Wall thickness referenced to myocardial volume: a new noninvasive framework for cardiac mechanics

Abstract

Dimensional variables measured for study of left ventricular mechanics are subject to errors arising from difficulty in determining zero-stress dimensions for use as a reference. Based on a method validated for measurements within individuals, we have devised an approach that facilitates comparison between individuals while minimizing random scatter. We define an exact mathematical index of strain, ln(h(0)/h), using wall thickness (h) referenced to extrapolated wall thickness at zero-luminal volume (h(0)). Noninvasive data from rabbits, pigs, and humans all yielded highly similar myocardial stress, ln(h(0)/h), and work values. The stress-ln(h(0)/h) relationship during afterload variation was constant among individual pigs with a twofold variation in ventricular mass. Stress-ln(h(0)/h) data from our analysis displayed lower scatter than either pressure-volume data normalized to myocardial mass or stress-ln(h(0)/h) data referenced to end-diastolic dimensions. A Frank-Starling-like curve with high correlation (r(2) = 0.96) was constructed from single points from different pigs, suggesting a low level of size and intersubject scatter. This method offers high precision for noninvasive characterization of ventricular and myocardial mechanics and for comparisons between subjects and between species.

Patterns of muscular strain in the embryonic heart wall

“…While recent years have been marked by significant increases in understanding of genetic regulation of cardiac development, epigenetic regulation has been the subject of less study. However, there has been increasing interest in factors such as myocardial stress/strain, blood fluid dynamics, and geometric constraints in both adult and developing hearts (Hogers et al, 1995; Taber, 1998a,b; Omens, 1998; Denslow et al, 1999; Gourdie et al, 1999, 2003; Hove et al, 2003; Sedmera et al, 2005). It has been suggested that, from the standpoint of physics, it is more likely for a cellular sensor to detect strain rather than stress (Arts et al, 1994; Omens, 1998).…”

“…Furthermore, observed plasticity of initial withdrawal from the cell cycle suggests that preexisting genetic state or molecular environment of these cells may not be the only mediators of this spatial pattern of withdrawal, that differences in physical parameters across the wall may directly affect cell proliferation (deAlmeida et al, 2007). Physical parameters that vary significantly with position across the condensed wall of a contracting and expanding tube include stress, strain, and energy consumption (Omens, 1998; Denslow et al, 1999); particularly pertinent here are biological sensors transducing strain (Morgan and Baker, 1991; Palmieri et al, 2002; Hoshijima, 2006). …”

Comparison of left ventricular contraction profiles among small, medium, and large dogs by use of two-dimensional speckle-tracking echocardiography

“…As explained by Laplace' s law, 25 anatomically large hearts may have increased left ventricular wall stress. It is reported 26 that the calculated wall stress at end diastole (which reflects the preload) and end systole (which reflects the afterload) are similar among species with remarkably different body weights. Therefore, the influence of preload and afterload should also be minimal within species.…”

The left ventricle undergoes biomechanical and gene expression changes in response to increased right ventricular pressure overload

“…Ideally, we were looking to correlate gene expression and fibrosis in the LV with an estimate of LV myocardial stress. Previous studies have derived estimates of LV myocardial stress based on a force‐balance between LV cavity pressure and the balancing stress of the myocardium (Arts, Bovendeerd, Prinzen, & Reneman, ; Denslow, Balaji, & Hewett, ). These equations are derived without any regard for the septal geometry or the influence of the RV.…”