超声检查对肥厚型梗阻性心肌病起搏治疗血液动力学变化的探讨

Echocardiographic Studies of Hemodynamic Changes in Hypertrophic Obstructive Cardiomyopathy Treated by Pacemarker.

用超声技术探讨起搏器对肥厚型梗阻性心肌病 (HCM)的作用机理。观察 4例HCM(左心导管和造影检查确诊 )患者的如下指标 :①起搏器置入前、后左室梗阻部位形态及运动变化情况 ;②不同起搏间期对左室心肌各部位收缩期运动顺序的影响 ;③观察自主心律与起搏心律对心功能的影响。结果 :①起搏后左室流出道动力性梗阻减轻 (76 .3± 5 2 .8vs 16 1.5± 47.4mmHg ,P <0 .0 5 )。但起搏后 ,肥厚的心肌收缩期梗阻左室流出道现象依然存在。②双腔起搏时 ,左室心肌激动顺序未见变化 ,但传导时限延长 (6 2 .5± 7.4vs 45 .5± 7.7ms,P <0 .0 5 )。③起搏后左室收缩、舒张诸项指标下降。结论 :起搏干扰心肌传导、激动和收缩的正常过程 ,使得其同步性劣于窦性心律时 。

Using ultrasound method to judge the mechanism of changes in hypertrophic constructive cardiomyopathy (HCM) with pacing.4 HCM patients they had received left ventricular (LV) catheterization and angiography were examined as followes echocardiographic parameters:①The shape and motion of LV obstructive muscles before and after pacing.②To measure the program of LV segments to be excited,when the atrial ventricular interval were changed by DDD pacemarker.③To measure the variation of LV function at sinus rhythm and pacing controlled.Result:①The gradient at obstructed region were decreased from 161.5±47.4 to 76.3±52.8 mmHg( P <0.05),but the hypertrophic muscles still contracted to obstruct LV outflow during pacing.②The program of exciting LV muscles controlled by DDD pacemarker was not different from that by sinus rhythm,but the interval of conduction course were prolonged (from 45.5±7.7 to 62.5±7.4 ms, P < 0.05). ③Some of LV functions turned to be inhibited.Conclusion:Pacing interrupted the normal course of cardiac muscles in conducting,exciting and contracting,so the synchronization ought to be worse than it controlled by physiological program,that LV systolic pressure and gradient of HCM could be decreased.