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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 ,由此可导致左室收缩压力以及狭窄处压力梯度的下降
Study the Mechanism of Pacemaker on Hypertrophic Obstructive Cardiomyopathy (HCM) with Ultrasound. The following indexes were observed in 4 cases of patients with HCM diagnosed by left heart catheterization and angiography: ①The shape and movement of left ventricular obstruction before and after pacemaker implantation; ②The contraction of left ventricular myocardium at different pacing intervals Period of the impact of exercise order; ③ observation of autonomic heart rate and pacemaker heart function. Results: (1) The dynamic obstruction of left ventricular outflow tract was reduced after pacing (76.3 ± 52.8 vs 16 1.5 ± 47.4mmHg, P <0.05). However, pacing, hypertrophy of myocardial systolic obstruction left ventricular outflow tract phenomenon still exists. ② In double-chamber pacing, the order of left ventricular myocardial activation was unchanged, but the conduction time was prolonged (62.5 ± 7.4 vs 45.5 ± 7.7ms, P <0.05). Left ventricular contraction after pacing, diastolic various indicators decreased. CONCLUSIONS: Pacing interferes with the normal process of myocardial conduction, activation and contraction so that its synchrony is inferior to sinus rhythm, which can result in a decrease in left ventricular systolic pressure and pressure gradient in the stenosis