridine-5'-triphosphate failed to cause stable increases of coronary conductance, caused desensitization of vasodilator responses, and were not antagonized by SCH 58261, 8-parasulphophenyltheophylline, or XAC. 7 Glibenclamide attenuated coronary vasodilations caused by ATP and adenosine by 88 and 89%, respectively, but failed to attenuate those caused by 2-methylthio-ATP.