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


Wenk, Jonathan F; Klepach, Doron; Lee, Lik Chuan; Zhang, Zhihong; Ge, Liang; Tseng, Elaine E; Martin, Alastair; Kozerke, Sebastian; Gorman, Joseph H; Gorman, Robert C; Guccione, Julius M (2012). First evidence of depressed contractility in the border zone of a human myocardial infarction. The Annals of Thoracic Surgery, 93(4):1188-1193.

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 (Tmax_B) and that developed in regions remote from the MI (Tmax_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 Tmax_B (73.1 kPa) was found to be greatly reduced relative to Tmax_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.

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 (Tmax_B) and that developed in regions remote from the MI (Tmax_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 Tmax_B (73.1 kPa) was found to be greatly reduced relative to Tmax_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.

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17 citations in Web of Science®
16 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Biomedical Engineering
Dewey Decimal Classification:170 Ethics
610 Medicine & health
Language:English
Date:2012
Deposited On:14 Feb 2013 09:48
Last Modified:05 Apr 2016 16:26
Publisher:Elsevier
ISSN:0003-4975
Publisher DOI:https://doi.org/10.1016/j.athoracsur.2011.12.066
Permanent URL: https://doi.org/10.5167/uzh-72389

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