Riordan Matt M, Kovács Sándor J
Department of Biomedical Engineering, School of Engineering and Applied Science, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Appl Physiol (1985). 2008 Feb;104(2):513-20. doi: 10.1152/japplphysiol.00848.2007. Epub 2007 Nov 21.
Cardiac output maintenance is so fundamental that, when regional systolic function is impaired, as during ischemia, nonischemic segments compensate by becoming hypercontractile. By analogy, diastolic compensatory mechanisms that maintain filling volume must exist but remain to be fully elucidated. Viewing filling in spatially distinct (longitudinal, radial) mechanistic terms facilitates elucidation of diastolic compensatory mechanisms. Because impairment of longitudinal (long axis) diastolic function (DF) in left ventricular hypertrophy (LVH) is established, we hypothesized that to maintain filling volume, radial (short-axis) filling function would compensate. In 20 normal left ventricular ejection fraction (LVEF) subjects (10 with LVH, 10 without LVH), we analyzed longitudinal function via Doppler tissue imaging of mitral annular motion and radial function as change in short-axis endocardial dimension via M-mode. The spatial (long axis, short axis) endocardial LV dimensions and their changes allowed assignment of E-wave filling volume into (cylindrical geometry-based) longitudinal and radial components. Despite indistinguishable (P = 0.70) E-wave velocity-time integrals (E-wave filling volume surrogate), systolic stroke volumes, and end-diastolic volumes in the LVH and control groups, longitudinal volume in absolute terms and the percent of E-wave volume accommodated longitudinally were reduced in the LVH group (P < 0.05 and P < 0.01, respectively), whereas the percent of E-wave volume accommodated radially was enhanced (P < 0.01). We conclude that, in normal LVEF (decreased longitudinal volume accommodation) LVH subjects vs. controls, spatially distinct compensatory mechanisms in diastole manifest as increased radial volume accommodation per unit of E-wave filling volume. Assessment of spatially distinct diastolic compensatory mechanisms in other pathophysiological subsets is warranted.
心输出量的维持至关重要，以至于当局部收缩功能受损时，比如在缺血期间，非缺血节段会通过变得过度收缩来进行代偿。同理，必然存在维持充盈量的舒张期代偿机制，但仍有待充分阐明。从空间上不同的（纵向、径向）机制角度看待充盈，有助于阐明舒张期代偿机制。由于左心室肥厚（LVH）时纵向（长轴）舒张功能（DF）受损已得到证实，我们推测为维持充盈量，径向（短轴）充盈功能会进行代偿。在20名左心室射血分数（LVEF）正常的受试者（10名有LVH，10名无LVH）中，我们通过二尖瓣环运动的多普勒组织成像分析纵向功能，并通过M型超声心动图分析径向功能，即短轴心内膜尺寸的变化。左心室心内膜的空间（长轴、短轴）尺寸及其变化，使得能够将E波充盈量分配为（基于圆柱几何形状的）纵向和径向分量。尽管LVH组和对照组的E波速度 - 时间积分（E波充盈量替代指标）、收缩期搏出量和舒张末期容积无显著差异（P = 0.70），但LVH组纵向容积的绝对值以及纵向容纳的E波容积百分比均降低（分别为P < 0.05和P < 0.01），而径向容纳的E波容积百分比则增加（P < 0.01）。我们得出结论，在正常LVEF（纵向容积容纳减少）的LVH受试者与对照组相比，舒张期空间上不同的代偿机制表现为每单位E波充盈量的径向容积容纳增加。有必要评估其他病理生理亚组中空间上不同的舒张期代偿机制。
