Abstract Body (Do not enter title and authors here): Background:
The progression of CHF after MI has been traditionally evaluated by serial changes in EF. However, mechanical parameters can provide a greater insight into cardiac function. Wall strain measures myocardial deformation, and reflects contractile function as a percentage change in length. Wall stress represents the force per unit area on the myocardium, as an evaluation of LV afterload. The relationship between wall stress and wall strain is termed Young’s modulus, and it represents cardiac elasticity. This study leverages in-vivo Young’s modulus analysis derived from cardiac MRI, which has the potential to quantify the extent of myocardial remodeling, and aid in early detection of heart failure progression.

Hypothesis:
We hypothesize that Young’s modulus offers a more detailed assessment of regional wall motion abnormality than conventional imaging measures alone.

Methods:
Male Yucatan mini-swine underwent 90-minute balloon occlusion-reperfusion of the left anterior descending coronary artery to induce MI (N=13). Cardiac MRIs were obtained at baseline and 1-month post-MI. Cardiac wall stress and wall strain were calculated separately in the anteroseptal (infarcted) and inferolateral (non-infarcted) regions, and in the longitudinal and circumferential fiber orientations. These measurements were correlated to determine the Young’s modulus of the LV.

Results:
Anteroseptal and inferolateral longitudinal Young’s modulus increased from 28.01±8.14 to 67.14±15.08 kPa (p < 0.05) from 13.88±1.92 to 38.80±7.29 kPa (p < 0.001), respectively. Anteroseptal and inferolateral circumferential Young’s modulus increased from 34.61±10.33 to 119.17±30.94 kPa (p < 0.05) and from 16.77±1.32 to 58.76±18.98 kPa (p < 0.001), respectively. The regional changes were accompanied by a decrease in EF from 60.6±1.5 to 50.9±3.3% (p < 0.01).

Discussion:
Our findings show that Young’s modulus is a valuable parameter in quantifying regional changes that occur with LV systolic dysfunction after ischemic insult; specifically that regional abnormalities occur in the non-infarcted area as well as the infarcted area––a change that would not be picked up by global LV EF. Thus, quantifying regional and directional cardiac elasticity non-invasively is a novel parameter that warrants further study. Prior research has explored the in-vitro characteristics of cardiac elasticity, but there is limited research that details the in-vivo changes within any disease affecting myocardial fiber contractility.