Mechanisms that initiate ventricular tachycardia in the infarcted human heart

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

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

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.

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).

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.