Barry H. Branham

Computerized activation sequence mapping of the human atrial septum

To delineate the propagation of electrical activation in the atrial septum, atrial epicardial and atrial septal maps were recorded intraoperatively using a 156-channel computerized mapping system in 12 patients during sinus rhythm (n = 10), supraventricular tachycardia associated with septal pathways in Wolff-Parkinson-White syndrome (n = 3), atrioventricular (AV) node reentrant tachycardia (n = 4), and atrial flutter (n = 5). The epicardial and septal data were recorded simultaneously from 156 atrial electrodes, digitized, analyzed, and displayed as isochronous maps on a two-dimensional diagram of the atria. During sinus rhythm, the activation wave fronts propagated most rapidly along the large muscle bundles of the atrial septum. During supraventricular tachycardia associated with Wolff-Parkinson-White syndrome, the earliest site of retrograde atrial activation usually corresponded to the position of atrial insertion of the septal pathways. However, the earliest site of activation during orthodromic supraventricular tachycardia was different from that during ventricular pacing in 1 patient with a posterior septal accessory pathway localized by the epicardial mapping study. The data document the rationale for dividing the ventricular end of the accessory pathways (ie, the endocardial technique) rather than the atrial end (ie, the epicardial technique) in patients with Wolff-Parkinson-White syndrome. During AV node reentrant tachycardia, atrial activation data suggested that atrial tissue lying outside the confines of the anatomical AV node is a necessary link in this common arrhythmia. Thus, these atrial septal maps explain why surgical dissection, or properly positioned small cryolesions placed in the region of the AV node, can ablate AV node reentrant tachycardia without altering normal AV node function. The maps recorded during atrial flutter suggest the importance of the atrial septum as one limb of a macroreentrant circuit responsible for the arrhythmia, and imply that atrial flutter is amenable to control by surgical techniques. These studies demonstrate the details of normal atrial septal activation, the importance of the atrial septum in a variety of different atrial arrhythmias, and the basis of and potential for surgical ablation of the most common types of supraventricular arrhythmias.

Noninvasive detection of cardiac allograft rejection by analysis of the unipolar peak-to-peak amplitude of intramyocardial electrograms.

The use of standard electrocardiographic monitoring to detect cardiac allograft rejection has become unreliable since the advent of cyclosporine immunosuppression. Unipolar peak-to-peak amplitude analysis has been shown to be a quantitative measure of ischemic myocardial injury. This study was performed to determine if unipolar peak-to-peak amplitude analysis could accurately detect cardiac allograft rejection as determined by blinded endomyocardial biopsies. Ten adult mongrel dogs underwent heterotopic (n = 7) or orthotopic (n = 3) cardiac transplantation with placement of sutureless screw-in electrodes (Medtronic, Inc, Minneapolis, MN) on the anterior and posterior aspect of each ventricle. Postoperatively, animals were immunosuppressed for seven to ten days with cyclosporine and prednisone and then allowed to reject the transplant. Digitally processed intramyocardial electrograms were obtained daily. Endomyocardial biopsy was performed 1 week postoperatively and then at three to five day intervals for histological correlation. A unipolar peak-to-peak amplitude decline of 15% or greater occurred one to three days before the biopsy detection in 10 of 10 episodes of rejection. There were no false negatives and one false positive (although a small focal lymphocytic infiltrate was present). Thus, noninvasive unipolar peak-to-peak amplitude analysis was 100% sensitive and 90% specific in predicting and detecting cardiac allograft rejection.

