Abstract
To quantitate the contractile mechanics of the heart, the ventricle is considered an elastic chamber with known end-systolic elastance (Ees). Ees can be calculated from a single pressure-ejected volume curve, which requires simultaneous records of left ventricular (LV) pressure and the aortic flow (Qm). In clinical settings, it is helpful to evaluate patients’ cardiac contractile status by using a minimally invasive approach to physiological signal monitoring, wherever possible, such as by using LV pressure alone. In this study, we evaluated a method for determining Ees on the basis of the measured LV pressure and an assumed aortic flow with a triangular wave shape (Qtri). Qtri was derived using a fourth-order derivative of the LV pressure to approximate its corresponding Qm. Values of EestriQ obtained using Qtri were compared with those of EesmQ obtained from the measured Qm. Healthy rats (NC; n = 28) and rats with type 1 diabetes (DM; n = 26) and chronic kidney disease (CKD; n = 20) were examined. The cardiodynamic conditions in both the DM and CKD groups were characterized by a decline in EesmQ and EestriQ. A significant regression line for Ees was observed (P < 0.0001): EestriQ = 2.6214 + 1.0209 × EesmQ (r2 = 0.9870; n = 74). Our finding indicates that the systolic pumping mechanics of the heart can be derived from a single LV pressure recording together with the assumed Qtri.
Highlights
The assessment of the cardiac contractile status is important under various physiological and pathological conditions [1]
Our finding indicates that the systolic pumping mechanics of the heart can be derived from a single left ventricular (LV)
Regarding the estimated peak isovolumic pressure (Pisomax), we discovered that the LV endsystolic elastance (Ees) can be approximately calculated using the assumed calibrated triangular flow wave (Qtri) and that it had a strong correlation with that derived from measured aortic flow wave (Qm)
Summary
The assessment of the cardiac contractile status is important under various physiological and pathological conditions [1]. In the 1960s and 1970s, a simple time-varying elastance model of left ventricular (LV) contraction was proposed to study the intrinsic contractility of the heart, which relates the end-systolic pressure–volume relationship (ESPVR) [2,3,4]. The ESPVR of the left ventricle has been reported to be approximately linear over a physiological range, and its slope is the endsystolic elastance (Ees), with the zero-pressure volume axis intercept of V0 [4,5,6]. Ees (but not V0) markedly varies in response to changes in contractility and is relatively www.impactjournals.com/oncotarget insensitive to changes in preload, afterload, and heart rate (HR) in a specific constant contractile status of the heart [4,5,6].
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