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主动脉瓣下室间隔膨出随年龄增长通过室间隔成角模拟肥厚型心肌病,与局灶性肥厚无关。一项超声心动图研究。

Subaortic septal bulge simulates hypertrophic cardiomyopathy by angulation of the septum with age, independent of focal hypertrophy. An echocardiographic study.

作者信息

Krasnow N

机构信息

Division of Cardiology, State University of New York Health Sciences Center at Brooklyn, USA.

出版信息

J Am Soc Echocardiogr. 1997 Jun;10(5):545-55. doi: 10.1016/s0894-7317(97)70009-9.

DOI:10.1016/s0894-7317(97)70009-9
PMID:9203495
Abstract

Focal hypertrophy of the basal anterior septum occurs not infrequently in elderly patients and is considered by some to be a significant form of hypertrophic cardiomyopathy; others consider it to be an unimportant anatomic variant associated with an angulated septum, called a septal bulge (SB). We analyzed 94 cases of SB collected prospectively and compared them with 88 patients with extensive hypertrophic cardiomyopathy (HCM), 20 patients with hypertrophic cardiomyopathy limited to the entire septum (ASH), and 20 age-matched controls. The SB cases were also divided into three groups, with marked, moderate, or no basal septal hypertrophy associated with the occurrence of an SB. All groups of SB patients had increased fractional shortening compared with controls (0.48 +/- 0.07 versus controls 0.40 +/- 0.07), comparable with HCM (0.48 +/- 0.12), and increased left ventricular outflow tract velocity both at rest and especially after amyl nitrite inhalation (3.42 +/- 1.35 versus 1.55 +/- 0.60 m/sec [controls]). Other features of HCM were not present: normal wall thickness except for the basal septal hypertrophy, no anterior malposition in SB patients, no age-independent reversal of ratio of early to late mitral inflow velocity (E/A), and no decrease in end-diastolic dimension. It is concluded that outflow tract narrowing by an angulated septum is the primary mechanism responsible for the increased outflow tract velocity, rather than the hypertrophic septum. The resultant increase in convective acceleration simulates the dynamics of hypertrophic cardiomyopathy. The focal hypertrophy may be secondary and contributory to the enhanced ventricular dynamics, but it does not appear to be a primary cardiomyopathy.

摘要

老年患者中,基底前间隔局灶性肥厚并不少见,一些人认为这是肥厚型心肌病的一种重要形式;另一些人则认为它是与成角间隔相关的一种不重要的解剖变异,称为间隔膨出(SB)。我们前瞻性收集了94例SB病例,并将其与88例广泛肥厚型心肌病(HCM)患者、20例局限于整个间隔的肥厚型心肌病(ASH)患者以及20例年龄匹配的对照进行比较。SB病例也分为三组,分别与SB的发生相关的明显、中度或无基底间隔肥厚。与对照组相比,所有SB患者组的缩短分数均增加(0.48±0.07对对照组0.40±0.07),与HCM相当(0.48±0.12),静息时尤其是吸入亚硝酸异戊酯后左心室流出道速度增加(3.42±1.35对1.55±0.60米/秒[对照组])。未出现HCM的其他特征:除基底间隔肥厚外,壁厚度正常,SB患者无前位异常,二尖瓣流入速度早期与晚期比值(E/A)无年龄无关的逆转现象,舒张末期内径无减小。结论是,成角间隔导致的流出道狭窄是流出道速度增加的主要机制,而非肥厚的间隔。由此产生的对流加速度增加模拟了肥厚型心肌病的动力学。局灶性肥厚可能是继发性的,有助于增强心室动力学,但它似乎不是原发性心肌病。

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