Mechanisms that initiate ventricular tachycardia in the infarcted human heart

Abstract

Background: Precise mechanisms that initiate ventricular tachycardia (VT) in the intact infarcted human heart have not been defined.

Objective: The purpose of this study was to investigate the mechanisms that underlie human postinfarct VT initiation.

Methods: Noncontact mapping of the left ventricle was performed in 9 patients (age 67.1 +/- 7.8 years, ejection fraction 34.4% +/- 5%) with previous myocardial infarction and sustained monomorphic VT.

Results: Circuits in which >/=30% of the diastolic pathway (DP) could be defined were identified in 12 VTs (cycle length 357 +/- 60 ms). Eighteen VT episodes were initiated with pacing, and one occurred spontaneously. Ten complete and two partial circuits were mapped (89% +/- 25% of the DP). In all complete circuits, pacing led to the development of unidirectional conduction block at the location of the subsequent VT exit site and the formation of functional block creating a border(s) for subsequent DP. Wavefront velocity in the DP region slowed from 1.22 +/- 0.2 m/s during sinus rhythm to 0.59 +/- 0.14 m/s during VT (P <.005). In 11 initiation episodes, lines of functional block and areas of slow conduction developed progressively over one to six reentrant cycles before a stable DP was established and sustained monomorphic VT ensued. The formation of unidirectional or functional lines of block was not identified during identical pacing protocols that failed to initiate VT (n = 14).

Conclusion: Initiation of sustained monomorphic VT requires the development of unidirectional block and formation of lines of functional block creating borders for a DP in areas of slow conduction. A transitional stage often exists during the initiation process before a stable VT circuit is established.

Figure 1

Schematic representation of left ventricular endocardium in all nine patients showing infarct scar (gray), pacing site location (black pacing symbols), diastolic pathway (DP; paired black lines), and transitional reentry zones. Numbered black dots indicate sites of the corresponding evolving transitional beat diastolic pathway. Patients 2, 3, and 9 have ≥2 pacing symbols representing the position of pacing for separate ventricular tachycardia episodes. See text for discussion.

Figure 2

Sequence of noncontact left ventricular isochronal maps demonstrating an episode of pacing-induced ventricular tachycardia initiation from patient 2. Flat maps represent the entire left ventricular endocardium cut along one border and laid open. Black region represents scar. Light blue lines represent lines of functional block. Arrows show direction of propagation of activation. Change of isochrone color represents 10-ms intervals in activation, progressing from white to purple (illustrated on the scale adjacent to panel 1). The corresponding surface ECG is shown at the top with numbers pertaining to map panels below and lines representing the point in time and duration of each map. In this and all subsequent figures, the base of the left ventricle is at the top of each panel and the apex at the bottom. See text for discussion.

Figure 3

Sequence of noncontact left ventricular isopotential maps from patient 8 demonstrating a transitional beat prior to monomorphic ventricular tachycardia. Flat isopotential maps represent the entire left ventricle cut along one border and laid open. Gray areas are infarct scar. Red rectangular symbol is the pacing site. Purple represents resting endocardial potential that changes through a spectrum of colors on activation, with white representing maximal change of negative potential. Arrows show direction of activation. Light blue lines represent lines of functional block. Panel at the top shows surface ECG lead III with reconstructed electrograms beneath (Virtual 1–6). White circles in panels 2 and 8 indicate sites where reconstructed electrograms were recorded. A ventricular premature beat occurs after S3, then a transitional beat and then sustained monomorphic ventricular tachycardia. Vertical red lines are lettered and correspond with the panels below. See text for discussion.

Figure 4

Sequence of noncontact left ventricular isochronal maps showing failure of ventricular tachycardia initiation due to formation of only a single line of functional block in patient 7. See text for discussion. Change of isochrones color represents 10-ms intervals in activation, progressing from white to purple.