Relationship of Multidirectional Myocardial Strain with Radial Thickening and Ejection Fraction and Impact of Left Ventricular Hypertrophy. A Study in a Community-Based Cohort

In clinical practice, left ventricular (LV) systolic function is commonly measured at the endocardial level (LV chamber function), and is usually assessed by echocardiographically determined ejection fraction (LVEF). The analysis of LV wall motion, which is often performed by visual estimation of systolic myocardial thickening, is also a widely used method for assessing LV systolic function.1,2 More recently, speckle-tracking echocardiography has made possible the non-invasive assessment of myocardial deformation (strain) over different spatial axes.3,4 Myocardial strain analysis has provided new insights in the understanding of LV mechanics far beyond the information provided by LVEF. Past studies showed that, even in the presence of a normal LVEF, LV strain may be selectively affected in the longitudinal or circumferential direction depending on the pathophysiology and the extension of the damage to the myocardial wall.5–7 Furthermore, the analysis of LV myocardial strain appears to carry prognostic value that is greater than, and additional to, the traditional LV systolic function evaluation by LVEF and wall motion analysis.8 In previous studies including a wide range of LV conditions, from normal to ischemic heart disease and heart failure, good correlations were found between LVEF and LV longitudinal strain,1,9 to the point that the latter has been proposed as an alternative method to quantify global LVEF.10 However, theoretical considerations and the evidence of the additional prognostic value of longitudinal strain over LVEF, along with its ability to uncover systolic dysfunction when LVEF is still normal, are reasons to believe that these two parameters express different aspects of LV function and should not be considered as equivalent.11,12 LVEF and LV wall thickening are, in fact, the final result of the contraction of a complex system of fibers in the myocardial wall,13 in which the subendocardial and subepicardial fibers have prevalent longitudinal direction and are arranged in counter-directional helical loops, and the midwall fibers have prevalent circumferential orientation.14 This architectural structure determines the systolic longitudinal shortening and torsion of the LV, and the thickening of the myocardium in the radial direction, which in turn causes the shift of the endocardium towards the LV cavity.15,16 Since the relationships of longitudinal and circumferential LV wall systolic components with radial thickening and LVEF have not been completely characterized especially in unselected populations without overt cardiac disease, we aimed at analyzing the association of the longitudinal and circumferential components of LV wall systolic function with LV radial thickening and global LVEF in participants from a community-based cohort study. Furthermore, we evaluated the impact of LV hypertrophy on these associations. The study of these relationships would provide a better understanding of LV mechanics and potentially clarify the basis for the additional prognostic information provided by the multidirectional assessment of myocardial deformation over the assessment of wall motion and global LVEF.