Human ventricular tachycardia: Precise intraoperative localization with potential distribution mapping

Electrophysiologically guided operations for ventricular tachycardia (VT) have been directed exclusively by activation time maps. Even with computer-assisted mapping, extensive editing is required, which prolongs the duration of the operation and which may introduce significant error. In contrast, potential distribution maps can be constructed in less than 3 minutes and can be viewed as a movie of developing and receding potentials. In 4 patients undergoing operation for VT, endocardial mapping was performed using form-fitting electrodes containing 160 points. A computerized mapping system, capable of simultaneously recording 256 channels of data, was used to analyze data and to display potential distribution maps sequentially at 1-millisecond intervals as a color movie. A total of eight morphologies of sustained VT were mapped. The mean VT cycle length was 340 +/- 40 milliseconds (range, 274 to 394 milliseconds). In 3 patients with ischemic heart disease, four VT morphologies originated from the subendocardium. All were successfully ablated with cryoablation alone or in conjunction with aneurysmectomy and endocardial resection. A fourth patient with VT secondary to cardiomyopathy had multiple morphologies and received an implantable cardioverter defibrillator. Potential distribution maps correlated well with the concomitant activation time maps. Thus, potential distribution mapping provides a rapid and accurate means of identifying the site of origin of VT facilitating intraoperative mapping in patients undergoing surgical ablation.

Computerized potential distribution mapping: A new intraoperative mapping technique for ventricular tachycardia surgery☆

This study evaluated potential distribution mapping as a method for localizing the site of origin of ventricular tachycardia (VT). In contrast to conventional activation time maps, potential distribution maps require less editing and thus can be more automated and rapidly processed for interpretation of multiple beats of VT. As a series of potential distribution maps during VT is required for detailed analysis, an on-line computerized system was designed to display potential distribution maps sequentially at 1-ms intervals as a color movie. Potential distribution maps and activation time maps were constructed from 182 epicardial and endocardial unipolar electrodes during 12 episodes of reproducible monomorphic VT in 9 dogs four to six days after experimental myocardial infarction (mean cycle length, 162 +/- 21 ms). At the onset of each depolarization during VT, a potential minimum abruptly developed on the surviving epicardium and another on the surviving endocardium of the left ventricle, both immediately adjacent to the subendocardial infarct. These two minima on the initial potential distribution maps corresponded to the sites of earliest epicardial and endocardial activation breakthrough recorded on the activation time maps. These two minima subsequently expanded or moved into the adjacent area and coincided with the spread of activation fronts on the epicardial and endocardial surfaces. Thus, the rapid display of sequential, computerized potential distribution maps of multiple beats of VT provides a dynamic means of identifying the site of origin of VT, and therefore should facilitate intraoperative mapping.

Anterior septal coronary artery infarction in the canine: a model of ventricular tachycardia with a subendocardial origin. Ablation and activation sequence mapping.

BackgroundIn humans, chronic ventricular tachycardia (VT) is usually associated with myocardial infarcts that involve the interventricular septum. In an effort to more closely mimic the anatomic substrate that gives rise to chronic VT in humans, we developed a canine model of VT in which the anterior septal coronary artery was ligated. The site of earliest activation, the subsequent activation sequence, and the mechanism of VT associated with the resultant ventricular septal infarct was then evaluated to determine if this model accurately reflected the characteristics of human VT. Methods and ResultsSeventeen dogs underwent occlusion-reperfusion ventricular septal infarcts. Four to 7 days later, electrophysiological studies were performed. VT was initiated by programmed electrical stimulation and terminated by pacing at a cycle length of 50% to 75% of the VT cycle length. Electrophysiological studies were performed using a 256-channel mapping system. A total of 15 VT morphologies were mapped in 9 animals. Fourteen of 15 morphologies had septal subendocardial sites of earliest activation and 1 had a septal midwall site of earliest activation. VT ablation was performed using a nitrous oxide cryoprobe and confirmed the site of earliest activation by subsequently rendering VT noninducible. Electrophysiological studies demonstrated four distinct VT activation sequences: (1) circular reentrant (n = 7), (2) concentric spread (n = 5), (3) figure-of-eight (n = 2), and (4) septal midwall (n = 1). ConclusionsThis canine model of ventricular septal infarction produces VTs with sites of earliest activation and activation sequences similar to those in humans. A reentrant mechanism as the basis of these arrhythmias is supported by the following observations: (1) all VT was initiated and terminated with programmed electrical stimulation; (2) VT activation sequences were consistent with reentry; and (3) precise interruption of the sequence terminated the VT and rendered it noninducible.