[Attenuated nodal response. Apropos of 30 cases]

In a population of 600 consecutive patients undergoing endocavitary electrophysiological study to assess nodal conduction, 40 had an atriohisian Wenckenbach point of over 200/mn. In 30 cases, vagal stimulation with ATP (10 to 40 mg IV) provoked an increase in atrioventricular conduction, with lengthening the AH interval by over 100 p. 100 or transient atrioventricular block. This increase allowed elimination of an accessory atriohisian pathway which could give similar high Wenckenbach points, but which do not show decremental conduction. In all our cases, the conduction passed through the artrioventricular node (AVN) whose response to rapid atrial stimulation was attenuated compared to normal. The parameter of this attenuated nodal response varied from case to case, but in general, the intervals were shorter than normal. The AH interval was less than 50 ms in 22 cases (N = 70 +/- 20 ms). The effective nodal refractory period was shorter than the functional atrial refractory period in 20 cases. The shortest atrial cycles transmitted 1/1 to the ventricles ranged from 230 to 300 ms (274 +/- 33 ms) (N = 375 +/- 40 ms). The functional structure of the AVN was studied by the lengthening of the AH interval with heart rate : 5 types were distinguished : 10 patients had progressive lengthening of AH interval greater than 100 ms (Type I) as in a normal AVN; 5 had progressive lengthening of AH interval of less than 50 ms (Type II), 5 had progressive lengthening of AH which then remained stable for a number of heart rates before lengthening again (Type III); 3 had an initial moderate lengthening of the AH interval which then became more rapid (Type IV) and 7 had no change in AH until 120/mn and then a progressive lengthening was observed (Type V). Two functional groups could also be identified depending on whether the lengthening was progressive, suggesting a single nodal pathway (Types I and II) or on whether differing increases were observed related to the atrial rate, suggesting two (Types IV and V) or even three (Type III) atrionodal or intranodal pathways with different refractory periods. Of these 30 patients, only 14 had documented supraventricular tachycardia, 13 being atrial fibrillation and the other a junctional tachycardia. Attenuated nodal behavior does not seem to be a direct cause of supraventricular arrhythmias but these arrhythmias were not tolerated as well because of the special properties of the atrioventricular node.