Relationship of Transmural Variations in Myofiber Contractility to Left Ventricular Ejection Fraction: Implications for Modeling Heart Failure Phenotype With Preserved Ejection Fraction

Figure 1. In normal conditions, contractility (Tmax) was uniform in all layers (scenario 1). To simulate no contraction in the subendocardial region, contractility in three layers in white was set to zero (scenario 2). The three layers in red were used to simulate alterations in subepicardial contractility (scenario 3). The three white layers, the two green layers, and the three red layers comprise subendocardial, midmyocardial, and subepicardial regions, respectively.

Figure 2. The passive material properties were determined such that the end diastolic pressure volume (ED PV) curve from finite element model was close to the experimental ED PV curve determined by Klotz et al. (2006).

Figure 3. The torsion of the LV was computed based on the apical and basal rotations, the apical and basal radius, and the distance between the apex and base. The formula used to compute the LV torsion (Equation 4) makes the LV torsion comparable for hearts of different sizes (Aelen et al., 1997; Rüssel et al., 2009). The positive rotation is counterclockwise when seen from apex.

Figure 4. When the subendocardial contractility was zero, EF reduced by 23.9% relative to scenario 1 (scenarios 1 and 2). Increased subepicardial contractility recovered EF to scenario 1 (scenarios 1 and 3).

Figure 5. A long-axis view showing that at end systole, with uniform Tmax (scenario 1), all layers experienced compressive strain in myofiber directions. When subendocardial contractility was zero, the strain pattern was altered (scenarios 1 and 2), but it partially recovered when subepicardial contractility increased (scenarios 1 and 3).

Figure 6. A short-axis view showing that the ES myofiber strain pattern altered when subendocardial contractility was zero (scenarios 1 and 2), but a partial recovery in strain pattern was observed when subepicardial contractility increased (scenarios 1 and 3).

Figure 7. The ES myofiber strain at various points along LV thickness. In the horizontal axis, 0% represents the endocardium and100% represents the epicardium. The alterations in strains in scenario 2 are noticeable, compared to scenario 1. In scenario 3, the tensile strains decreased compared to scenario 2.

Figure 8. A long-axis view showing the ES myofiber compressive stress decreased when the subendocardial contractility was zero (scenarios 1 and 2). The stress pattern became partially similar to the normal case when subepicardial contractility increased (scenarios 1 and 3).

Figure 9. The ES longitudinal deformation was altered when subendocardial contractility was zero (scenarios 1 and 2). Deformation partially recovered when subepicardial contractility increased (scenarios 1 and 3).