There has been a fascination with the preexcitation syndromes that has spanned decades and led to a rich history of discovery (Figure 7-1). Over a century ago investigators began looking into the mechanism of how an atrial impulse activated the ventricle.1 Stanley Kent reported on an atrioventricular (AV) connection in mammalian hearts. This nodelike structure most likely does not represent the AV muscle connection more typically described by anatomists in patients with preexcitation, and Sir Thomas Lewis dismissed this alternative theory of AV conduction. However, Mines was more visionary and postulated the use of this AV connection in a reentrant circuit using the main AV bundle for anterograde activation and the accessory pathway (AP) for retrograde conduction. Electrocardiographic (ECG) evidence of preexcitation was reported by Cohn and Fraser, as well as Wilson, who also demonstrated intermittent preexcitation in one of the figures. The mechanism for the delta wave of preexcitation had several postulates including mechanical, chemical, and electrical. Holzmann and Scherf, and Wolferth and Wood suggested that the abnormal ventricular depolarization was due to conduction over the anomalous AV connection.
History of the preexcitation syndromes. (See text for details.)
Wolff, Parkinson, and White in 1930 reported on a “combination of bundle-branch block, abnormally short P-R interval, and paroxysms of tachycardia … in young, healthy patients with normal hearts” as a distinctive entity. Years later they published a follow-up of the original series of patients and made some key observations: congestive heart failure could rarely occur from uncontrolled tachycardia (now referred to as tachycardia-induced cardiomyopathy); the delta wave disappeared in many patients; and digitalis ineffectively controlled the ventricular rate in a patient with atrial fibrillation (now it is know that digitalis can also increase the risk of sudden death in some patients with preexcitation).
Anatomic confirmation of typical APs was reported separately by both Wood and Ohnell, and Mahaim described accessory nodoventricular and fasciculoventricular connections (NOT atriofascicular connections that are often incorrectly called Mahaim fibers). Lev and Brechenmacher made additional anatomic findings of preexcitation, including ones that connect the atria with the His bundle (atrio-Hisian tract). The clear demonstration of an AP as the cause of preexcitation was shown by several investigators: Durrer, Burchell, and Wallace, and Wellens in Amsterdam and Gallagher at Duke contributed many observations to our understanding of the preexcitation syndrome. The decades of research led to possibly the most important event in nonpharmacologic therapy for cardiac arrhythmias—the first successful surgical dissection of an AP with the cure of the patient by Dr. Will C. Sealy at Duke University.
Under usual circumstances, an impulse originating in the atrium conducts over the normal AV node–His-Purkinje system to activate the ventricles. When an accessory pathway is present, the opportunity exists to bypass some or ...