Mapping of reset of anatomic and functional reentry in anisotropic rabbit ventricular myocardium.

Abstract

BACKGROUND Premature stimulation is used to characterize the reentrant circuit during ventricular tachycardia (VT) in patients. The goal of this study was to compare the effects of premature stimulation on functional and anatomic reentrant VT. METHODS AND RESULTS In 18 Langendorff-perfused rabbit hearts, thin layers of anisotropic left ventricular subepicardium were created by a cryoprocedure. In 8 hearts, rapid pacing induced reentry around a line of functional conduction block; in 10 hearts, reentry occurred around a fixed epicardial obstacle created by a cryoprobe. The cycle lengths (CL) of functional and anatomic VT were 110 +/- 10 and 167 +/- 17 milliseconds, respectively. During anatomic VT, the excitable gap measured 43% of the CL and premature stimuli could always reset VT (44 +/- 12 milliseconds). During early premature beats, conduction of the orthodromic wave was slightly depressed, but anatomic VT was never terminated. Reset curves at different sites in the ventricle revealed three different response types, both determined by and characterizing the spatial and temporal relation between pacing and recording sites. Premature stimulation during functional VT revealed a local excitable gap at the pacing site measuring 27% of the cycle length of VT. However, in only 3 of 8 hearts, premature stimuli could reset functional VT by 8%. In 5 VTs, advancement of the paced activation was fully compensated by prolongation of the return cycle, and VT was not reset. Due to slow conduction both toward and inside the circuit, the paced orthodromic wave lost its prematurity already within a distance of 6 to 10 mm from the pacing site. CONCLUSIONS Both during anatomic and functional reentry, an excitable gap is present in the reentrant circuit. Three different response curves reveal the localization of the pacing and recording sites in the circuit. Anatomic VT can always be reset by premature stimuli, whereas in 5 of 8 hearts, functional VT could not be reset. In the other 3 hearts, VT could only be reset for less than 7% to 11% of the VT interval. Therefore, it seems very unlikely that clinical VT based on functional reentry can be reset.

Rectification of the Background Potassium Current

“…20 Similarly, in our experiments, rotors have significantly briefer CLs (Ϸ30 to 40 ms) than expected from the guinea pig heart whose action potential duration (APD) is Ϸ200 ms during sinus rhythm. 12 Computer simulations suggest that extremely fast rotors may be the result of the strong repolarizing influence exerted by their core, which activates I K1 and leads to extreme abbreviation of the APD in its proximity.…”

Polymorphic Reentrant Ventricular Tachycardia in the Isolated Rabbit Heart Studied by High-Density Mapping

“…In this model, sustained monomorphic VT based on functional reentry may be provoked by aggressive programmed electrical stimulation. 11,12 …”

“…Conduction block was defined as a local velocity Ͻ5 cm/s (50 ms over 2.5 mm or 30 ms over 1.5 mm) associated with a change in direction of the impulse at the other side of the line of block. This was stricter than the criteria used in previous studies with this model 11,12 to minimize the inclusion of very slow local conduction or pseudoblock. Similar criteria have been used by other investigators.…”

“…9 -12 In this model, aggressive programmed electrical stimulation can provoke monomorphic VT based on a functional reentry circuit. 11,12 We extended the model by creating a central area of prolonged refractoriness in the wall of the left ventricle by local cooling. As a result of this intervention, single or multiple premature beats induced short episodes of rapid polymorphic VT based on a functional reentrant circuit that continuously changed its reentrant pathway.…”

Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

“…In this setting, reentry can occur as the result of shortening of activation wavelength below the physical length of a preformed reentry circuit. [35][36][37] Conduction slowing and action potential shortening both shorten activation wavelength. Given little or no change in APD, a fourfold increase in conduction time as observed with propafenone in this study decreases activation wavelength fourfold (Table 4) and possibly below the perimeter of the heart, a setting that allows for macroreentry around the circumference of the whole heart in this model.…”