Estimation of left-ventricular systolic performance and its determinants in man from pressures and dimensions of one beat: Effects of aortic valve stenosis and replacement

Abstract

Within a thick heart-chamber wall, there is a midwall element or layer whose displacements best express systolic performance. The volume enclosed by that midwall element (Vm) and the average stress in that element (sigma m) can be calculated accurately by simple formulae. From simultaneous left-side pressure tracings and contrast cine-ventriculograms, Vm and sigma m were calculated at 20-ms intervals for an entire cardiac cycle in five normal subjects and in eight patients before and one year after replacement of stenotic aortic valves. Prior to surgery, the overloaded left ventricles were not hypertrophied enough to restore normal mid- and end-ejection stresses. Four had subnormal cavity ejection fractions, but all had subnormal midwall ejection fractions. All had subnormal fractional midwall ejection rates and prolonged active intervals (from the beginning of activation to the end of deactivation). Judging from pre-ejection pressure-development rates, the pressure-developing ability was not consistently elevated by concentric hypertrophy, because the stress-developing ability (contractility) was usually subnormal. The ability to shorten in the absence of afterload appeared to be subnormal in about half of the cases. The subnormal midwall ejection fractions appeared to be due to various combinations of increased mid- and late-ejection stresses, reduced contractility, and reduced shortening ability. On average and in several cases, reduced shortening ability appeared to be the main cause of the reduced performance. The effect of the slowed fractional midwall ejection rate to reduce the midwall ejection fraction was partially compensated by a prolonged active interval, by prolonged ejection time relative to the active interval, and by a more sustained ejection rate. Valve replacement partially restored all values except contractility towards normal, but the restorations of wall/cavity ratio and active interval were slight.

Speckle-tracking echocardiography correctly identifies segmental left ventricular dysfunction induced by scarring in a rat model of myocardial infarction

“…Thus, with a constant contractility assumed, an increase in stress must lead to a decrease in strain. Stress, in turn, is determined by local radii of curvature (21,29), which for radial and meridional stress can be approximated by endsystolic diameters (8). As a confirmation, Bogaert et al (3) used magnetic resonance imaging to show that strains decrease in the remote regions after myocardial infarct and that this decrease is associated with increased circumferential and longitudinal radii of curvature (3).…”

Mechanical characteristics of tachycardia-induced left-ventricular failure as evaluated in isolated dog hearts

“…Reference midwall volume was used only in the calculation of shortening ability [18,19] or mobility [14][15][16][17], the midwall ejection fraction with reference preload and no afterload. It can be calculated as the difference between reference cavity volume (Vcu) and apparent (extrapolated) cavity dead space (Vcx) divided by reference midwall volume (Vmu):…”

“…For example, it is accurate for any chamber shape, thickness distribution and segmental stress distribution, and for a variety of fiber-orientation distributions. At each of these two candidate reference volumes (diastolic-transition volume, standard-diastolic-stress volume), the volume enclosed by a midwall layer was calculated by the formula [14][15][16][17]:…”

“…While shape abnormalities were demonstrable statistically, they were limited to the initial and final phases, the body of the wave being normally shaped. Therefore, the curve-fitting method to predict peak isovolumic pressure from the pressure time course of an ejecting beat [17,[21][22][23][24] is valid for failing and dilated chambers. This pressure is a measure of contractile vigor and a determinant of systolic performance, and its välue at end-diastolic volume can be combined with the end-systolic V,P point to estimate the end-systolic P-V relation in vivo [17,[21][22][23][24].…”

“…First, we wished to determine the mix of mechanical abnormalities contributing to hypokinesis in this failure model. According to the analysis used [14][15][16][17], properties are defined in terms of a positive-strain reference dimension intended to express chamber size. In the hydraulic context, one such dimension is the "standard-diastolicstress volume", where diastolic stress has a particular value [18][19][20].…”