ArticleScientific reports2026
Changes in myocardial elasticity derived from in-vivo cardiac MRI in a swine model of ischemic heart failure.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The progression of chronic heart failure after myocardial infarction (MI) is traditionally evaluated by serial changes in left ventricular (LV) ejection fraction (EF), a measure of systolic function. Our study evaluated how a combined wall stress and wall strain analysis of myocardial elasticity (secant modulus) offers a more complete assessment of myocardial changes that occur after MI. Using a clinically relevant ischemic swine model, we calculated secant modulus in-vivo from cardiac magnetic resonance imaging (MRI), to better understand changes in cardiac remodeling and to identify potential early detection markers. Male Yucatan mini swine (N = 15) underwent 90-min occlusion-reperfusion of the left anterior descending coronary artery to induce MI. Cardiac MRIs were obtained at baseline (before MI) and 1-month post-MI. Secant modulus was calculated in the anteroseptal (infarcted) and inferolateral (non-infarcted) regions, in the longitudinal and circumferential fiber directions. This method applied both strain and stress, the latter utilizing invasive hemodynamic LV pressure data acquired prior to MRIs. Anteroseptal and inferolateral longitudinal secant modulus increased from 28.01 ± 8.14 to 67.14 ± 15.08 kPa (p < 0.05) and from 13.88 ± 1.92 to 38.80 ± 7.29 kPa (p < 0.001), respectively. Anteroseptal and inferolateral circumferential secant 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 with a decrease in EF from 60.6 ± 1.5 to 50.9 ± 3.3% (p < 0.01). Secant modulus has value in quantifying regional changes with LV dysfunction after ischemic insult; specifically, that regional abnormalities in elasticity occur in non-infarcted and infarcted areas. Although prior research has explored the ex-vivo characteristics of cardiac elasticity, there is limited research detailing in-vivo changes associated with diseases affecting myocardial fiber contractility. A better understanding of how the elasticity of the non-infarcted myocardium is adversely affected in-vivo may offer future opportunities for therapies preventing heart failure progression.
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