Henein M Y, Gibson D G
Cardiac Department, Royal Brompton National Heart and Lung Hospital, London.
Br Heart J. 1995 Feb;73(2):151-7. doi: 10.1136/hrt.73.2.151.
To assess how early diastolic transmitral flow is suppressed in a group of patients in whom effective ventricular filling occurred exclusively with atrial systole.
Prospective examination of the left ventricular transverse and longitudinal axes and transmitral Doppler flow.
A tertiary referral centre for cardiac diseases.
20 patients (mean (SD) age 65 (10) years) with isolated transmitral late diastolic flow were studied. None had sinus tachycardia, prolonged PR interval or a summation flow pattern. 21 normal individuals of similar age served as controls.
The left ventricle was usually dilated, end diastolic diameter (6.6 (1.0) v 4.9 (0.5) cm, P < 0.001) and end systolic diameter (5.4 (1.1) v 3.3 (0.5) cm, P < 0.001) were both increased, and fractional shortening of the minor axis reduced (16 (7)% v 30 (10)%, P < 0.001) in patients in whom left ventricular early diastolic filling was absent compared with those of normal controls. Mitral valve opening was late after aortic valve closure (A2) (115 (30) v 60 (10) ms, P < 0.001). The minor axis increased during this period (30 (20)% v 8.6 (2.5)%, P < 0.001). Onset of detectable transmitral flow was further delayed after cusp separation (85 (25) v 25 (10) ms, P < 0.001). Left ventricular long axis function was very abnormal. Onset of shortening was delayed with respect to the q wave at the left and septal sites (150 (40) v 90 (20) ms and 145 (30) v 80 (10) ms respectively, P < 0.001) and major shortening occurred after, rather than before, A2 (25 (12) v -10 (2.5)% and 50 (30) v -6.6 (0.3)% total excursion, P < 0.001). Although the long axis lengthened a little at the start of early diastole, its dominant component occurred in late diastole to coincide with atrial systole. The relative A wave was thus greatly increased at both sites (67 (17) v 29 (6)% and 77 (13) v 33 (8)%, P < 0.001).
Prolonged left ventricular long axis shortening and delayed onset of lengthening effectively suppress early diastolic transmitral flow even though the minor axis increases and mitral cusps separate apparently normally. This grossly asynchronous left ventricular relaxation may interfere with filling by dissipating normal ventricular restoring forces.
评估在一组仅通过心房收缩实现有效心室充盈的患者中,舒张早期经二尖瓣血流是如何被抑制的。
对左心室横轴和纵轴以及经二尖瓣多普勒血流进行前瞻性检查。
一家三级心脏病转诊中心。
研究了20例(平均(标准差)年龄65(10)岁)仅有舒张晚期经二尖瓣血流的患者。无一例有窦性心动过速、PR间期延长或血流叠加模式。21名年龄相仿的正常个体作为对照。
与正常对照组相比,左心室舒张末期直径(6.6(1.0)对4.9(0.5)cm,P<0.001)和收缩末期直径(5.4(1.1)对3.3(0.5)cm,P<0.001)均增加,短轴缩短分数降低(16(7)%对30(10)%,P<0.001),这些患者左心室舒张早期充盈缺失。二尖瓣开放在主动脉瓣关闭(A2)后延迟(115(30)对60(10)ms,P<0.001)。在此期间短轴增加(30(20)%对8.6(2.5)%,P<0.001)。瓣叶分离后可检测到的经二尖瓣血流起始进一步延迟(85(25)对25(10)ms,P<0.001)。左心室长轴功能非常异常。在左心室和室间隔部位,缩短起始相对于q波延迟(分别为150(40)对90(20)ms和145(30)对80(10)ms,P<0.001),主要缩短发生在A2之后而非之前(总偏移分别为25(12)%对 -10(2.5)%和50(30)%对 -6.6(0.3)%,P<0.001)。尽管在舒张早期开始时长轴略有延长,但其主要成分出现在舒张晚期与心房收缩一致。因此,在两个部位相对A波均显著增加(67(17)%对29(6)%和77(13)%对33(8)%,P<0.001)。
尽管短轴增加且二尖瓣瓣叶分离看似正常,但左心室长轴缩短延长和延长起始延迟有效地抑制了舒张早期经二尖瓣血流。这种严重不同步的左心室舒张可能通过消散正常的心室恢复力而干扰充盈。