Quantification of circumferential, longitudinal, and radial global fractional shortening using steady‐state free precession cines: A comparison with tissue‐tracking strain and application in fabry disease. Issue 2 (13th March 2014)

• Record Type: Journal Article
• Authors: Cheng‐Baron, June; Chow, Kelvin; Pagano, Joseph J.; Punithakumar, Kumaradevan; Paterson, D. Ian; Oudit, Gavin Y.; Thompson, Richard B.
• Is Part Of: Magnetic resonance in medicine. Volume 73:Issue 2(2015:Feb.)
• Page Start: 586
• Page End: 596
• Publication Date: 2014-03-13
• Subjects: Nuclear magnetic resonance -- Periodicals; Electron paramagnetic resonance -- Periodicals; 616.07548
• DOI: 10.1002/mrm.25166
• Languages: English
• ISSNs: 0740-3194

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mrm25166-sec-0001" sec-type="section"> <title>Purpose</title> <p>Conventional calculation of myocardial strain requires tissue‐tracking. A surrogate for strain called global fractional shortening (GFS) is proposed based on changes in dimensions of endocardial and epicardial surfaces without tissue‐tracking.</p> </sec> <sec id="mrm25166-sec-0002" sec-type="section"> <title>Methods</title> <p>Three‐dimensional endocardial and epicardial left ventricular surfaces traced at end‐diastole and end‐systole using conventional steady‐state free precession cine images were used to calculate <italic>GFS<sub>cc</sub></italic> (circumferential), <italic>GFS<sub>ll</sub></italic> (longitudinal), and <italic>GFS<sub>rr</sub></italic> (radial) using fractional length changes in each direction over the heart surface. GFS values were validated using finite element models (FEM) and in vivo using tagging‐derived strains (<italic>ε<sub>cc</sub>, ε<sub>ll</sub>, ε<sub>rr</sub></italic>) in patients with a wide range of ejection fraction (EF) and diagnosis (n = 32). GFS was also measured in 31 patients with Fabry disease and matched healthy controls.</p> </sec> <sec id="mrm25166-sec-0003" sec-type="section"> <title>Results</title> <p>GFS values were within 3% of average FEM‐derived Lagrangian strains and had good agreement in vivo (<italic>GFS<sub>cc</sub></italic> = −14 ± 4%, <italic>ε<sub>cc</sub></italic> = −14 ± 4%, R<sup>2</sup> = 0.85; <italic>GFS<sub>ll</sub></italic> = −12 ± 4%, <italic>ε<sub>ll</sub></italic> = −12 ± 4%, R<sup>2</sup> = 0.72; <italic>GFS<sub>rr</sub></italic> = 46 ± 21%). <italic>ε<sub>rr</sub></italic> could not be measured reliably from tagging. Compared with healthy controls with matched EF, patients with Fabry disease had significantly increased <italic>GFS<sub>cc (Endo)</sub></italic> (−28 ± 3% versus −25 ± 2%), decreased <italic>GFS<sub>cc(Epi)</sub></italic> (−10 ± 2% versus −11 ± 2%) and decreased <italic>GFS<sub>ll</sub></italic> for all components.</p> </sec> <sec id="mrm25166-sec-0004" sec-type="section"> <title>Conclusion</title> <p>GFS yields similar values to conventionally measured strains without requiring tissue‐tracking. Compared with controls, patients with Fabry disease have significant differences in several GFS components. <bold>Magn Reson Med 73:586–596, 2015. © 2014 Wiley Periodicals, Inc.</bold></p> </sec> </abstract>