Improved Strain Analysis of Left Ventricular Function Post Myocardial Infarction in Mice

Abstract

A myocardial infarction (MI), caused by an arterial blockage preventing blood from flowing to a part of the heart, restricts tissue oxygenation and results cell death and myocardial tissue damage. This compromises contractility, resulting either in sudden death, or ventricular remodeling and eventually heart failure. Echocardiography is the standard, non-invasive cardiac imaging technique for humans and small animals. The standard measurements obtained from M-mode echocardiography to assess left ventricle (LV) function lack the sensitivity to detect subtle changes in regional LV performance at the early stages of disease. Speckle tracking techniques in conjunction with strain analysis overcome this issue by tracking the movement of the myocardium across 6 transverse segments of the LV. Analysis of strain in more regions of the heart from the apex (bottom) to base (top) would reveal earlier, localized detection of LV dysfunction. The purpose of this study is to develop a methodology to improve regional specificity in the analysis of strain and strain rate (SR) relative to the site of injury in mouse hearts in 12 equal segments along the myocardium and compare these results to the VevoStrain software (VisualSonics) strain values. Echocardiographic images obtained from the Vevo 3100 (VisualSonics) ultrasound in uninjured hearts or after acute ischemia/reperfusion (30minI/24hr R) injury induced by ligation of the left anterior descending coronary artery were analyzed using MATLAB (MathWorks). To quantify strain, the motion of the speckles was tracked between the epicardium and endocardium for 3 consecutive cardiac cycles. Perpendicular lines were generated connecting these contours. Displacement of these lines were calculated from the starting location to end location to calculate strain. The LV was divided into 12 equal segments. The peak % strain values across the region of interest were averaged for the 12 segments to obtain global strain measurements. To measure SR, the change in strain was divided by the time between frames. The novel strain analysis was compared to the VevoStrain software data to validate the results. These values were used to measure the contractile function of the LV between sham, MI, and MI+ephrinA1-Fc mice. Feasibility of the proposed algorithm has been demonstrated, but due to some limitations, more work is needed to improve this method. With further work, this method could optimize the treatment process by determining the location being treated and extent of treatment to the infarct and remote regions of the heart.