Obstruction is unimportant in the pathophysiology of hypertrophic cardiomyopathy.

Obstruction is unimportant in the pathophysiology of hypertrophic cardiomyopathy.
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梗阻在肥厚型心肌病的病理生理学中并不重要。

DOI:
10.1136/pgmj.62.728.515
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发表时间:
1986
影响因子:
5.1
通讯作者:
R. Siegel
R. Siegel
中科院分区:
医学4区
文献类型:
--
作者:
J. Criley;R. Siegel

文献摘要

被引文献

相似文献

关于肥厚型心肌病(HCM)中腔内压力梯度的重要性一直存在争议。人们普遍认为梯度是“阻塞”的结果,它阻碍了左心室流出,并且可以通过手术干预来缓解。在发现 HCM 后的第一个十年(1957-66),“梗阻”部位被认为是左心室下区的肌肉括约肌或收缩环,并开发了旨在模拟幽门肌切除术(用于肥厚性幽门狭窄)的手术。在对“收缩环”的存在提出质疑以及对压力梯度的另一种非阻塞性解释之后,“阻塞”部位被转移到二尖瓣前叶和室间隔之间的并置点,这是二尖瓣收缩期前移(SAM)的结果。尽管“梗阻”的部位和机制发生了易位,但“解梗阻”的操作并没有发生明显的变化。新的“阻塞”部位受到了质疑,因为心室的排空并未明显受到阻碍;当引起梯度时,心室排空比没有梯度时更快、更完全。除了对梯度的非阻塞性解释之外,其他被认为表明“阻塞”的现象可以通过心室的快速且完全排空(空洞闭塞)来解释。由于无压力梯度的有症状 HCM 患者的发病率和死亡率可能超过有压力梯度的患者,因此建议“梗阻”在 HCM 的病理生理学中可能并不重要,应重点关注舒张功能异常和危及生命的心律失常。
There has been a longstanding controversy about the significance of intracavitary pressure gradients in hypertrophic cardiomyopathy (HCM). It has been generally assumed that the gradient is the result of an 'obstruction' that impedes left ventricular outflow and which can be relieved by operative intervention. In the first decade after the discovery of HCM (1957-66), the site of 'obstruction' was thought to be a muscular sphincter or contraction ring in the submitral region of the left ventricle, and operations designed to emulate pyloromyectomy (for hypertrophic pyloric stenosis) were developed. Following a challenge to the existence of the 'contraction ring' and an alternative non-obstructive explanation of the pressure gradient, the site of 'obstruction' was translocated to a point of apposition between the anterior mitral leaflet and the interventricular septum, a result of systolic anterior motion (SAM) of the mitral valve. Despite the translocation of the site and mechanism of 'obstruction', the operation for 'relief of obstruction' has not changed significantly. The newer site of 'obstruction' has been challenged on the grounds that the ventricle is not demonstrably impeded in its emptying; when a gradient is provoked, the ventricle empties more rapidly and more completely than it does without a gradient. In addition to a non-obstructive explanation of the gradient, other phenomena thought to be indicative of 'obstruction' can be explained by rapid and complete emptying of the ventricle (cavitary obliteration). Since the morbidity and mortality of symptomatic HCM patients without pressure gradients may exceed that of patients with pressure gradients, it is suggested that 'obstruction' may be unimportant in the pathophysiology of HCM and attention should be focused on abnormal diastolic function and life threatening arrhythmias.