Moustakidis Pavlos, Maniar Hersh S, Cupps Brian P, Absi Tarek, Zheng Jie, Guccione Julius M, Sundt Thoralf M, Pasque Michael K
Department of Surgery, Division of Cardiothoracic Surgery, Washington University, St. Louis, Mo, USA.
Circulation. 2002 Sep 24;106(12 Suppl 1):I168-75.
Left ventricular aneurysm (LVA) is a significant complication of myocardial infarction that may lead to global left ventricular (LV) dysfunction. However, the exact mechanism underlying the abnormal function has not been elucidated. In this study we tested the hypothesis that changes in LV geometry cause both an increase in wall stress and a change in the temporal distribution of stress in the LVA border zone (BZ) during systole.
Transmural anteroapical infarcts were created in adult Dorsett sheep (n=8) and were allowed to mature into LVAs for 10 weeks. Animals were imaged subsequently using MRI with simultaneous recording of intraventricular pressures. Cardiac models were constructed from the MRI images at end-diastole, isovolumic systole, peak-systole and end-systole. Two short-axis slices, 1 basal and 1 apical were analyzed. The apical slice included the septal and anterior component of the aneurysm as well as the corresponding BZs and normal myocardium. Regional wall stresses were calculated using finite element analysis and compared with stresses in corresponding regions from normal control sheep (n=7).
In the LVA group, stress was significantly increased in the BZ at the end-diastolic, isovolumic, peak-systolic, and end-systolic instants (P<0.001 for all). In addition the temporal distribution of stress was significantly altered with maximum stress occurring at peak instead of isovolumic systole.
Geometric changes in the LVA hearts increased wall stress and altered its temporal distribution in the BZ region. Correlation of this finding with the corresponding regional blood flow, oxygen consumption, and mechanical systolic performance may help elucidate the mechanism underlying the observed global LV dysfunction.
左心室室壁瘤（LVA）是心肌梗死的一种严重并发症，可能导致左心室（LV）整体功能障碍。然而，功能异常背后的确切机制尚未阐明。在本研究中，我们检验了这样一个假设，即左心室几何形状的改变会导致收缩期左心室室壁瘤边缘区（BZ）壁应力增加以及应力的时间分布改变。
在成年多塞特羊（n = 8）中制造透壁性前尖部梗死，并使其发展为左心室室壁瘤达10周。随后使用磁共振成像（MRI）对动物进行成像，并同步记录心室内压力。从舒张末期、等容收缩期、收缩期峰值和收缩期末期的MRI图像构建心脏模型。分析两个短轴切片，一个为基底部，一个为尖部。尖部切片包括室壁瘤的间隔和前部成分以及相应的边缘区和正常心肌。使用有限元分析计算局部壁应力，并与正常对照羊（n = 7）相应区域的应力进行比较。
在左心室室壁瘤组中，舒张末期、等容收缩期、收缩期峰值和收缩期末期边缘区的应力均显著增加（所有P < 0.001）。此外，应力的时间分布发生了显著改变，最大应力出现在收缩期峰值而非等容收缩期。
左心室室壁瘤心脏的几何形状改变增加了壁应力，并改变了边缘区壁应力的时间分布。将这一发现与相应区域的血流、氧消耗和机械收缩性能相关联，可能有助于阐明观察到的左心室整体功能障碍的潜在机制。
