Kirchhof P F, Fabritz C L, Zabel M, Franz M R
Cardiology Division, Veterans Administration, Medical Center, Washington, DC 20422, USA.
Cardiovasc Res. 1996 Jun;31(6):953-62.
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.
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.
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.
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.
T波电击诱发心室颤动(VF)与复极离散有关,但该假说仅有间接证据。像d - 索他洛尔这类延长复极的药物对T波电击易损性的影响尚不清楚。
在9个离体兔心脏中,同时记录7个单相动作电位(MAP)和一份心电图。在基线状态以及d - 索他洛尔使动作电位延长后,使用两种不同的电击强度来确定易损期,一种接近颤动阈值,另一种接近易损性上限。
较低电击强度下易损期持续时间为30±14毫秒,较高电击强度下为34±12毫秒(P =无显著差异)。与较低电击强度相比,较高电击强度下易损期的耦合间期短13±10毫秒(P <0.005)。低电击强度下的易损期与90%复极时的MAP离散一致(r = 0.87 - 0.92,P <0.005),高电击强度下的易损期与70%复极时的离散一致(r = 0.82 - 0.93,P <0.005)。心电图参数预测易损期的准确性不如MAP复极(r≤0.72)。d - 索他洛尔在70%复极时平均使MAP持续时间延长33毫秒,在90%复极时延长39毫秒,但未改变所述关系,也未减少复极离散或易损期持续时间。
复极离散决定易损期,可能是促进T波电击诱发VF的致心律失常基质的一部分。易损期的耦合间期取决于施加的电击强度以及复极情况,接近颤动阈值的电击强度在90%复极离散时诱发VF,接近易损性上限的电击强度在7%复极离散时诱发VF。在这个离体心脏模型中,d - 索他洛尔既不降低对T波电击的易损性,也不减少复极离散。