Effect of adjustable passive constraint on the failing left ventricle: a finite-element model study

Abstract

Background: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

Figure 1

(A) 3-dimensional finite element mesh of the unloaded dilated canine LV, 16x5x1 (longitudinal x transmural x circumferential), (B) cut away view of the interior cavity and wall cross-section.

Figure 2

Epicardial pressure loading profile; P = 3, 5, 7, and 9 mmHg (Time points for ED and ES are not drawn to scale).

Figure 3

The effect of constraint on end-diastolic compliance; at baseline, 3, 5, 7, and 9 mmHg of constraint. The compliance is shifted to the left as the level of passive constraint increases.

Figure 4

The effect of adjustable passive constraint on the stroke volume/end-diastolic pressure (Starlings) relationship at baseline, 3, 5, 7, and 9 mmHg of constraint.

Figure 5

Mean volume weighted end-diastolic fiber stress; as the level of passive constraint increases. Fiber stress at end-diastole was reduced by 18.3% (Inner wall), 15.3% (Mid wall), and 14.2% (Outer wall) at a constraint level of 2.3 mmHg.

Figure 6

Relationship between stroke volume at initial end-diastolic pressure (17 mm Hg). Note that any amount of constraint is associated with a reduction in stroke volume. A line of 10% reduction in stroke volume occurs at 2.3 mmHg.