Journal
JOURNAL OF THE MECHANICAL BEHAVIOR OF BIOMEDICAL MATERIALS
Volume 8, Issue -, Pages 165-177Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jmbbm.2011.12.006
Keywords
Biomechanics; Infarct; Heart failure; Growth; Remodeling; Strain
Funding
- US National Institutes of Health [R01 HL 29589, R01 HL67025]
- US National Science Foundation [CMMI-0952921]
- Swiss National Science Foundation [PBELP2-130913]
- Div Of Civil, Mechanical, & Manufact Inn
- Directorate For Engineering [0952021] Funding Source: National Science Foundation
- Swiss National Science Foundation (SNF) [PBELP2-130913] Funding Source: Swiss National Science Foundation (SNF)
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Progressive growth and remodeling of the left ventricle are part of the natural history of chronic heart failure and strong clinical indicators for survival. Accompanied by changes in cardiac form and function, they manifest themselves in alterations of cardiac strains, fiber stretches, and muscle volume. Recent attempts to shed light on the mechanistic origin of heart failure utilize continuum theories of growth to predict the maladaptation of the heart in response to pressure or volume overload. However, despite a general consensus on the representation of growth through a second order tensor, the precise format of this growth tensor remains unknown. Here we show that infarct-induced cardiac dilation is associated with a chronic longitudinal growth, accompanied by a chronic thinning of the ventricular wall. In controlled in vivo experiments throughout a period of seven weeks, we found that the lateral left ventricular wall adjacent to the infarct grows longitudinally by more than 10%, thins by more than 25%, lengthens in fiber direction by more than 5%, and decreases its volume by more than 15%. Our results illustrate how a local loss of blood supply induces chronic alterations in structure and function in adjacent regions of the ventricular wall. We anticipate our findings to be the starting point for a series of in vivo studies to calibrate and validate constitutive models for cardiac growth. Ultimately, these models could be useful to guide the design of novel therapies, which allow us to control the progression of heart failure. (C) 2011 Elsevier Ltd. All rights reserved.
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