Key result
Mean longitudinal strain measured by TFE velocity encoded CMR was significantly lower in patients with recent myocardial infarction (-0.15) compared to healthy volunteers (-0.18).
Why the study?
Does velocity encoded cardiovascular magnetic resonance accurately quantify longitudinal strain compared to optical tracking in healthy volunteers and MI patients?
Observational (n=46)
No
Does velocity encoded cardiovascular magnetic resonance accurately quantify longitudinal strain compared to optical tracking in healthy volunteers and MI patients?
Absolute Event Rate: -0.15% vs -0.18%
p-value: p=<0.05
Velocity encoded CMR with a novel tracking algorithm provides a robust, clinically applicable method for quantifying longitudinal strain and regional myocardial wall function.
Simple velocity-encoded CMR strain method offers quantitative regional assessment; leaves open clinical adoption pending prospective validation.
BACKGROUND: Regional myocardial function is typically evaluated by visual assessment by experienced users, or by methods requiring substantial post processing time. Visual assessment is subjective and not quantitative. Therefore, the purpose of this study is to develop and validate a simple method to derive quantitative measures of regional wall function from velocity encoded cardiovascular magnetic resonance (CMR), and provide associated normal values for longitudinal strain. METHOD: Both fast field echo (FFE) and turbo field echo (TFE) velocity encoded CMR images were acquired in three long axis planes in 36 healthy volunteers (13 women, 23 men), age 35±12 years. Strain was also quantified in 10 patients within one week after myocardial infarction. The user manually delineated myocardium in one time frame and strain was calculated as the myocardium was tracked throughout the cardiac cycle using an optimization formulation and mechanical a priori assumptions. A phantom experiment was performed to validate the method with optical tracking of deformation as an independent gold standard. RESULTS: There was an excellent agreement between longitudinal strain measured by optical tracking and longitudinal strain measured with TFE velocity encoding. Difference between the two methods was 0.0025 ± 0.085 (ns). Mean global longitudinal strain in the 36 healthy volunteers was -0.18 ± 0.10 (TFE imaging). Intra-observer variability for all segments was 0.00 ± 0.06. Inter-observer variability was -0.02 ± 0.07 (TFE imaging). The intra-observer variability for radial strain was high limiting the applicability of radial strain. Mean longitudinal strain in patients was significantly lower (-0.15± 0.12) compared to healthy volunteers (p<0.05). Strain (expressed as percentage of normal strain) in infarcted regions was lower compared to remote areas (p<0.01). CONCLUSION: In conclusion, we have developed and validated a robust and clinically applicable technique that can quantify longitudinal strain and regional myocardial wall function and present the associated normal values for longitudinal strain.
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Heiberg et al. (2013) conducted an observational in Myocardial Infarction (n=46). Recent myocardial infarction vs. Healthy volunteers was evaluated on Mean global longitudinal strain measured by TFE velocity encoded CMR (p=<0.05). Mean longitudinal strain measured by TFE velocity encoded CMR was significantly lower in patients with recent myocardial infarction (-0.15) compared to healthy volunteers (-0.18).