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左束支传导阻滞:一个不断演变的概念。

Left bundle branch block: a continuously evolving concept.

作者信息

Flowers N C

出版信息

J Am Coll Cardiol. 1987 Mar;9(3):684-97. doi: 10.1016/s0735-1097(87)80065-7.

Abstract

Eppinger and Rothberger in 1909 and 1910 first acknowledged the importance of the conduction system, yet a confusion of the pattern of left bundle branch block with right bundle branch block resulted which persisted for 25 years. In left bundle branch block, right ventricular endocardial activation begins before, and is often completed before, initiation of left ventricular endocardial activation. Most likely, right to left septal activation then follows, resulting in left ventricular endocardial activation. Although it is hazardous to make definitive diagnoses of infarction in the presence of left bundle branch block, clues do exist. Benign left bundle branch block is rare; usually disease becomes manifest. Electrocardiographic criteria of hypertrophy are not as helpful in older patients with chronic left bundle branch block (mainly because of the very high incidence of left ventricular hypertrophy) as in younger patients with block of nonatherosclerotic origin. Left bundle branch block is often associated with other abnormalities of the conduction system. Fascicular blocks may mask or mimic myocardial infarction. Left posterior fascicular block is most often an indicator of left ventricular myocardial deficit if right ventricular enlargement is eliminated. Mortality is higher in patients with associated left axis deviation than in those with a normal axis, although the incidence of progression of atrioventricular (AV) block is low. In symptomatic patients with prolonged His to ventricular intervals, the incidence of progression of AV block is higher (12%). Preexisting left bundle branch block in the absence of clinical evidence of heart disease is rare, yet carries with it a slightly increased mortality. Newly acquired left bundle branch block carries a 10-fold increase in mortality; the incidence of sudden death as the first manifestation of heart disease is increased 10-fold.

摘要

1909年和1910年,埃平格(Eppinger)和罗特贝格尔(Rothberger)首次认识到传导系统的重要性,但左束支传导阻滞模式与右束支传导阻滞模式出现混淆,这种情况持续了25年。在左束支传导阻滞时,右心室心内膜激活在左心室心内膜激活开始之前就已开始,并且通常在左心室心内膜激活开始之前就已完成。很可能随后是从右向左的间隔激活,从而导致左心室心内膜激活。尽管在存在左束支传导阻滞的情况下做出明确的梗死诊断存在风险,但线索确实存在。良性左束支传导阻滞很少见;通常疾病会显现出来。肥厚的心电图标准在患有慢性左束支传导阻滞的老年患者中(主要是因为左心室肥厚的发生率非常高)不如在患有非动脉粥样硬化性起源阻滞的年轻患者中有用。左束支传导阻滞常与传导系统的其他异常相关。分支阻滞可能掩盖或模拟心肌梗死。如果消除右心室扩大,左后分支阻滞最常是左心室心肌损害的指标。伴有左轴偏移的患者死亡率高于轴正常的患者,尽管房室(AV)传导阻滞进展的发生率较低。在有症状且希氏束至心室间期延长的患者中,AV传导阻滞进展的发生率较高(12%)。在没有心脏病临床证据的情况下预先存在左束支传导阻滞很少见,但死亡率略有增加。新获得的左束支传导阻滞使死亡率增加10倍;作为心脏病首发表现的猝死发生率增加10倍。

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