Electrophysiologic investigations with programmed stimulation of the human heart have clearly established the participation of the atrioventricular (A-V) junction in three different types of junctional reciprocating tachycardia: (1) paroxysmal supraventricular tachycardia in the Wolff-Parkinson-White syndrome: (2) the vast proportion of "paroxysmal atrial tachycardia" without evidence of preexcitation during sinus rhythm with antegrade conduction; and (3) the permanent or almost permanent (chronic relapsing) form of supraventricular tachycardia with its characteristic rate-dependent initiating mechanism. The obvious presence of the Wolff-Parkinson-White syndrome during sinus rhythm does not necessarily imply that the accessory pathway will be utilized during supraventricular tachycardia. Conversely, in the absence of preexcitation, the mechanism of A-V junctional reciprocating tachycardia has been traditionally attributed to pure intranodal dissociation, often without definite direct proof. Concealed accessory pathways (with unidirectional block) may be more frequent than realized and should be carefully searched for. Proof that supraventricular tachycardia utilizes an accessory pathway for retrograde conduction to the atrium often requires meticulous electrophysiologic studies- Conslucions based on the absence of various findings may be misleading. Emphasis must be placed on positive viagnostic features. One or more of the following observations may prove or disprove participation of a Kent bundle during supraventricular tachycardia: (1) induction of A-V block during tachycardia: (2) influence of electrically induced ventricular premature beats upon tachycardia; (3) patterns of retrograde atrial activation during tachycardia; or (4) influence of functional bundle branch block on the rate of the tachycardia. Analysis of events at the onset of rather than during the tachycardia is probably less important but may also provide suggestive clues about the mechanism of reentry. Observation of the following variables may be helpful: (1) behavior of antegrade conduction at the onset of tachycardia; (2) relation of atrial and ventricular activation at the onset of tachycardia; (3) presence of retrograde ventriculoatrial (V-A) conduction; (4) prolongation of the H-V interval at the onset of tachycardia; and (5) atrial stimulation at various sites. Precise understanding of the pathophysiology of supraventricular tachycardia is important because specific therapy (pharmacologic, pacemaker or surgical) may ultimately depend on accurate knowledge of the underlying mechanisms.