Gras D, Daubert C, Mabo P
Service de cardiologie A, Hôtel-Dieu/CHRU, Rennes.
Arch Mal Coeur Vaiss. 1995 Apr;88(4 Suppl):577-83.
Recent studies have shown that dual-chamber cardiac pacing could improve patients with hypertrophic obstructive cardiomyopathy resistant to medical treatment. After a brief historical review, the authors report the present status of this original therapeutic option. The results of different studies are in agreement and show that the functional improvement is associated with a large reduction of the intraventricular pressure gradient with permanent DDD pacing. Although the exact mechanism of the improvement remains unknown, all groups underline the importance of complete and permanent ventricular capture. This requires precise regulation of the atrioventricular delay which in most cases must be programmed at a value inferior to 90 ms, which compromises ventricular filling which is already abnormal under basal conditions. The inefficacy of pacing in some cases is explained by the necessity of selecting a very short atrioventricular delay which alters diastolic function and finally masks the benefits of ventricular capture. In this particular situation, the authors propose improving atrioventricular synchrony by pharmacological prolongation of the PR interval, or, when unsuccessful, by ablation of the atrioventricular junction. This attitude was adopted in 5 cases when pacing with an AVD programmed between 20 and 70 ms, provided only a partial haemodynamic result. Improved atrioventricular synchrony allowed selection of an AVD of 100 to 150 ms, so reducing the gradient by more than 70%, compared with 30% under the initial programming parameters. The authors conclude that a positive and sustained benefit of cardiac pacing can only be obtained by an individualised regulation of pacing parameters to optimize atrioventricular synchrony which seems to be the key element of success.
近期研究表明,双腔心脏起搏可改善药物治疗无效的肥厚性梗阻性心肌病患者。在简要回顾历史后,作者报告了这一创新治疗方法的现状。不同研究结果一致,表明功能改善与永久DDD起搏导致的心室内压力梯度大幅降低有关。尽管改善的确切机制尚不清楚,但所有研究组都强调完全且永久的心室夺获的重要性。这需要精确调节房室延迟,在大多数情况下,房室延迟必须设置为小于90毫秒的值,这会损害在基础状态下就已异常的心室充盈。某些情况下起搏无效的原因是需要选择非常短的房室延迟,这会改变舒张功能并最终掩盖心室夺获的益处。在这种特殊情况下,作者建议通过药物延长PR间期来改善房室同步性,或者在药物治疗失败时,通过消融房室结来改善。在5例患者中,当将房室延迟设置在20至70毫秒之间进行起搏时,仅获得了部分血流动力学结果,于是采用了这种方法。改善后的房室同步性允许选择100至150毫秒的房室延迟,与初始程控参数下降低30%相比,梯度降低了70%以上。作者得出结论,只有通过个体化调节起搏参数以优化房室同步性,才能获得心脏起搏积极且持续的益处,而房室同步性似乎是成功的关键要素。