Key result
Biphasic T wave shocks inducing ventricular fibrillation resulted in a repolarization dispersion of 64 +/- 15 msec, compared to 41 +/- 17 msec for shocks above the upper limit of vulnerability (P<0.01).
Why the study?
How do shock timing and intensity affect shock-induced dispersion of ventricular repolarization and ventricular fibrillation induction in an intact heart model?
How do shock timing and intensity affect shock-induced dispersion of ventricular repolarization and ventricular fibrillation induction in an intact heart model?
Absolute Event Rate: 64% vs 41%
p-value: p=<0.01
This preclinical study demonstrates that shock-induced dispersion of ventricular repolarization depends on shock timing and intensity, offering a mechanistic explanation for the upper and lower limits of vulnerability to ventricular fibrillation.
Should not inform clinical defibrillation yet; leaves open mechanistic studies on shock timing in intact hearts.
INTRODUCTION: Shock-induced dispersion of ventricular repolarization (SIDR) caused by an electrical field stimulus has been suggested as a mechanism of ventricular fibrillation (VF) induction; however, this hypothesis has not been studied systematically in the intact heart. Likewise, the mechanism underlying the upper (ULV) and lower (LLV) limit of vulnerability remains unclear. METHODS AND RESULTS: In eight Langendorff-perfused rabbit hearts, monophasic action potentials were recorded simultaneously from ten different sites of both ventricles. Truncated biphasic T wave shocks were randomly delivered at various coupling intervals and strengths, exceeding the vulnerable window, ULV, and LLV, SIDR, defined as the difference between the longest and shortest postshock repolarization times, was 64 +/- 15 msec for shocks inducing VF. SIDR was 41 +/- 17 msec for shocks delivered above the ULV, and 33 +/- 14 and 27 +/- 8 msec for shocks delivered 10 msec before and after the vulnerable window, respectively (all P < 0.01 vs VF-inducing shocks). Although SIDR was larger for shocks delivered below the LLV (93 +/- 24 msec, P < 0.01 vs VF-inducing shocks), the repolarization extension was significantly smaller for shocks below the LLV (10.3% +/- 3.9% vs 16.3% +/- 4.9%, P < 0.01). CONCLUSION: SIDR is influenced by the shock timing and intensity. Large SIDR within the vulnerable window and an SIDR decrease toward its borders suggest that SIDR is essential for VF induction. The decrease in SIDR toward greater shock strengths may explain the ULV. Small repolarization extension for shocks below the LLV may explain why these shocks, despite producing large SIDR, fail to induce VF.
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Behrens et al. (1997) studied Ventricular fibrillation (n=8). Truncated biphasic T wave shocks vs. Shocks above ULV, below LLV, or outside vulnerable window was evaluated on Shock-induced dispersion of ventricular repolarization (SIDR) (p=<0.01). Biphasic T wave shocks inducing ventricular fibrillation resulted in a repolarization dispersion of 64 +/- 15 msec, compared to 41 +/- 17 msec for shocks above the upper limit of vulnerability (P<0.01).
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