Abstract 4367288: Effect of Myocardial Scar Burden on Blood-Tissue Interaction in Chronic Myocardial Infarction

Abstract

Background: Hemodynamic force (HDF) analysis calculates intraventricular pressure gradients using blood volume geometry and velocity data derived from cardiac magnetic resonance (CMR). HDF analysis offers a comprehensive assessment of cardiac function by integrating myocardial contractility with blood flow dynamics. We aim to determine the relationship between scar burden (defined by late gadolinium enhancement [LGE]), HDF, and strain. We hypothesize that scar burden is inversely correlated with HDF, offering a novel, non-invasive approach to assess the effect of myocardial scar on blood–tissue interactions. Methods: 62 patients with stress cardiac Positron Emission Tomography (PET) underwent 3.0T CMR. 21 patients had fixed and 41 had reversible defects on PET. Patients with fixed PET defects underwent CMR with cine and late gadolinium enhancement imaging. Feature-tracking global longitudinal strain (GLS) and global circumferential strain (GCS) were derived from long- and short-axis (SAX) cine views, respectively. HDFs were calculated as root mean squares (RMS) in longitudinal (apical-basal, A-B) and transverse (lateral-septal, L-S) directions. Scar burden was quantified from LGE images using full width at half maximum (FWHM). Point-biserial Spearman correlations compared strain and HDF by scar presence. Spearman correlation matrices incorporated LGE extent, with scar burden (LGE) categorized as small (≤15% of myocardium) or large (>15%). Results: Patients with scar had reduced median GCS, GLS, A-B RMS, and L-S RMS compared to those without scar (Table 1). GLS was significantly associated with scar (p=0.02). Both GLS and A-B RMS were significantly different when comparing patients with large scar to no scar (both p-values < 0.05). There were moderate negative correlations and decreased median GLS (19.3% vs 13.5%, p=0.01) and A-B RMS (12.5% vs 9.2%, p=0.04) with scar burden (Fig 1). GCS was higher in the group with small scar (34.6% vs 27.0%, p=0.06). HDF and strain from two patients are shown in Fig 2. Conclusion: In patients with chronic ischemic heart disease, an inverse relationship between scar burden and HDF was associated with impaired mechanical function, supporting abnormal blood-tissue interactions. Our findings suggest a potential role for HDF in characterizing structure-function relationships. Further analysis is warranted in a larger population.