Journal of the American Society of Echocardiography
Real-Time Strain Rate Imaging of the Left Ventricle by Ultrasound☆,☆☆,★,★★
Section snippets
The Strain Rate
The temporal derivative of the strain, ie, the strain rate, is a measure of the rate of deformation. This measure is equivalent to the spatial derivative of the velocity as described in the Appendix. A negative strain rate means that the tissue segment is becoming shorter (or thinner), whereas a positive strain rate means that the segment is becoming longer (or thicker). The strain rate is also equivalent to the shortening velocity per fiber length. This measure is a part of the
Long-Axis Function and Regional Wall Thickening
In conventional 2-dimensional (2D) echocardiography, global left ventricle (LV) function is estimated by the shortening fraction or ejection fraction, whereas regional LV function is evaluated using segmental endocardial excursion or wall thickening. Although endocardial excursion generally is the most used parameter, it does not differentiate actively contracting segments from passively drawn segments (eg, postinfarction scars). Wall thickening, on the other hand, is more difficult to evaluate
Tissue Doppler
Tissue Doppler imaging (TDI) maps local tissue velocities (point velocities) in the ventricle, thus increasing the physiologic information about the LV. In color mapping, particularly in M-mode, the TDI can accurately delineate the phases of the heart cycle with high temporal resolution.25 TDI cine loops can be collected with a sampling frequency (frame rate) of above 50 frames/s. In color M-mode or pulsed wave Doppler, the frame rate can be increased to above 200 frames/s.
The point velocity of
The Strain Rate Imaging Method
The strain rate (S) is equivalent to the spatial gradient of the velocity. The longitudinal velocity component v of every point in the muscle is available from TDI, so the gradient can be estimated from 2 points along the ultrasound beam, as described in Equation 1: where r is the distance along the beam, and Δr is the small offset between the 2 points, as shown in Figure 2.
RESULTS
We obtained a frame rate of 50 to 70 frames/s. Thus the M-modes could be reconstructed from single cine-loops, with true simultaneity in all parts of the ventricle in each plane. The temporal resolution (sampling frequency) of the M-mode is equal to the frame rate in 2D echocardiography, and far greater than that available with MRI.
In the healthy subjects, the systole appeared as an ordered sequence of negative strain rate (longitudinal shortening) during the ejection period. This wave of
Limitations
Strain rate imaging by ultrasound has a superior temporal resolution compared with MRI, but can only account for one direction of strain rate. Strain rates in the directions transverse to the ultrasound beam as well as shear strain rates are currently not accessible.
Besides being performed in real-time, SRI imaging differs from the MVG method in that the strain rate is calculated for all points in the image simultaneously, allowing a color display of the deformations. In addition, because the
CONCLUSIONS
In this pilot study, we demonstrated that the strain rate can be measured in real-time by ultrasound, and that SRI gives additional, qualitative physiologic information to other echocardiographic modalities, both in healthy subjects and in patients with infarctions. The method seems to differentiate clearly between normal and reduced regional LV function. We believe that the longitudinal strain rate, assessed in apical views, is the most informative examination. Strain rate imaging may be the
Acknowledgements
We thank Annette Vanvik Lund, MSc, for practical help with the radiofrequency data after processing; Bjørn Olstad, PhD, at Vingmed Sound, and Sevald Berg, MSc, for the strain rate curved M-mode implementation; and Torbjørn Bakke, MSc, at Vingmed Sound, and Tor Urdalen, MSc, for the real-time implementation. We also thank Marek Belohlavek, MD, at the Mayo Clinic, Rochester, Minn, for helpful review and comments.
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Cited by (0)
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From the Department of Physiology and Biomedical Engineering, Norwegian University of Science and Technology, and the Department of Cardiology, University Hospital of Trondheim, Norwegian University of Science and Technology, Trondheim, Norway.
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Supported by the Norwegian Research Council and the Norwegian Council for Cardiovascular Disease.
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Reprint requests: Andreas Heimdal, MSc, Department of Physiology and Biomedical Engineering, Medisinsk Teknisk Senter, N-7005 Trondheim, Norway.
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