Myocardial Function Abnormalities in Obesity: Assessment Via Standard Doppler Indices, Myocardial Speckle-Tracking and Kinematic Modeling of Early Diastolic Filling

Background: Obesity is an established risk factor for heart failure. We aimed to comprehensively characterize early subclinical obesity-related abnormalities in diastolic and systolic function in a large general population sample. Methods: We studied 1,603 middle-aged adults enrolled in the Asklepios study. We assessed standard Doppler indices of diastolic function, speckle-tracking echocardiography-derived myocardial systolic deformation and parameters describing the elastic recoil-driven early diastolic suction attribute of the left ventricle (LV), obtained via kinematic modeling of early mitral inflow. All models were adjusted for, age, gender and LV size. Results: Speckle tracking echocardiography revealed decreased longitudinal peak systolic strain in obesity (-17.3; 95%CI=-17. 7 to -16.8; P=0.001), with preserved circumferential strain (P=0.35). Obesity was also independently associated with lower stored elastic strain energy (9013 vs. 10695 m 2 /s 2 ; P<0.0001) available at mitral valve opening, resulting in a lower peak force driving early diastolic filling (1824 vs. 2013 m/s2; P<0.001). Despite exhibiting a lower early diastolic mitral annular tissue velocity (8.32 vs. 9.6 cm/s; P<0.001), obese subjects demonstrated a significantly greater early diastolic mitral inflow propagation velocity (81.5 vs. 73.8 cm/s; P<0.001) and a lower damping constant c (15.1 vs. 16.7 /s; P<0.01), which represents the dampening effects of slow LV relaxation and increased tissue viscoelasticity preventing rapid LV filling). Conclusions: Our results suggest that the main abnormality underlying abnormal early diastolic LV filling in obesity is a reduced stored elastic strain / potential energy during systolic contraction, leading to decreased mechanical recoil during early diastole. This may be related to loss of longitudinal (but not circumferential) systolic function. Our findings have implications for our understanding the underlying mechanisms of obesity-related LV dysfunction.