EDITORIAL COMMENT
Strain rate imaging
why do we need it?*
Otto A. Smiseth, MD, PhD, FACC*,* and
Halfdan Ihlen, MD, PhD*
* Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway
* Reprint requests and correspondence: Dr. Otto A. Smiseth, Department of Cardiology, Rikshospitalet, N-0027 Oslo, Norway.
o.a.smiseth{at}klinmed.uio.no
The most widely used method for evaluating cardiac function is transthoracic echocardiography, and myocardial function is assessed from M-mode or two-dimensional images. These modalities have significant limitations, and tissue Doppler imaging (TDI) has been introduced as a more objective and quantitative method for assessing myocardial function. The implementation of TDI in clinical routine, however, has been relatively slow, and so far TDI has not replaced the conventional echocardiographic methods. One important limitation of TDI is that velocities in one myocardial segment are determined by function in other segments as well, which is due to tethering between segments and cardiac translational motion. This limitation of TDI is best illustrated when left ventricular (LV) longitu- dinal velocities are measured from an apical window. During the cardiac cycle the ventricular apex is essentially stationary, while the mitral ring moves toward and away from the apex during systole and diastole, respectively. Mitral ring motion is in essence the sum of all longitudinal shortening and lengthening between the apex and the base. Thus, when an infarct occurs in the apical region, this causes reduced myocardial velocities not only in the apex but also in the nonischemic basal portion of the ventricle (1,2). Importantly, the reduced TDI velocities in basal segments do not mean there is a reduction in function in these segments. Likewise, owing to tethering, contractions in nonischemic regions may cause velocities in neighboring ischemic regions; accordingly, nonviable myocardium appears to contract (1). Therefore, although TDI provides very important clinical information it has significant limitations. Recently, a new TDI-based modality has been introduced that may overcome these limitations, namely strain Doppler echocardiography or strain rate imaging (SRI).
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What is strain?
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Strain means "deformation," and it can be calculated as change in length (L – L0) divided by original length (L0): strain = (L – L0)/L0 (3). Thus, strain is a dimensionless quantity and represents the fractional or percentage change in dimension. Because myocardial deformation or strain is caused by fiber contraction, strain is a measure of myocardial contractile function. Myocardial strain can be measured accurately by tagged magnetic resonance imaging (MRI) (4). This method provides quantitative data about myocardial deformation in multiple plans, and it has substantial potential in cardiac research. Unfortunately, tagged MRI is not suited for clinical routine and, owing to limited temporal resolution, does not provide measures of rate of deformation (i.e., strain rate).
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Can strain and strain rate be measured by doppler echocardiography?
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Quinones et al. (5) suggested measuring myocardial strain rate from echocardiographic data, but this principle was never implemented clinically. More recently, Heimdal et al. (1) introduced a clinical method to calculate strain rate from regional Doppler velocity gradients, and Urheim et al. (2) demonstrated that strain could be measured as the time integral of the spatial velocity gradients. Since then, various studies have confirmed the validity of these measures (6–8).
Strain rate reflects how fast regional myocardial shortening or lengthening occurs. Strain rate is calculated from myocardial Doppler velocities (V1 and V2) measured at two different locations separated by a distance (L). If V1 and V2 are different, there is a spatial velocity gradient, and this in turn implies that there is deformation of the tissue in-between. In the situation where the two locations are getting closer, there is myocardial shortening, and when the two locations are moving apart, there is lengthening. Strain rate is calculated as the instantaneous spatial velocity gradient and has units of 1/s: strain rate = (V2 – V1)/L. Some investigators present the measurements as velocity gradient instead of strain rate (9,10). Strain is calculated as the time integral of strain rate, most often using end-diastole as a reference (2).
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What is the clinical meaning of strain and strain rate?
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The introduction of the terms strain and strain rate in echocardiographic imaging has created some confusion as they apparently do not fit in with conventional terminology. There is, however, no reason to change conventional clinical terminology when reporting SRI data. Analogous to the convention of reporting global LV function in terms of LV ejection fraction, one can report regional strain by SRI as regional shortening fraction when measurements are done in the long axis (longitudinal strain), and as regional thickening fraction in the short axis (radial strain). Alternatively, one may use percentage shortening and percentage thickening. Strain rate means deformation per time, and as clinical terminology one may use shortening rate and thickening rate, respectively.
