The Ventricular-Arterial Coupling: From Basic Pathophysiology to Clinical Application in the Echocardiography Laboratory
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Tags: VA coupling
Abstract
The interplay between cardiac function and arterial system, which in turn affects ventricular performance, is defined commonly ventricular-arterial coupling and is an expression of global cardiovascular efficiency. This relation can be expressed in mathematical terms as the ratio between arterial elastance (EA) and end-systolic elastance (EES) of the left ventricle (LV). The noninvasive calculation requires complicated formulae, which can be, however, easily implemented in computerized algorithms, allowing the adoption of this index in the clinical evaluation of patients. This review summarizes the up-to-date literature on the topic, with particular focus on the main clinical studies, which range over different clinical scenarios, namely hypertension, heart failure, coronary artery disease, and valvular heart disease.
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(9/11/2022, 8:49:17 PM)
“[4] However, aortic input impedance is described in the frequency domain, whereas measures of LV contractility are best described in the time domain; consequently direct comparisons between arterial and LV function is difficult.” Go to annotation (Antonini-Canterin et al., 2013, p. 1)
“ventricular-arterial coupling is commonly calculated by the ratio of effective arterial elastance (EA), a measure of afterload, to LV end-systolic elastance (EES), a relatively load independent measure of LV chamber performance. Both these measures are expressed in mmHg/ml and therefore comparable mathematically.” Go to annotation (Antonini-Canterin et al., 2013, p. 1)
“a rough estimate of ventricular-arterial coupling could be obtained using such a simplified approach: EA = ESP/SV, EES = ESP/ESV where ESP is the end systolic pressure, SV is the stroke volume, and ESV is the end systolic volume. So: EA/EES = (ESP/SV)/(ESP/ESV) and then simplifying, eliminating ESP: EA/EES = ESV/SV The problem with this simplified approach is that the ESV/ SV ratio is related in mathematical terms to the ejection fraction (1/EF - 1) and therefore it does not add substantial information to the traditional ejection fraction measurement.” Go to annotation (Antonini-Canterin et al., 2013, p. 2)
“In a patient with a failing heart, EES is reduced and EA is increased. In this situation, LV and arterial system are coupled in a suboptimal way resulting in a EA/EES ratio >1.0.[6] An increase in heart rate will further increase EA, worsening the coupling.[7] On the contrary, vasodilator therapy, lowering EA, brings the EA/EES ratio back down toward 1.0, improving the coupling. Similarly, inotropic therapy, increasing EES, improves the coupling.” Go to annotation (Antonini-Canterin et al., 2013, p. 2)
“end-systolic pressure can be estimated as 0.9 times the peak brachial systolic pressure. Thus, EA can be easily calculated as 0.9 times the brachial systolic pressure divided by stroke volume, determined at LV outflow tract level by Doppler techniques” Go to annotation (Antonini-Canterin et al., 2013, p. 2)