Houck Philip D, Jones Billy, Patel Rikin, Olsovsky Greg
Department of Medicine Division of Cardiology, Baylor Scott & White Health, Temple, Texas, USA.
BMJ Case Rep. 2019 Aug 5;12(8):e229339. doi: 10.1136/bcr-2019-229339.
The pathophysiology of narrow complex dilated cardiomyopathy is not defined, so therapeutic options are limited. By utilising the velocity equation, the pathophysiology of narrow complex cardiomyopathy allows above normal conduction propagation velocities. There are two pathophysiological theories that allow above normal conduction velocities and failure to capture the myocardium: (1)insulating fibres of the conduction system extending beyond the apex and (2) reduction of axon branching. A patient with narrow complex cardiomyopathy was subjected to graded increase in amplitude and pulse width pacing to overcome the failure of native conduction to capture the myocardium. Peak systolic strain maps demonstrated a progressive increase in apical contractility with increasing pulse width and amplitude. Ejection fraction improved from 17% to 31%. Understanding the pathophysiology of narrow complex cardiomyopathy leads to proposed therapies. One potential pacing therapy is multi-lead pacing at high amplitude and pulse width to capture myocardial cells not captured by native conduction.
窄QRS波型扩张型心肌病的病理生理学尚不明确，因此治疗选择有限。通过运用速度方程，窄QRS波型心肌病的病理生理学表现为传导传播速度高于正常。有两种病理生理理论可以解释传导速度高于正常以及无法激动心肌的现象：（1）传导系统的绝缘纤维延伸至心尖以外；（2）轴突分支减少。一名窄QRS波型心肌病患者接受了递增幅度和脉宽的起搏治疗，以克服自身传导无法激动心肌的问题。收缩期峰值应变图显示，随着脉宽和幅度的增加，心尖收缩力逐渐增强。射血分数从17%提高到了31%。了解窄QRS波型心肌病的病理生理学有助于提出相应的治疗方法。一种潜在的起搏治疗方法是采用高幅度和脉宽的多导联起搏，以激动未被自身传导所激动的心肌细胞。
