First evidence of depressed contractility in the border zone of a human myocardial infarction

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Figure 1

(a) Short axis view from 3D CSPAMM image of patient LV, with the posterior retion circled in blue, and (b) FE model that was reconstructed from the MR images, showing the remote (red), borderzone (green), and infarct (tan) regions.

Figure 2

Convergence plots of (a) T_{max_R} and (b) T_{max_B} during the numerical optimization process. Note that the solution was stable after roughly 10 iterations.

Figure 3

End-systolic myofiber strain distribution. (a) View of epicardial surface with infarct and borderzone outlined, (b) interior view of posterior endocardial wall with infarct and borderzone outlined, (c) mid-ventricular slice through remote, borderzone, and infarct. Note the elevated strain in the borderzone.