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Residual strain in ischemic ventricular myocardium.
S R Summerour1, J L Emery, B Fazeli
1Department of Bioengineering, Institute of Biomedical Engineering, University of California, San Diego, La Jolla 92093-0412, USA.
Journal of Biomechanical Engineering
|July 21, 1999
Summary
Acute myocardial infarction significantly alters left ventricular residual strain, indicated by increased opening angles in rat hearts. This change is not due to collagen content or overstretch-induced softening.
Area of Science:
- Cardiovascular Physiology
- Myocardial Infarction Research
- Biomechanical Analysis
Background:
- Acute myocardial infarction (AMI) causes structural remodeling, impacting ventricular wall stress and strain.
- Understanding changes in residual stress and strain in the left ventricle (LV) is crucial for comprehending cardiac function post-infarction.
Purpose of the Study:
- To investigate whether acute myocardial infarction alters residual stress and strain in the left ventricle.
- To explore the relationship between altered residual strain and potential mechanisms like strain softening due to systolic overstretch.
Main Methods:
- Measurement of opening angles in rat hearts subjected to 30 minutes of left coronary artery occlusion (ischemia).
- Assessment of opening angles in isolated hearts passively inflated to high LV pressures to induce strain softening.
- Quantification of mean collagen area fractions in the myocardium of ischemic and control groups.
Main Results:
- Hearts with ischemia exhibited significantly greater mean opening angles (51 +/- 20 deg) compared to sham-operated controls (29 +/- 11 deg).
- Strain-softened hearts showed no significant difference in mean opening angles compared to controls (34 +/- 27 deg).
- Myocardial collagen area fractions were not significantly different between ischemic and non-ischemic groups.
Conclusions:
- Acute ischemia leads to significant alterations in left ventricular residual strain, evidenced by changes in opening angles.
- These alterations do not appear to stem from changes in extracellular collagen content or strain softening associated with overstretch.
- The observed changes in residual strain may be linked to modifications in collagen fiber structure, myocyte structure, or the metabolic state of the myocardium.