Acharya, Tushar

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.

Background: Normative changes in right ventricular (RV) structure and function have not been characterized in the context of treatment-associated functional recovery (RV functional recovery [RVFnRec]). The aim of this study is to assess the clinical relevance of a proposed RVFnRec definition. Methods: We evaluated 63 incident patients with pulmonary arterial hypertension by right heart catheterization and cardiac magnetic resonance imaging at diagnosis and cardiac magnetic resonance imaging and invasive cardiopulmonary exercise testing following treatment (≈11 months). Sex, age, ethnicity matched healthy control subjects (n=62) with 1-time cardiac magnetic resonance imaging and noninvasive cardiopulmonary exercise testing were recruited from the PVDOMICS (Redefining Pulmonary Hypertension through Pulmonary Vascular Disease Phenomics) project. We examined therapeutic cardiac magnetic resonance imaging changes relative to the evidence-based peak oxygen consumption (VO 2peak )>15 mL/(kg·min) to define RVFnRec by receiver operating curve analysis. Afterload was measured as mean pulmonary artery pressure, resistance, compliance, and elastance. Results: A drop in RV end-diastolic volume of −15 mL best defined RVFnRec (area under the curve, 0.87; P =0.0001) and neared upper 95% CI RV end-diastolic volume of controls. This cutoff was met by 22 out of 63 (35%) patients which was reinforced by freedom from clinical worsening, RVFnRec 1 out of 21 (5%) versus no RVFnRec 17 out of 42, 40% (log-rank P =0.006). A therapy-associated increase of 0.8 mL/mm Hg in compliance had the best predictive value of RVFnRec (area under the curve, 0.76; [95% CI, 0.64–0.88]; P =0.001). RVFnRec patients had greater increases in stroke volume, and cardiac output at exercise. Conclusions: RVFnRec defined by RV end-diastolic volume therapeutic decrease of −15 mL predicts exercise capacity, freedom from clinical worsening, and nears normalization. A therapeutic improvement of compliance is superior to other measures of afterload in predicting RVFnRec. RVFnRec is also associated with increased RV output reserve at exercise.