Validation of an automated method to quantify stress-induced ischemia and infarction in rest-stress myocardial perfusion SPECT.

BACKGROUND: Myocardial perfusion SPECT (MPS) is one of the frequently used methods for quantification of perfusion defects in patients with known or suspected coronary artery disease. This article describes open access software for automated quantification in MPS of stress-induced ischemia and infarction and provides phantom and in vivo validation. METHODS AND RESULTS: A total of 492 patients with known or suspected coronary artery disease underwent both stress and rest MPS. The proposed perfusion analysis algorithm (Segment) was trained in 140 patients and validated in the remaining 352 patients using visual scoring in MPS by an expert reader as reference standard. Furthermore, validation was performed with simulated perfusion defects in an anthropomorphic computer model. Total perfusion deficit (TPD, range 0-100), including both extent and severity of the perfusion defect, was used as the global measurement of the perfusion defects. Mean bias ± SD between TPD by Segment and the simulated TPD was 3.6 ± 3.8 (R(2) = 0.92). Mean bias ± SD between TPD by Segment and the visual scoring in the patients was 1.2 ± 2.9 (R (2)= 0.64) for stress-induced ischemia and -0.3 ± 3.1 (R(2) = 0.86) for infarction. CONCLUSION: The proposed algorithm can detect and quantify perfusion defects in MPS with good agreement to expert readers and to simulated values in a computer phantom.

Longitudinal strain from velocity encoded cardiovascular magnetic resonance: a validation study.

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.