Iwao Sotohata

Body surface isopotential mapping in Wolff-Parkinson-White syndrome: Noninvasive method to determine the localization of the accessory atrioventricular pathway

The body surface isopotential maps of 22 patients with WPM syndrome were obtained from the 85 unipolar lead ECGs using the on-line minicomputer system newly devised by the authors group. The map patterns were classified into three types-I, II, and III (Type I, eight; Type II, seven; Type III, three; and unclassified, four cases). In Type I, the back surface displayed the negative potential throughout the entire ventricular activation, and at the terminal stage the lower precordial area displayed the positive potential and the upper precordial area, the negative one. Type II was characterized by two longitudinal lines, one staying at its place on the back and the other moving right to left on the precordial area following the process of ventricular activation. In Type III, the right precordial area displayed negative potential in the early stage, and in the terminal stage the upper part of the right side of chest surface displayed positive potential and the lower part, negative potential. It was surmised from these patterns that the pre-excited area was located at the posterior region of the ventricles in Type I, at the right ventricle in Type II, and the right ventricular base near the posterior margin of the ventricular septum in Type III. Type A patients in the conventional ECG classification fell under Type I; Type C patients, under Type III; Type B patients under either Type I or Type II.

Comparative evaluation of depressed automaticity in sick sinus syndrome by Holter monitoring and overdrive suppression test

To ascertain whether the long cardiac pauses on the Holter ECGs of patients with the sick sinus syndrome were related to the spontaneously occurring overdrive suppression, the heart rates for the 12 seconds preceding the cardiac pauses longer than 5 seconds were compared with that averaged for 24 hours. Even in six out of seven patients with bradycardia-tachycardia syndrome the former rate was not significantly greater than the latter, indicating that episodes of such long cardiac pauses may not result from spontaneously occurring overdrive suppression. This observation was also consistent with the result that no statistically significant correlation was obtained between the maximum pauses measured from Holter ECGs of sick sinus syndrome and those obtained by the overdrive suppression test. In conclusion, many episodes of long life-threatening cardiac pauses observed in sick sinus syndrome may be attributed to accidental depression of the sinus nodal and subsidiary pacemaker activity rather than to spontaneously occurring overdrive suppression; therefore, Holter monitoring may be useful as an additional tool for diagnosis of sick sinus syndrome.