Noninvasive quantification of left ventricular elastance and ventricular-arterial coupling using three-dimensional echocardiography and arterial tonometry

Abstract

Gayat E, Mor-Avi V, Weinert L, Yodwut C, Lang RM. Noninvasive quantification of left ventricular elastance and ventricular-arterial coupling using three-dimensional echocardiography and arterial tonometry. Am J Physiol Heart Circ Physiol 301: H1916-H1923, 2011. First published September 9, 2011; doi:10.1152/ajpheart.00760.2011.-Most techniques previously used to assess left ventricular (LV) end-systolic elastance (E es) and ventricular-arterial coupling (CLV-A) relied on invasive measurements and data acquisition over a wide range of loading conditions. Our goals were to 1) assess the feasibility of noninvasive assessment of E es and CLV-A using real-time three-dimensional echocardiography (RT3DE) and arterial tonometry; 2) test the ability of this approach to detect changes in LV contractility; and 3) study its reproducibility. We studied pharmacologically induced changes in inotropic state (5 and 10 g·kg Ϫ1 ·min Ϫ1 dobutamine) in normal volunteers (N ϭ 8) and compared 10 normal volunteers with 10 patients with dilated cardiomyopathy (DCM; ejection fraction Ͻ 35%). RT3DE LV images, calibrated carotid artery tonometry, and Doppler tracings were obtained to noninvasively estimate Ees and CLV-A, using two alternative calculations. Dobutamine caused a significant stepwise increase in blood pressure, heart rate, ejection fraction, and Ees and a decreased CLV-A. In patients with DCM, Ees was significantly reduced and CLV-A elevated, compared with controls. Both inter-and intraobserver variability were good for all measured parameters, as reflected by intraclass correlation coefficients (Ͼ0.8) and coefficients of variation (Ͻ20%). While both Ees estimates showed significant differences between DCM patients and controls, one estimate resulted in no overlap and better reproducibility (interobserver intraclass correlation coefficient: 0.83 vs. 0.47, coefficients of variation: 20 vs. 29%). This is the first study to test the feasibility of using RT3DE-derived LV volumes in conjunction with arterial tonometry to noninvasively quantify LV elastance and CLV-A. This approach was found to be sensitive enough to detect expected differences in LV contractility and reproducible. Due to its noninvasive nature, this methodology may have clinical implications in various disease states. left ventricular contractility LEFT VENTRICULAR (LV) pressure-volume loops provide valuable information on LV systolic and diastolic function, as well as on LV-arterial coupling (C LV-A ) (8). End-systolic elastance (E es ), the slope of the end-systolic pressure (ESP)-volume relationship, has been used as a load-independent index of myocardial contractility (2). In the past, to obtain pressure-volume loops, invasive pressure and volume measurements were required to be obtained under a wide range of loading conditions, thus limiting the clinical applicability of this technique. To avoid these limitations, several investigators have proposed invasive solutions to estimate E es from a single cardiac cycle (23,24,27), and, more recently, the accuracy of ...

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“…The main finding was that these often used prediction equations 15, 16 overpredict LV ESP in this population. Furthermore, changes in LV ESP following the exercise perturbation were inaccurate using either prediction equation.…”

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“…3E). Typical values for E es summarized by Gayat et al[105] are: Ees ~2.0 mm Hg/ml in normal hearts, E es <1.0 mm Hg/ml in dilated failing hearts and E es ~4.0 mm Hg/ml inhypertrophied hearts.…”

Ventricular–vascular coupling in hypertension

“…64,85 In an attempt to overcome these limitations, new approaches have been proposed to calculate from a single beat reliable estimates of both V 0 and end-systolic ventricular elastance. 86,87 Wave intensity analysis In the last years, a new approach, the 'wave intensity analysis', has been proposed for the assessment of ventricular-arterial coupling. 88,89 Wave intensity considers changes in pressure and velocity at any point in the arterial tree as a result of interaction between forwardtravelling and backward-travelling wavelets carrying energy from the heart and vasculature, respectively.…”