Similar to LV ejection fraction, strain is load-dependent and, therefore, it is not a perfect measure of contractility (2). On the other hand, strain rate appears to be less load-dependent and is a better measure of contractility (7).
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Strain rates in different myocardial layers
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In a report in this issue of the Journal, Hashimoto et al. (11) utilize SRI to measure strain rate in different layers of the LV myocardium. In a sheep model they demonstrate a transmural gradient of systolic and diastolic strain rates, with the highest strain rates in the subendocardium and lowest in the subepicardium. The study was done in open-chest anesthetized sheep and was limited to measurements in the LV free wall. The strain rate gradient changed in parallel with changes in absolute strain rate, and peak systolic and early-diastolic strain rates correlated with indices of LV contractility and relaxation, respectively. Consistent with the gradient in strain rate, there was also a gradient in strain from the endocardium to the epicardium.
These findings are consistent with experimental studies that have shown systolic strains in the subendocardial layer that exceed strains in the subepicardial layer (12,13). Studies in humans with tagged MRI have confirmed these findings (14,15). These measurements have been done predominantly for radial and circumferential strains, but there appears to be a similar but smaller gradient for longitudinal strains (16,17). Very limited data exist on strain rate in different layers, but experimental studies indicate that strain rate is highest in the deepest layers (12).
In patients with coronary artery stenosis the subendocardial zones are more susceptible to ischemia and infarction than the subepicardial ones. Experimental studies have demonstrated that a reduction in coronary flow causes reductions in strain and strain rate in the subendocardial layer that far exceed those in the subepicardial layer (12). However, it is not obvious that strain in one myocardial layer reflects function within the same layer. Simple spherical and ellipsoidal models predict that the subendocardium should thicken more than the subepicardium (18). Thus, even if active contraction occurs only in the subepicardial layer and the subendocardial layer does not contract at all, it will thicken more (i.e., higher strain) than the subepicardial layers. This is a consequence of geometry and tissue incompressibility, which imply that concentric shells of myocardium have proportionally greater changes in dimension with decreasing radius.
Therefore, it may be difficult to use strain as a marker of injury in one particular myocardial layer. In contrast, experimental data suggest that recovery of postischemic systolic thickening is delayed in the subendocardium relative to the subepicardium (19). Therefore, potentially the timing of peak strains might reflect local function. More studies are needed to resolve these questions, and SRI may provide new insights.
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Study limitations
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The study by Hashimoto et al. (11) was done in an open-chest model where measurement conditions could be easily optimized. When SRI is used in a clinical environment, a significant problem arises with random noise and other artefacts. Because strain is obtained by integrating strain rate, the noise problem is significantly reduced but is still present. The SRI is also more angle-dependent than other Doppler techniques. It remains to be demonstrated that strain rate imaging by Doppler has the ability to measure transmural gradients in patients. One obvious technical limitation is the density of the echocardiographic beams needed to measure strain rates separately in multiple regions in the LV wall. The scanning sector angle should therefore be as narrow as possible. Another problem is that the beam width increases with lower ultrasonic frequency, as used in adult patients. Furthermore, because the entire heart is moving during the cardiac cycle it will be necessary to move the sampling volume continuously to keep it over the same area of tissue. This type of tracking was done by Hashimoto et al. (11).
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Future perspectives
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Strain-rate imaging may have considerable potential as a clinical method for quantifying myocardial function in terms of regional shortening fraction and thickening fraction, respectively. Recent developments in three-dimensional cardiac imaging could allow more comprehensive visualization of myocardial strains. The theoretical advantages of measuring strain and strain rate as opposed to measuring myocardial velocities are that the former are less influenced by cardiac translation and motion due to tethering to other regions. It remains to be shown, however, that these advantages outweigh the disadvantages of noise and stronger angle dependency, which are the main limitations of SRI. It is likely that SRI will become a clinically useful method, but some refinement of the technology is needed.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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3. Mirsky I, Parmley WW. Assessment of passive elastic stiffness for isolated heart muscle and the intact heart. Circ Res. 1973;33:233–243[Abstract/Free Full Text]
4. Axel L, Dougherty L. Heart wall motion: improved method of spatial modulation of magnetization for MR imaging. Radiology. 1989;172:349–350[Abstract/Free Full Text]
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What is strain?
Can strain and strain...