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Systolic function and ejection

Teaching Course on cardiac function and mechanics organised jointly with the American Society of Echocardiography

  • How does the heart pump? From sarcomere to ejection volume, presented by P Claus (Leuven, BE)  
  • Quantifying ventricular function: why do we need to go beyond ejection fraction, presented by K O'Connor (Quebec, CA)  
  • Stressing the ventricle: what happens and how can we detect it, presented by A La Gerche (Brussels, BE)  
  • Illustrative clinical cases: how to detect subtle changes in systolic function, presented by V Delgado (Leiden, NL)  

This course was aimed at providing insight into cardiac mechanics and cardiac physiology, since this knowledge is essential in order to be able to correctly interpret deformation data that can be obtained by the latest technologies in strain (-rate) imaging.
In the first session of the course, systolic function was discussed in more detail. Several aspects were presented, including the basics of fibre mechanics and how this translated into efficient pressure build up and ejection. Next, the limitations of ejection fraction were discussed and it was illustrated how deformation analysis can provide complementary information. It was further illustrated how stressing the ventricles can provide more information on function and functional capacity, especially knowing which are the expected physiological changes during exercise and how deviations to this can help in assessing function. Finally, some studies were shown where a more comprehensive assessment of myocardial tissue and deformation provided more detailed information for addressing clinical questions.

In summary, these concepts were discussed:

  • Intrinsic cardiac function consists of two essential components: force development by the myocytes, to develop pressure needed to open the ventricular-arterial valve, and deformation of the cavity to displace volume into the circulation. Since force development is very difficult to assess in clinical practice (invasive ventricular pressure would be the closest), we mainly have to rely on interpreting deformation since more and more imaging tools become available to quantify this. However, deformation is the result of the sum of forces generated by a tissue segment and generated upon a segment by the internal cavity pressure and the surrounding segment. Therefore, all of these aspects have to be taken into account to interpret segmental function. Especially pressure loading and segment interaction are key to interpret deformation.
  • Local shape of the myocardium is crucial to interpret the stresses on the wall and the myofibres. Intrinsic shape of the ventricle means that different segments will react differently to e.g. acute pressure overload and some segments (especially the septum) can change their shape in order to better cope with changes in loading. This will obviously impact on local deformation and thus has to be taken into account when interpreting changes in strain values and profiles.
  • Ejection fraction, although shown to contain important prognostic value for groups of patients, has inherent limitations in the individual. One of the main problems, besides the technical difficulties to accurately assess it, is the fact that it either measures predominantly global radial/circumferential function (when using a Teichholz approach) or an average of all deformation components (using Simpson’s).  Since most cardiac diseases are associated with an early change in longitudinal deformation, as compared to radial/circumferential, a much more sensitive approach is to measure longitudinal function (either using global longitudinal strain or mitral ring displacement) to quantify (subclinical) changes in systolic function.
  • Stressing the ventricle provides a way to look at its functional capacity. Whereas looking at a segmental response provides useful information in e.g. CAD, assessing the global response to stress has important prognostic value. A normal heart copes with stress by using a combination of a heart rate (HR) response, a slight increase in end-diastolic volume (preload increase) and an important decrease in end-systolic volume (ESV), by increased contractility and reduced afterload, to increase stroke volume. The combination of HR reserve and decrease in ESV, ideally combined with the change in blood pressure, is a powerful prognostic predictor.
  • The left (LV) and right ventricle (RV) have distinctly different responses to exercise. While the LV can increase stroke volume with only a slight increase in pressure, the pressure in the RV increases significantly more when its volume load is increased. This implies that intensive exercise will translate into a combined volume and pressure overload at the right side.


In order to assess systolic function, a framework, describing the physiological changes in global and local parameters, in different conditions, and their mal-adaptations in diseases, combined with measurements of (global and regional) deformation, provides a powerful approach to assess the status and prognosis in an individual patient.




Systolic function and ejection

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.