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The effects of abnormal ventricular activation upon the contractile pattern of the ventricles in patients with the Wolff-Parkinson-White syndrome (WPW) remain uncertain. Therefore we compared the motion of the anterior right ventricular wall (RV), the interventricular septum (IVS), and left ventricular posterior wall (LVPW) on echogram in nine patients with WPW and one patient with a coronary sinus pacemaker (CSP) to 20 normal subjects. Normal subjects manifested posterior RV motion which began and reached maximal excursion at 175 and 366 msec (group mean), respectively, after the onset of the QRS complex; posterior movement of the IVS which started and peaked at 90 and 30 msec, respectively; and anterior contraction of the LVPW which began and peaked at 159 and 406 msec, respectively. Five of seven patients with Type A WPW demonstrated a localized area of premature contraction of the LVPW occuring during the initial 100 msec interval following the onset of the QRS complex which was accompanied by paradoxic anterior motion of the IVS. Thereby in Type A patients initial and maximal posterior motion of the IVS occurred later, 230 (P less than 0.001) and 400 (P less than 0.05) msec, and anterior motion of the LVPW occurred earlier, 75 (P less than 0.001) and 367 (P less than 0.05) msec as compared to normal. The amplitude and duration of early contraction could be related to the prominence of the delta wave during atrial pacing. Similar premature contraction was also observed in the patient with CSP during paced beats. One Type B WPW patient exhibited abnormal IVS motion while the additional patient manifested premature LVPW contraction similat to that seen in Type A patients. The contractile pattern of the right ventricular anterior wall was recorded in five of seven Type A Wolff-Parkinson-White patients and manifested prolongation of the interval from the onset of the QRS complex to the initial posterior movement (group mean 234 msec, P less than 0.05) as compared to normal. Thus echocardiography can be used to confirm the diagnosis and to improve understanding of the pathophysiology of the Wolff-Parkinson-White syndrome.

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