First Evidence of Depressed Contractility in the Border Zone of a Human Myocardial Infarction

Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California, United States
The Annals of thoracic surgery (Impact Factor: 3.85). 02/2012; 93(4):1188-93. DOI: 10.1016/j.athoracsur.2011.12.066
Source: PubMed


The temporal progression in extent and severity of regional myofiber contractile dysfunction in normally perfused border zone (BZ) myocardium adjacent to a myocardial infarction (MI) has been shown to be an important pathophysiologic feature of the adverse remodeling process in large animal models. We sought, for the first time, to document the presence of impaired contractility of the myofibers in the human BZ myocardium.
A 62-year-old man who experienced an MI in 1985 and had recently had complete revascularization was studied. Myofiber systolic contractile stress developed in the normally perfused BZ adjacent to the MI (T(max_B)) and that developed in regions remote from the MI (T(max_R)) were quantified using cardiac catheterization, magnetic resonance imaging, and mathematical modeling.
The resulting finite element model of the patient's beating left ventricle was able to simulate the reduced systolic strains measured using magnetic resonance imaging at matching left ventricular pressures and volumes. The T(max_B) (73.1 kPa) was found to be greatly reduced relative to T(max_R) (109.5 kPa). These results were found to be independent of assumptions relating to BZ myofiber orientation.
The results of this study document the presence of impaired contractility of the myofibers in the BZ myocardium and support its role in the post-MI remodeling process in patients. To fully establish this important conclusion serial evaluations beginning at the time of the index MI will need to be performed in a cohort of patients. The current study supports the importance and demonstrates the feasibility of larger and longer-term studies.

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    • "Fortunately, ex vivo biaxial tissue testing is not required to quantify in vivo regional contractilities for the case of a posterobasal or posterolateral MI because the thickness of the infarcted wall segment is at least 50% of normal [3] [6] [13]. In the previous studies [3] [6] [13], we could measure 3D myocardial strain in the MI. In all three of those studies, however, it was not necessary to use a nonzero T max value in the MI for the LV finiteelement models to predict strain fields as measured with tagged MRI. "
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    • "The material passive stiffness (C) and the tissue contractility (T max ) were chosen so that the predicted LV volumes (without injection) matched the corresponding EDV (197 ml) and ESV (122 ml) measured from the MR images. All other parameters had values equal to those used in large animal studies (Sun et al., 2009) and human study (Wenk et al., 2012). "
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    • "Fig. 4 Cyclical loading in the ELLISPOID and HUMAN models consisting of five high pressure cycles and five low pressure cycles. Every growth step lasts one characteristic time of the growth model which correspond to the values defined in the human modeling study by Wenk et al. (2012). For the growth parameters, we chose τ g = τ rg = 1 s and γ g = γ rg = 1. "
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