Assessment of the Left Ventricular-Arterial Coupling: A More Reasonable Method.

Abstract

To the Editor: We read with great interest the article by Li et al. recently published in Shock(1) which investigated the performance of left ventricular–arterial coupling (VAC) in septic shock patients who are unresponsive to fluid administration. As described in the article (1), the formula for calculating the effective arterial elastance (Ea), left ventricular (LV) end-systolic elastance (Ees), and VAC (defined as Ea/Ees) is shown as follows: Ea = ESP/SV, Ees = ESP/(ESV-V0), and VAC = (ESV-V0)/SV, where V0 was defined as the volume axis intercept of the end-systolic pressure–volume relationship (see the Figure 1 in the article (1), ESP represents end-systolic pressure of ventricular, ESV represents end-systolic volume of ventricular, and SV represents stroke volume). We respectfully disagreed with the method applied in this study for evaluating the VAC because the abovementioned approximated calculations are unreliable and may overestimate the actual value measured by the invasive method. First, to simplify the formula for calculation, the authors made a simple assumption that the V0 is negligible. Indeed, the parameter V0 is, theoretically, near to 0 when the heart load is in the physiologic range (2, 3). However, in some case, particularly in cardiac dysfunction, the V0 is not equal to 0 and should not be neglected. A study by Ky et al. (4) revealed a median V0 of 43 mL (interquartile range: −2.6 mL to 113 mL) for patients with chronic systolic heart failure, and the V0 was positively associated with the New York Heart Association (NYHA) functional class (ρ = 0.31; P < 0.001), indicating that the worse the cardiac function, the greater the V0. In the study by Li et al. (1), we can guess that the patients included in this study had a cardiac dysfunction according to the data regarding the global end-diastolic ventricular volume index (GEDVI) and stroke volume index (SVI), despite a normal cardiac index. Hence, roughly neglecting the V0 in this study would, inevitably, result in an overestimation of the true VAC. Second, the ratio ESP/ESV was used to calculate Ees by Li et al (1); however, this formula was proven as a suboptimal method for estimating Ees in the study by Chen et al. (5). Chen et al. found that the approximately calculated Ees (ESP/ESV) was not well correlated with the invasively measured Ees (y = 0.18x + 0.69; r = 0.56, P < 0.001), and the residuals of the calculated Ees to the invasively measured Ees were significantly different from 0, averaging 2.2 mmHg/mL (5). Meanwhile, a novel method, named the “single-beat” method, was proposed by Chen et al. (5) to estimate Ees; this method was validated as more well correlated with the invasively measured Ees (y = 0.78x + 0.55; r = 0.81, P < 0.0001) compared with the ratio ESP/ESV. Importantly, the “single-beat” method just requires several parameters that can be noninvasively measured by echocardiography; it thus seems to be more reasonable and suitable for evaluating Ees and VAC in critically ill patients. Lastly, the authors (1) used the arterial systolic pressure (ASP) of the femoral artery to represent the LV ESP; this method for assessing LV ESP is also not reasonable. The invasive method using LV catheterization is the “gold-standard” for the assessment of LV ESP; however, it is an unrealistic practice in the intensive care unit at present. Alternatively, the researchers have commonly used the mean aortic pressure (MAP) (3, 6) and 90% of the ASP (7, 8) as surrogate for LV ESP, and the ratio of MAP/SV was confirmed as a robust surrogate for Ea and is interchangeably in any peripheral artery (9). Therefore, this unreasonable approximation for LV ESP used in this study (1) may also lead to an overestimation of Ea and VAC. Overall, the inappropriate method for assessing the Ea, Ees, and VAC will downgrade the credibility of their evidence to some extent.