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J Am Coll Cardiol, 2006; 47:1313-1327, doi:10.1016/j.jacc.2005.11.063 (Published online 14 March 2006).
© 2006 by the American College of Cardiology Foundation
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Measurement of Strain and Strain Rate by Echocardiography

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Thomas H. Marwick, MD, PhD*

University of Queensland Department of Medicine, Princess Alexandra Hospital, Brisbane, Australia.


Figure 1
Figure 1
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  		Figure 1 Derivation of strain rate (SR) and strain from tissue Doppler data. A series of velocity curves (comprising isovolumic contraction [IVC], systolic [S] and diastolic [E and A] components) show a velocity gradient along a length of the wall (labeled d in the color Doppler image in A). A regression calculation between adjacent tissue velocity data points along this length generates the strain rate curve (B), which is then integrated to calculate strain (C). Timing of end-systole can be confirmed from the tissue Doppler waveform—in a separate example, the aortic valve closure (AVC) is marked by a transient wave in the adjacent septum and anterior mitral leaflet (D). ES = end-systolic; IVR = isovolumic relaxation.

 

Figure 2
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  		Figure 2 Variations in strain rate (SR) signal quality. A good-quality curve has well-defined components and limited signal noise (A). Increasing degrees of signal noise compromise the definition of peak SR (initially influencing timing parameters, (B) and if sufficiently severe may preclude even the measurement of amplitude parameters (C).

 

Figure 3
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  		Figure 3 Pitfalls of tissue Doppler-derived strain rate. (A) Reverberation (here related to rib artifact marked by an arrow and shown on the yellow curve) compromises the strain rate signal, contrasted with an adjacent normal strain rate signal (blue curve). (B) The importance of avoiding blood-pool activity, in which a noisy strain rate curve (yellow) is compared with a smaller sample size, tracked to myocardial movement (blue). (C) The limited spatial resolution of tissue Doppler, in which the blue curve (sample volume outside of the cardiac contour), although noisy, is comparable with the yellow curve that is appropriately tracked to the wall.

 

Figure 4
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  		Figure 4 The impact of aliased peak stress tissue velocity data on strain rate calculation. (A) The presence of aliased tissue Doppler data is identified by the golden coloration of the inferior wall on the color tissue Doppler image (lower left), which in turn produces a mottled appearance of the color strain rate image (upper left) and a meaningless strain rate curve (note the absence of negative systolic deflection [arrows]). (B) The tissue velocity data have been gathered with a higher aliasing velocity—note the different color map appearances and typical waveform.

 

Figure 5
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  		Figure 5 Impact of angulation on strain rate imaging. Interrogation parallel with the wall (mid-septum, shown in blue) identifies long-axis shortening, and at right angles to the wall (apex, shown in red) identifies short-axis thickening. However, an intermediate angle (apical septum, shown in yellow) causes underestimation—a mixture of vectors at 45% produces a net absence of recordable strain. Scan planes are shown as continuous lines, longitudinal and radial contraction vectors as broken lines.

 

Figure 6
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  		Figure 6 Two-dimensional (2D) strain is based on comparison of the image texture (i.e., pattern of individual speckle elements) from frame to frame. The distortion of this pattern permits assessment of strain in the axis of movement rather than the axis of the ultrasound beam.

 

Figure 7
Figure 7
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  		Figure 7 Quantification of the biphasic response using strain rate imaging. This dobutamine echo was performed 3 months after anterior infarction. Resting images are in the upper left with 5 µg in the upper right, 10 µg in the lower left, and 40 µg in the lower right. The two-dimensional images (A) show a resting wall motion abnormality in the apical septal and lateral walls, both of which seem to improve at low dose and deteriorate at peak dose. Strain profiles (B) of the apical lateral segment show lengthening at rest, shortening at low dose, and lengthening at peak stress, and a similar pattern of augmentation and deterioration is apparent on the strain rate curves. There are no changes in the apical septal segment, consistent with infarction. Gadolinium-contrast magnetic resonance confirmed the presence of scar in the apex. For an accompanying video, please see the .

 

Figure 8
Figure 8
Figure 8
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  		Figure 8 Quantification of ischemic changes using strain rate imaging. In these views of a standard dobutamine echocardiograph, resting images are shown in the upper left, 10 µg in the upper right, 30 µg in the lower left, and 40 µg in the lower right. End-systolic frames of the apical two-chamber (A) and four-chamber (B) views are shown, inferior and septal walls are outlined, and stress-induced wall motion abnormalities in the basal inferior (A) and septal (B) segments are marked by arrows in the pre-peak and peak dose images. Strain and strain rate profiles in the basal inferior (C) and septal (D) segments show reduction of basal strain (<10%) and strain rate (<1/s) at peak stress, with no changes in the mid/apical segments. Coronary angiography (E) shows significant right coronary disease. For an accompanying video, please see the .

 

Figure 9
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  		Figure 9 Use of two-dimensional (2D) strain to quantify changes in wall thickening in ischemic territories. The baseline images showed apical septal hypokinesis, manifest as reduced amplitude of the strain-rate curve (green, marked with short arrow), but this worsened to display systolic lengthening and post-systolic shortening with stress (long arrow). The patient had critical disease of the left anterior descending artery at coronary angiography.

 




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