Abstract Body: Introduction. Partial or complete blockage of the coronary arteries leads to cardiomyocyte death, known as myocardial infarction (MI). MI causes the formation of a fibrotic scar, impairing the mechanical behavior of the left ventricular (LV) free wall (LVFW) tissue. The fibrotic scar is expected to subdue viscoelastic behavior in the LVFW; however, the dependence of LVFW viscoelasticity on diastolic stretching remains unexplored. Our objective in this study was to determine the dependence of LVFW stress relaxation behavior on the initial tissue stretch in MI.

Methods. The LAD artery of WKY rats was ligated to induce MI, and hearts were harvested at three timepoints: sham, 2-week (2wk), and 4wk post-MI (n=3 for each group). Echocardiography was performed prior to sacrifice to estimate the change in ejection fraction (EF) relative to EF prior to ligation. LVFW specimens were isolated and used to perform viscoelastic stress relaxation tests. The specimens were stretched to 3, 6, and 9% along the circumferential and longitudinal directions and allowed to relax. The stress was normalized against the peak (initial) stress for each specimen for proper comparison across the groups.

Results. There was a substantial loss of EF at 2wk and 4wk specimens compared to the sham specimens (Fig. 1A). In contrast to the stress relaxation behavior for the sham and 2wk specimens, the 4wk post-MI specimens showed a faster relaxation relaxing from 3% stretch (Fig. 1B), and nearly elastic behavior when the initial stretch was set to 6 and 9% (Figs. 1C, D). The relaxation times suggested that the viscoelastic response was dependent on the initial stretch in the sham and 2wk timepoints while the stretch-dependency was diminished at 4wk timepoint (Fig. 1E).

Conclusions. Our results suggested that the healthy LVFW is strongly viscoelastic, and its viscous behavior is enhanced by increased initial (diastolic) stretch, whereas the late-stage MI myocardium tends to exhibit a nearly elastic behavior independent of diastolic stretching. This behavior in late-stage-MI can be attributed to significant compositional and structural alterations, particularly the expected presence of a mature fibrotic scar. Future studies will aim to determine the effects of such viscoelastic remodeling events on LV diastolic dysfunction in MI.