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Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Piet Claus
Over the past decade strain (-rate) imaging has emerged as a powerful tool for the assessment of myocardial function. Originally tissue Doppler-based deformation imaging was developed and turned out to be a useful experimental and clinical research tool. However, it was the availability and the ease-of-use of speckle-tracking technology that made echocardiographic deformation imaging a highly accessible clinical tool. This session was devoted to the discussion of the physiological determinants of strain and strain-rate. The sensitivity of strain-rate to changes in inotropic state has been clearly shown, but the load dependence of these strain parameters remains a subject of study.
Christian Hassager presented an overview of the evidence for the load dependency of strain and strain-rate imaging starting from the theoretical relationships of increased strain and strain-rate with increased preload and decreased values with increased afterload. Several experimental animal studies in large animals as well as small animals elucidated this load dependency, where strain was shown to be definitely load dependent and strain rate as being less load dependent and more reflecting changes in inotropic state. Several clinical models with acute variation in pre- and afterload, such as saline infusion, hemodialysis, but also parabolic flights showed the same results, but always to a lesser extent. Strain response to load was compared to the response of ejection fraction. However, it is acknowledged that strain could provide more information by distinguishing radial from longitudinal deformation which is often impaired at an earlier stage. Also in that respect a note of caution was raised for the translation of animal data to the clinical setting, since in the animal lab mainly radial deformation is measured in the closed chest setting.
Antonello D’Andrea continued on this theme, discussing the impact of loading on the left ventricle. He discussed the changes mentioned above in the context of successful valve replacement, which again show the expected load dependence. An important note was made on dyssynchrony time-based measurements, that are highly load dependent and for which an assessment of changes during a preload change would be of benefit. A clinical advise that resulted from this talk is to always report blood pressures together with strain(-rate) measurements, to have at least a crude estimate on the load.
Andre La Gerche presented data on the load dependence of right ventricular (RV) function. In contrast to the left ventricle, the normal RV at rest works at a very low contractility. Indeed, the success of the Fontan procedure shows that the RV at rest has no role to play and “RV output” can be purely generated by left ventricular contraction. However, when the afterload of the RV increases, the RV needs to increase contractility. A clinical model of this is pulmonary hypertension, where longitudinal deformation is lost and radial and circumferential take over. Radial function in the apical parts is severely impaired in the short-term survivors as opposed to long-term survivors. However, the most important message is that RV function at rest can be misleading and an exercise test is important to evaluate RV functional status. The RV has a completely different response to exercise than the left ventricle, while left ventricular output can be increased with a limited increase in developed pressure, the RV output increase requires a disproportional higher increase in RV pressure. The RV exhibits dramatic loading changes in the RV as measured by a higher wall stress increase with respect to the left ventricle during exercise. This response is also closely related to changes in the compliance and resistance of the lung vasculature.
Finally, Arco Teske discussed if the responses in strain and strain rate to increased preload could be used in the individual patient to assess intrinsic contractility. This would exploit different measurements on a Frank-Starling relation, during a preload changing challenge. Given that parabolic flights would be a logistic nightmare in clinical practice, he presented data on the response of LV performance to leg-lifting. Using end-diastolic volume from 3D echocardiography as a measure of preload and stroke volume, he showed the feasibility of deriving a Frank-Starling curve during a protocol with head-up position, normal position and Trendelenburg. These gave the expected higher slopes in normal controls and flatter responses in dilated cardiomyopathy patients. Also monitoring left-ventricular volumes and deformation in the septum was shown to be feasible. Timing of peak response was delayed in the DCM patients.
Strain imaging: are we really measuring contractility?