Department of Surgery, University of California, San Francisco, California, USA.
Ann Thorac Surg. 2010 Jan;89(1):132-7. doi: 10.1016/j.athoracsur.2009.08.075.
Passive constraint is used to prevent left ventricular dilation and subsequent remodeling. However, there has been concern about the effect of passive constraint on diastolic left ventricular chamber stiffness and pump function. This study determined the relationship between constraint, diastolic wall stress, chamber stiffness, and pump function. We tested the hypothesis that passive constraint at 3 mm Hg reduces wall stress with minimal change in pump function.
A three-dimensional finite-element model of the globally dilated left ventricle based on left ventricular dimensions obtained in dogs that had undergone serial intracoronary microsphere injection was created. The model was adjusted to match experimentally observed end-diastolic left ventricular volume and midventricular wall thickness. The experimental results used to create the model were previously reported. A pressure of 3, 5, 7, and 9 mm Hg was applied to the epicardium. Fiber stress, end-diastolic pressure-volume relationship, end-systolic pressure-volume relationship, and the stroke volume-end-diastolic pressure (Starling) relationship were calculated.
As epicardial constraint pressure increased, fiber stress decreased, the end-diastolic pressure-volume relationship shifted to the left, and the Starling relationship shifted down and to the right. The end-systolic pressure-volume relationship did not change. A constraining pressure of 2.3 mm Hg was associated with a 10% reduction in stroke volume, and mean end-diastolic fiber stress was reduced by 18.3% (inner wall), 15.3% (mid wall), and 14.2% (outer wall).
Both stress and cardiac output decrease in a linear fashion as the amount of passive constraint is increased. If the reduction in cardiac output is to be less than 10%, passive constraint should not exceed 2.3 mm Hg. On the other hand, this amount of constraint may be sufficient to reverse eccentric hypertrophy after myocardial infarction.
被动约束用于防止左心室扩张和随后的重塑。然而，人们一直担心被动约束对舒张左心室腔刚度和泵功能的影响。本研究旨在确定约束、舒张壁应力、腔刚度和泵功能之间的关系。我们检验了这样一个假设，即在 3mmHg 的被动约束下，舒张壁应力减小，而泵功能几乎没有变化。
根据在接受连续冠状动脉微球注射的犬中获得的左心室尺寸，创建了一个基于整体扩张的左心室的三维有限元模型。该模型被调整以匹配实验中观察到的舒张末期左心室容积和中室壁厚度。用于创建模型的实验结果先前已有报道。将 3、5、7 和 9mmHg 的压力施加到心外膜。计算纤维应力、舒张末期压力-容积关系、收缩末期压力-容积关系以及每搏量-舒张末期压力（Starling）关系。
随着心外膜约束压力的增加，纤维应力降低，舒张末期压力-容积关系向左移位，Starling 关系向下和向右移位。收缩末期压力-容积关系没有改变。约束压力为 2.3mmHg 时，每搏量减少 10%，平均舒张期纤维应力降低 18.3%（内室壁）、15.3%（中室壁）和 14.2%（外室壁）。
随着被动约束量的增加，应力和心输出量呈线性下降。如果要将心输出量的减少量控制在 10%以内，则不应超过 2.3mmHg 的被动约束量。另一方面，这种程度的约束可能足以在心肌梗死后逆转离心性肥厚。
