INTRODUCTION: The induction of ventricular fibrillation (VF) by T-wave shocks has been related to dispersion of repolarisation, but only indirect evidence of this hypothesis exists. The effects of drugs prolonging repolarisation like d-sotalol on the vulnerability to T-wave shocks remain unknown. METHODS: In 9 isolated rabbit heart, 7 monophasic action potentials (MAPs) and an ECG were recorded simultaneously. Vulnerable periods were determined using two different shock strengths, one close to the fibrillation threshold and the other close to the upper limit of vulnerability, at baseline and after action potential prolongation by d-sotalol. RESULTS: The vulnerable period had a duration of 30 +/- 14 ms for the lower and 34 +/- 12 ms for the higher shock strength (P = NS). Coupling intervals of the vulnerable periods were 13 +/- 10 ms shorter for higher shock strengths as compared to lower shock strengths (P < 0.005). The vulnerable period for low shock strengths coincided with dispersion of MAPs at 90% repolarisation (r = 0.87-0.92, P < 0.005), and the vulnerable period for high shock strengths coincided with dispersion at 70% repolarisation (r = 0.82-0.93, P < 0.005). ECG parameters predicted the vulnerable periods less precisely than MAP repolarisation (r < or = 0.72). d-Sotalol prolonged MAP durations by an average of 33 ms at 70% and 39 ms at 90% repolarisation but did not alter the described relations, nor did it reduce dispersion of repolarisation or duration of the vulnerable periods. CONCLUSIONS: Dispersion of repolarisation determines vulnerable periods and might be part of the arrhythmogenic substrate promoting induction of VF by T-wave shocks. The coupling intervals of the vulnerable periods depend on the applied shock strength as well as repolarisation, with shock strengths close to the fibrillation threshold inducing VF during dispersion at 90% repolarisation and shock strengths close to the upper limit of vulnerability inducing VF during dispersion at 70% repolarisation. d-Sotalol reduces neither vulnerability to T-wave shocks nor dispersion of repolarisation in this isolated heart model.
INTRODUCTION: The induction of ventricular fibrillation (VF) by T-wave shocks has been related to dispersion of repolarisation, but only indirect evidence of this hypothesis exists. The effects of drugs prolonging repolarisation like d-sotalol on the vulnerability to T-wave shocks remain unknown. METHODS: In 9 isolated rabbit heart, 7 monophasic action potentials (MAPs) and an ECG were recorded simultaneously. Vulnerable periods were determined using two different shock strengths, one close to the fibrillation threshold and the other close to the upper limit of vulnerability, at baseline and after action potential prolongation by d-sotalol. RESULTS: The vulnerable period had a duration of 30 +/- 14 ms for the lower and 34 +/- 12 ms for the higher shock strength (P = NS). Coupling intervals of the vulnerable periods were 13 +/- 10 ms shorter for higher shock strengths as compared to lower shock strengths (P < 0.005). The vulnerable period for low shock strengths coincided with dispersion of MAPs at 90% repolarisation (r = 0.87-0.92, P < 0.005), and the vulnerable period for high shock strengths coincided with dispersion at 70% repolarisation (r = 0.82-0.93, P < 0.005). ECG parameters predicted the vulnerable periods less precisely than MAP repolarisation (r < or = 0.72). d-Sotalol prolonged MAP durations by an average of 33 ms at 70% and 39 ms at 90% repolarisation but did not alter the described relations, nor did it reduce dispersion of repolarisation or duration of the vulnerable periods. CONCLUSIONS: Dispersion of repolarisation determines vulnerable periods and might be part of the arrhythmogenic substrate promoting induction of VF by T-wave shocks. The coupling intervals of the vulnerable periods depend on the applied shock strength as well as repolarisation, with shock strengths close to the fibrillation threshold inducing VF during dispersion at 90% repolarisation and shock strengths close to the upper limit of vulnerability inducing VF during dispersion at 70% repolarisation. d-Sotalol reduces neither vulnerability to T-wave shocks nor dispersion of repolarisation in this isolated heart model.
Authors: Barbara Mali; Tomaz Jarm; Selma Corovic; Marija Snezna Paulin-Kosir; Maja Cemazar; Gregor Sersa; Damijan Miklavcic Journal: Med Biol Eng Comput Date: 2008-04-16 Impact factor: 2.602
Authors: M J Killeen; G Thomas; I S Gurung; C A Goddard; J A Fraser; M P Mahaut-Smith; W H Colledge; A A Grace; C L-H Huang Journal: Acta Physiol (Oxf) Date: 2007-01 Impact factor: 6.311