The term cardiac preexcitation was originally used to describe premature activation of the ventricle in patients with the Wolff-Parkinson-White syndrome. This term has been broadened to include all conditions in which antegrade ventricular activation or retrograde atrial activation occurs partially or totally via an anomalous pathway distinct from the normal cardiac conduction system.
The classic form of cardiac preexcitation remains the Wolff-Parkinson-White (WPW) syndrome, which is characterized by a short PR interval (less than 0.12 sec) and a broad QRS complex with a delta wave. The anatomic substrate for WPW syndrome is a band of myocytes, also known as the bundle of Kent, which bridges the fibrous atrioventricular junction. The electrocardiographic features are a result of premature ventricular activation due to conduction over the accessory pathway. (See "Anatomy, pathophysiology and localization of accessory pathways in the preexcitation syndrome" and "Epidemiology, clinical manifestations, and diagnosis of the Wolff-Parkinson-White syndrome", section on 'Electrocardiographic (ECG) findings'.)
Several other pathways have been postulated to result in cardiac preexcitation. However, most lack the histopathologic correlation that has been demonstrated for the WPW syndrome. The Lown-Ganong-Levine (LGL) syndrome and enhanced atrioventricular nodal conduction (EAVNC) share some common features and have often been considered to have a similar etiology. The mechanisms proposed to account for these conditions include more rapid conduction within or bypass of the normal AV nodal tissue (figure 1). The LGL syndrome and EAVNC will be discussed in detail here. Mahaim fiber tachycardia, another non-WPW form of preexcitation, is discussed separately. (See "Mahaim fiber tachycardias".)
The Lown-Ganong-Levine (LGL) syndrome is characterized by the presence of a short PR interval and normal QRS complex on the surface electrocardiogram (ECG). This finding may represent a perinodal accessory pathway or enhanced AV nodal conduction (waveform 1).
Patients with palpitations who had a short PR interval but normal QRS complex on the resting electrocardiogram were first described in 1938 and then further evaluated by Lown, Ganong, and Levine in 1952 [1,2]. The latter report consisted of a retrospective examination of 13,500 consecutive ECGs at a single tertiary care center. 200 subjects were identified with a short PR interval, most of whom had a normal QRS complex . The incidence of paroxysmal supraventricular tachycardia was significantly higher in these patients when compared to a control group with a normal PR interval (11 versus 0.5 percent).