Assessing left ventricular performance: a rashomon effect.

The physiology of conduit arteries can be approximated noninvasively. One simple method to estimate arterial load is by computation of effective arterial elastance (Ea). Ea incorporates the steady component (peripheral resistance) and the pulsatile components of arterial load, including total arterial compliance and aortic characteristic impedance. Invasive studies and simulations have shown that Ea can be approximated by the ratio of left ventricular (LV) end-systolic pressure to stroke volume in normal and hypertensive human subjects.1,2 An important practical advantage of the calculation of Ea is the merging of all components of arterial load into a single quantitative variable, although it has the limitations of not separating the relative contributions of steady and pulsatile components2 and of relative sensitivity to variation of heart rate.3 Ea influences stroke volume and is related to LV contractility, as assessed at end ejection by the pressure-volume loop and determination of the LV elastance (Emax). Thus, Ea has been combined with Emax, the slope of a regression line connecting end-systolic pressures and volumes obtained at different loading conditions. The ratio Ea/Emax is widely used as a measure of LV-arterial coupling. As emphasized recently by Baicu et al,6 LV function, LV performance, LV contractility, and myocardial contractility are not interchangeable terms. Experimental studies suggest that LV performance, measured as stroke work (SW),6 is maximal when Emax Ea. LV performance increases its efficiency when, for a given SW, myocardial oxygen consumption is lower. The optimal efficiency of LV performance is achieved at Ea 0.5Emax. However, beyond these clear-cut limits, there is also evidence that SW may remain near maximal for a broad range of Ea/Emax values,7 mostly depending on the magnitude of preload and preload-recruitable SW.8 In addition to end-ejection phase indices, LV contractility can also be measured by isovolumic phase indices (peak positive dP/dt) and ejection phase indices (end-systolic wall stress versus fractional shortening). Because measures of LV contractility using LV volumes or shortening assess the inotropic state of the LV chamber, they may be influenced by LV geometric changes that alter the relation of the chamber to myocardial contractility.9