Abstract
Introduction: Myocardial infarction (MI) leads to myofiber death and the formation of a fibrotic scar in the left ventricular free wall (LVFW) myocardium. Acute MI induces remodeling events in the LV consisting of alterations in the architecture and biomechanical properties of the LVFW, collectively leading to LV systolic dysfunction. We implemented a multi-modality pipeline bridging architectural remodeling, LVFW passive behavior adaptation, and ventricular dysfunction in MI. We hypothesize that biomechanical remodeling of the LV serves as an important predictor of clinical outcomes in MI. Methods: MI was induced in rats via the ligation of the LAD artery, and hearts were harvested at five time points: pre-MI, and 1-wk to 4-wk post-MI (n=6 for each time point). Echocardiography and terminal LV catheterization were performed. LVFW specimens were harvested and subjected to biaxial testing, followed by picrosirius red staining. Histological slides were analyzed to quantify fiber architecture. Results: Comparisons for 3-wk MI versus control groups are reported (animal-specific results for representative rats are shown in Fig. 1). Echocardiography imaging showed a decrease in EF (84±5 vs 73±10%; p=0.053) and a decrease in ESV (0.122±0.045 vs 0.31±0.195ml; p=0.013). LV catheterization revealed a decrease in SV (50±0.86 vs 10±0.38μL; p<0.001) and an increase in peak systolic pressure (36.62±0.87 vs 44.91±0.99 mmHg; p<0.001), indicating systolic dysfunction. Biaxial testing revealed longitudinal stiffening of the LVFW at 3-wk post-MI. Scarring and a shift in myofiber orientation towards the longitudinal direction corroborated changes in the LVFW mechanical behavior in the MI group. Conclusions: LV systolic dysfunction in MI is significantly influenced by disruption in myofiber architecture and fiber orientation remodeling in the LVFW. Assessment of LVFW remodeling events provides important incremental information over traditional organ-level indices.
Published Version
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