Madariaga I, Carmona J R, Mateas F R, Lezaun R, de los Arcos E
Division of Cardiology, Hospital de Navarra, Pamplona, Spain.
Eur Heart J. 1994 Jan;15(1):134-7. doi: 10.1093/oxfordjournals.eurheartj.a060366.
Electrophysiological studies with simultaneous echocardiographic control and invasive measurement of intravascular pressures were carried out in a 13-year-old boy with hypertrophic cardiomyopathy who was hospitalized after an episode of aborted sudden death. Ventricular stimulation did not induce ventricular tachycardia, but atrial stimulation induced atrial fibrillation, atrial flutter and non-sustained ventricular tachycardia. Atrial stimulation (S1) at 200 beats.min-1 (10-15 s) also induced significant repolarization abnormalities in the 5-10 post-stimulation beats. Akinesia of the ventricular septum and posterior wall without opening of the mitral valve was documented by echocardiography. A complete anterior systolic motion, not observed under basal conditions, was detected in the first post-stimulation beat. Atrial stimulation at rates over 120 beats.min-1 caused a drop in systolic blood pressure, a rise in pulmonary artery pressure, and a decrease in cardiac output. Despite therapy with propranolol and amiodarone, the patient died suddenly.
对一名13岁肥厚型心肌病男孩进行了电生理研究，该男孩在一次猝死未遂发作后住院，研究过程中同时进行超声心动图监测和血管内压力的有创测量。心室刺激未诱发室性心动过速，但心房刺激诱发了心房颤动、心房扑动和非持续性室性心动过速。以200次/分钟的频率进行心房刺激（S1，持续10 - 15秒）也在刺激后5 - 10个搏动中诱发了明显的复极异常。超声心动图记录显示室间隔和后壁运动减弱，二尖瓣未开放。在刺激后的第一个搏动中检测到一种在基础状态下未观察到的完全性收缩期前运动。心率超过120次/分钟的心房刺激导致收缩压下降、肺动脉压升高和心输出量减少。尽管使用了普萘洛尔和胺碘酮治疗，该患者仍突然死亡。
