Abstract 10265: Association of Myocardial Mechanical Markers of Extracellular Volume Expansion With Heart Failure and All-Cause Mortality: The Multi-Ethnic Study of Atherosclerosis

Abstract

Introduction: Characteristic myocardial deformation indices have been proposed to be associated with extracellular volume (ECV) expansion and differentiate cardiac pathologies that induce cardiac remodeling. Hypothesis: Our hypothesis was that such mechanical markers are associated with (1) pathologic ECV expansion and cardiac remodeling and (2) clinical outcomes of heart failure and mortality. Methods: Our analysis included 2778 participants who underwent cardiac MRI at the Multi-Ethnic Study of Atherosclerosis Exam 5 (2010-2012). The following deformation indices were calculated: relative apical strain ratio (RAS), septal apical basal ratio (SAB) and ejection fraction circumferential strain ratios (EFSR). We used linear regression to analyze the associations of these deformation indices with cardiac remodeling and ECV expansion. We used Cox proportional models to investigate the associations of mechanical deformation indices with incident HF and all-cause mortality. Results: The mean (SD) age of the cohort at Exam 5 was 69.1 (9.3) years; 53% were female. MRI tagging and T1 mapping analyses showed that higher levels of EFSR were associated with 0.2% greater ECV and 4.4ms higher native T1. In addition, EFSR was associated with 3.59ml lower LV end-diastolic volume, 1.98g higher LV mass and 0.13 ⃘ higher torsion. EFSR was associated with greater LA volume, decreased total emptying fraction and reduced maximal strain (Table 1). During a follow-up period of 7.5 years (Figure 1), there were 101 incident heart failure events, and 228 all-cause deaths. In the multivariable cox regression analysis, hazard ratios (95% CI) of incident HF and all-cause mortality for each unit increase of EFSR were 1.36 (1.04,1.78) and 1.31 (1.05,1.64) (Table 2), respectively. Conclusion: Mechanical markers of extracellular expansion are associated with adverse cardiac remodeling, incident HF and all-cause mortality.