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a Department of Surgery, University of California, San Francisco, California
b Department of Bioengineering, University of California, San Francisco, California
c Department of Veterans Affairs Medical Center, San Francisco, California
d Henry Ford Hospital, Detroit, Michigan
Accepted for publication August 31, 2009.
* Address correspondence to Dr Ratcliffe, Surgical Service (112), San Francisco Veterans Affairs Medical Center, 4150 Clement St, San Francisco, CA 94121 (Email: mark.ratcliffe{at}va.gov).
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.
Related Article
Ann. Thorac. Surg. 2010 89: 137-138.
This article has been cited by other articles:
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  S. T. Wall, J. M. Guccione, M. B. Ratcliffe, and J. S. Sundnes Electromechanical feedback with reduced cellular connectivity alters electrical activity in an infarct injured left ventricle: a finite element model study Am J Physiol Heart Circ Physiol, January 1, 2012; 302(1): H206 - H214. [Abstract] [Full Text] [PDF]
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 J. A. Dixon, A. M. Goodman, W. F. Gaillard II, W. T. Rivers, R. A. McKinney, R. Mukherjee, N. L. Baker, J. S. Ikonomidis, and F. G. Spinale Hemodynamics and myocardial blood flow patterns after placement of a cardiac passive restraint device in a model of dilated cardiomyopathy J. Thorac. Cardiovasc. Surg., November 1, 2011; 142(5): 1038 - 1045. [Abstract] [Full Text] [PDF]
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 R. Mukherjee Invited Commentary Ann. Thorac. Surg., January 1, 2010; 89(1): 137 - 138. [Full Text] [PDF]
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