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(Circulation. 1997;95:1658-1660.)
© 1997 American Heart Association, Inc.

Articles

Human Left Ventricular Endocardial Activation Mapping Using a Novel Noncontact Catheter

Nicholas S. Peters, MD, MRCP; Warren M. Jackman, MD; Richard J. Schilling, MB, MRCP; Graydon Beatty, MS; D. Wyn Davies, MD, FRCP

Correspondence to Dr Nicholas S. Peters, Department of Cardiology, St Mary's Hospital, Praed St, London W2 1NY, UK. E-mail n.peters{at}ic.ac.uk.

	Introduction

Top Introduction

 
The patient was a 39-year-old male who had recurrent sustained monomorphic ventricular tachycardia, satisfying the electrocardiographic criteria for fascicular tachycardia, in a structurally normal heart.

These isopotential maps were acquired from the patient's left ventricle during an otherwise routine electrophysiology study by deploying a catheter-mounted multielectrode array consisting of a wire braid on the surface of an 8-mL balloon (Endocardial Solutions Inc). Without endocardial contact, this system uses inverse solution mathematics (boundary-element method) to reconstruct 3360 "virtual" electrograms onto a shell model of the endocardium. A manually selected line of virtual electrograms shows a normal sequence of high-frequency potentials consistent with fascicular activation during sinus rhythm, which correlates with the activation process shown by isopotential mapping (Fig 1). During a brief, nonsustained episode of the patient's clinical tachycardia (Fig 2) the sequence of these presumed fascicular potentials is clearly altered in a manner consistent with the diagnosis of fascicular tachycardia and corresponding to an altered activation sequence on isopotential mapping. Despite its short duration, the tachycardia could be characterized in a single beat.

View larger version (35K): [in this window] [in a new window]   Figure 1. Sinus rhythm: A sequence of isopotential maps of the left ventricular endocardium (purple) modeled to the patient's chamber dimensions and opened along its anteroseptal margin. The location of the multielectrode array is represented by the yellow ellipsoid. Surface ECG lead I and selected virtual electrograms from a line following fascicular activation (I-P on the map) are shown beneath each map. The timing of each map is indicated by the white cursor, which progresses through the presystolic fascicular potentials (A and B). Fascicular activation propagates toward the apex, where it initiates ventricular activation (C).

View larger version (37K): [in this window] [in a new window]   Figure 2. Fascicular tachycardia: During tachycardia, the fascicular activation sequence is altered, starting near the left ventricular apex (A) and propagating toward the His bundle (B). This rapid retrograde fascicular activation is closely followed by ventricular activation (C). The relative delay in right ventricular activation produces a QRS complex with right bundle-branch block pattern in ECG lead I.

This case illustrates the use of a novel catheter-based technology in acquiring extensive simultaneous data to create unique maps of endocardial activation during electrophysiological study of a conscious patient.

	Acknowledgments

 
This work was supported by the British Heart Foundation.

	Footnotes

 
From the Department of Cardiology (N.S.P., R.J.S., D.W.D.), St Mary's Hospital and Imperial College School of Medicine, London, UK; Department of Medicine (W.M.J.), University of Oklahoma Health Sciences Center, Oklahoma City, Okla; and Endocardial Solutions, Inc (G.B.), Saint Paul, Minn.

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.

Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner, MC 4-265, Houston, TX 77030.

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