Experimental electrophysiology and arrhythmogenicity. Anisotropy and ventricular tachycardia.

In a 2-D model of anisotropy, created by freezing the intramural and endocardial layers of a Langendorf perfused rabbit heart, sustained ventricular tachycardia (VT) with a cycle length of 130 ms and an excitable gap of 30 ms could be initiated by rapid pacing. High resolution mapping (256 points) of the thin surviving epicardial layer revealed that the VT was based on epicardial re-entry without the involvement of a gross anatomic obstacle and a central line of functional conduction block oriented parallel to the fibre. Microelectrode recordings from the centre of the ellipsoid circuit showed markedly prolonged action potentials, leading to 2:1 or 3:1 cellular responses. At the pivoting points prolonged action potentials with a 1:1 response were recorded. Immediately after termination of VT the same sites showed 1:1 responses with normal action potential duration. The various degrees of prolongation of the action potentials in the centre of functional anisotropic re-entry were caused by electrotonic current flow between the two limbs of the circuit, which were closely opposed but activated with a large time difference. Towards the pivoting points the phase difference between the two limbs of the circuit decreased, but because of slow transverse conduction around the pivoting points was still 30 ms. We conclude that the electrotonic prolongation of the action potentials at the pivoting points of anisotropic re-entry enlarges both the size and the cycle length of the circuit. Anisotropy thus contributes to the creation of stable VT with an excitable gap.