Origins Of Clinical Cardiac Electrophysiology

Clinical cardiac electrophysiology was "born" in the late 1960s. The technique of programmed electrical stimulation of the heart was developed independently by Durrer and colleagues (10) in Amsterdam and Coumel and colleagues (11) in Paris. Scherlag's technique for transcutaneous recording of the His potential was an invaluable contribution (12), and led to the first systematic evaluation of normal and abnormal function of the A-V node, by Damato and colleagues in Staten Island, NY (13). Another key development was the combination of programmed electrical stimulation with multiple intracardiac recordings by Wellens to discern arrhythmia mechanisms (14). (see Fig. 1). Shortly thereafter, three American electrophysiology centers, established by investigators trained in Staten Island, began making important contributions. These centers included Gallagher at Duke, Rosen at the University of Illinois, and Josephson at the University of Pennsylvania. These three centers and the facility established by Wellens in Maastricht have contributed tremendously to the development of electrophysiology, both in terms of scientific discovery, and in training other investigators in cardiac electrophysiology. Wellens and Josephson continue to train electrophysiologists and make major contributions to the field as the twenty-first century begins.

The early years of electrophysiology were largely descriptive. Programmed stimulation was used to define the electrophysiologic parameters of the atria, A-V node, bundle

| 580 | 580 | 280 | 340 | 310 | 300 | 265 | 265 | 265 |

Fig. 1. Figure from the seminal publication of Wellens et al., which first demonstrated the use of programmed stimulation to initiate VT. From top to bottom are surface leads I and III, intracardiac recordings from the right atrium (RA) and His position (HIS), and surface leads Vi and V6. Annotated at the bottom are timing intervals in ms. Shown are the last two beats of a right ventricular drive train at 580 ms, and then a single stimulus (coupling interval 280 ms). Monomorphic VT is induced. (With permission from Wellens HJ, Schuilenburg RM, Durrer D. Electrical stimulation of the heart in patients with ventricular tachycardia. Circulation 1972;46:216-226.)

| 580 | 580 | 280 | 340 | 310 | 300 | 265 | 265 | 265 |

Fig. 1. Figure from the seminal publication of Wellens et al., which first demonstrated the use of programmed stimulation to initiate VT. From top to bottom are surface leads I and III, intracardiac recordings from the right atrium (RA) and His position (HIS), and surface leads Vi and V6. Annotated at the bottom are timing intervals in ms. Shown are the last two beats of a right ventricular drive train at 580 ms, and then a single stimulus (coupling interval 280 ms). Monomorphic VT is induced. (With permission from Wellens HJ, Schuilenburg RM, Durrer D. Electrical stimulation of the heart in patients with ventricular tachycardia. Circulation 1972;46:216-226.)

of His, Purkinje system, and the ventricles, and then to assess the effects of various pharmacologic agents on these parameters. The reentrant nature of the vast majority of clinical arrhythmias was established using programmed stimulation. Serial drug testing was the first real therapeutic advance in electrophysiology; the ability of a drug to acutely render an arrhythmia noninducible in the laboratory implied a lower risk of recurrence when the drug was administered chronically. Despite this advance, the limitations of this methodology, in which a clinical recurrence of VT could be fatal, were also recognized.

With increasing experience came the confidence to place multiple electrode catheters in multiple cardiac chambers. Endocardial catheter mapping techniques, in which catheters were sequentially moved to many sites in multiple chambers, allowed identification of the sites of origin of VT, definition of the mechanisms of supraventricular tachycardia (SVT), and delineation of the location of accessory pathways (15,16) (see Fig. 2). These technologies paved the way for surgical treatment of Wolff-Parkinson-White Syndrome (WPW), VT, and other arrhythmias (17).

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