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• W2896532004 abstract "To the Editor: Morimont et al.1 highlighted the discordance between left ventricular ejection fraction (LVEF) and end-systolic elastance (Ees), and concluded that “LVEF may be misleading in the assessment of LV function during VA-ECMO.” However, such discordant changes are predictable through an examination of LVEF physiology. Mathematically, , where V0 is the maximum ventricular volume at zero pressure and ESP is end-systolic pressure; Rearranging the equation, Dividing by EDV, Equation 1 shows that LVEF is related to ventricular contractility, the arterial load, preload, and ventricular remodeling (Ees, ESP, EDV, and V0). In this regard, LVEF is related to but is not a simple measure of contractility. Left ventricular ejection fraction encapsulates two physiologic concepts of ventricular interaction with arterial load: 1) preload–afterload matching; and 2) ventriculoarterial coupling. First, Ross2 described the reduction in stroke volume when afterload is increased in the presence of limited preload reserve at any given level of inotropy (afterload mismatch). If two of the three major determinants (preload, afterload, and contractility) of ventricular performance are held constant, a change in the third will independently affect the stroke volume and EF. Expressed mathematically (Equation 1): at a fixed EDV (limited preload reserve), an increase in ESP/Ees ratio (increase in afterload relative to contractility) must lead to reduction in LVEF. Second, Sunagawa et al.3 showed that the arterial load could be characterized by arterial elastance (Ea), and coupled it with Ees (both share the same unit of measurement) to describe ventriculoarterial coupling—expressed mathematically as Ea/Ees ratio. Ejection fraction is intrinsically related to Ea/Ees ratio: If V0 is assumed to be negligible in normal individuals, Burkhoff and Sagawa4 showed that optimal mechanical efficiency occurred when Ea approximated half of Ees (normal LVEF of 0.67). Higher Ea/Ees ratio (ventriculoarterial mismatch) would result in a lower LVEF (Equation 3). Of note, V0 increases with LV remodeling, which results in greater reduction in LVEF (Equation 2). The data by Morimont et al.1 are consistent with the mathematical expressions of these two concepts. The unchanged LVEF despite near doubling of Ees in the first case can be explained by lower EDV and higher arterial pressure (afterload mismatch) and higher Ea/Ees (ventriculoarterial uncoupling). Thus, LVEF does not mislead the assessment of LV function, because LVEF is not simply a measure of LV function. Left ventricular ejection fraction should be interpreted in the context of its determinants to avoid misleading conclusions about LV function. Hoong Sern LimQueen Elizabeth Hospital BirminghamUniversity Hospital Birmingham NHS Foundation TrustEdgbaston, Birmingham, United Kingdom[email protected]" @default.
• W2896532004 created "2018-10-26" @default.
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• W2896532004 date "2019-08-01" @default.
• W2896532004 modified "2023-09-26" @default.
• W2896532004 title "The Physiologic Basis of Ejection Fraction" @default.
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• W2896532004 doi "https://doi.org/10.1097/mat.0000000000000899" @default.
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