Ventricular–arterial coupling: Invasive and non-invasive assessment

Abstract

Interactions between the left ventricle (LV) and the arterial system, (ventricular–arterial coupling) are key determinants of cardiovascular function. Ventricularearterial coupling is most frequently assessed in the pressure–volume plane using the ratio of effective arterial elastance (EA) to LV end-systolic elastance (EES). EA (usually interpreted as a lumped index of arterial load) can be computed as end-systolic pressure/stroke volume, whereas EES (a load-independent measure of LV chamber systolic stiffness and contractility) is ideally assessed invasively using data from a family of pressure–volume loops obtained during an acute preload alteration. Single-beat methods have also been proposed, allowing for non-invasive estimations of EES using simple echocardiographic measurements. The EA/EES ratio is useful because it provides information regarding the operating mechanical efficiency and performance of the ventricular–arterial system. However, it should be recognized that analyses in the pressure–volume plane have several limitations and that “ventricular–arterial coupling” encompasses multiple physiologic aspects, many of which are not captured in the pressure–volume plane. Therefore, additional assessments provide important incremental physiologic information about the cardiovascular system and should be more widely used. In particular, it should be recognized that: (1) comprehensive analyses of arterial load are important because EA poorly characterizes pulsatile LV load and does not depend exclusively on arterial properties; (2) The systolic loading sequence, an important aspect of ventricular–arterial coupling, is neglected by pressure–volume analyses, and can profoundly impact LV function, remodeling and progression to heart failure. This brief review summarizes methods for the assessment of ventricular–arterial interactions, as discussed at the Artery 12 meeting (October 2012).

Pulse wave velocity to global longitudinal strain ratio in hypertension

“…Both E a and E es are derived from pressure volume loops and are measured with the same units. [4][5][6] There are, however, some endogenous limitations in the clinical use of the echocardiography-derived E a /E es ratio that may account for the negative results in our study. Firstly, E a is highly dependent on vascular resistance and heart rate, while simplifications in its calculation are not adequately validated.…”

“…Several adaptive alterations in the aorta, peripheral arteries and left ventricle (LV) of hypertensive patients have been linked with disease severity; however, arterial-ventricular (AV) coupling has not been clearly associated with target organ damage and clinical outcomes [1][2][3] Effective arterial elastance (E a ) is derived from the end systolic pressure to stroke volume (SV) curve and provides a measure of overall afterload, incorporating arterial elastance and peripheral vascular resistance. [4][5][6] Left Ventricular (LV) performance is better expressed from the LV end-systolic elastance (E es ), a marker calculated invasively from the LV end-systolic pressure-volume slope as a change in pressure for a given change in volume noninvasively or by echocardiography. 4,6 The interaction of the arterial and ventricular component is described by the ratio of E a /E es and is considered optimal over a broad range of E a /E es ratios (0.3-1.3).…”

“…[4][5][6] Left Ventricular (LV) performance is better expressed from the LV end-systolic elastance (E es ), a marker calculated invasively from the LV end-systolic pressure-volume slope as a change in pressure for a given change in volume noninvasively or by echocardiography. 4,6 The interaction of the arterial and ventricular component is described by the ratio of E a /E es and is considered optimal over a broad range of E a /E es ratios (0.3-1.3). [4][5][6] However, in hypertensives arterial stiffness may be increased in parallel with LV myocardial stiffness, and E a /E es ratio may remain relatively unchanged, despite the fact that in these patients a given increase in stroke volume (SV) may be associated with an exaggerated systolic blood pressure increase especially after exertion.…”

“…4,6 The interaction of the arterial and ventricular component is described by the ratio of E a /E es and is considered optimal over a broad range of E a /E es ratios (0.3-1.3). [4][5][6] However, in hypertensives arterial stiffness may be increased in parallel with LV myocardial stiffness, and E a /E es ratio may remain relatively unchanged, despite the fact that in these patients a given increase in stroke volume (SV) may be associated with an exaggerated systolic blood pressure increase especially after exertion. [5][6][7] In the last decades, more valid markers of arterial and ventricular performance in hypertensives have emerged.…”

“…[4][5][6] However, in hypertensives arterial stiffness may be increased in parallel with LV myocardial stiffness, and E a /E es ratio may remain relatively unchanged, despite the fact that in these patients a given increase in stroke volume (SV) may be associated with an exaggerated systolic blood pressure increase especially after exertion. [5][6][7] In the last decades, more valid markers of arterial and ventricular performance in hypertensives have emerged. Specifically, carotid-femoral pulse wave velocity (PWV) has been linked to cardiovascular events in this group and is recommended as a "gold standard" measure of aortic stiffness.…”