The Mechanical Consequences

SINCE its description as a clinical entity in 1930,1 the Wolff-Parkinson-White (WPW) syndrome has been the object of much study and speculation. The essential feature of the disorder is early anomalous activation of at least a portion of the ventricular myocardium as indicated by the "delta" deformity of the QRS complex. Shortening of the P-R segment to 0.12 second or less is accompanied by varying degrees of prolongation or aberration of the QRS complex. Exidence has been adduced in support of the hypothesis that preactivation occurs via a functioning accessory atrioventricular conduction pathway.2-6 The mechanical consequences of this unique abnormality have received less attention. A number of technics have been employed in previous studies. Prinzmetal and co-workers7 used a high-speed movie camera during electrical stimulation of dog ventricles, and observed a localized area of contraction preceding the normal contraction wave in the same ventricle. Pick and Katz8 have questioned, however, whether true WPW complexes were produced. Bandiera and Antognetti,9 employing an improved method or roentgenkymography, reported precontracting areas high in the ventricle, on the left side when the electrocardiogram exhibited predominantly positive QRS complexes in right precordial leads (type A),10 and on the right side when predominant S waves were recorded in the same leads (type B) .10 Curiously, the same aberrant border motion persisted when the WPW morphology was replaced by normal complexes.