title: Blood correction reduces variability and gender differences in native myocardial T1 values at 1.5 T cardiovascular magnetic resonance - a derivation/validation approach.
abstract: BACKGROUND
  Myocardial native T1 measurements are likely influenced by intramyocardial blood. Since blood T1 is both variable and longer compared to myocardial T1, this will degrade the precision of myocardial T1 measurements. Precision could be improved by correction, but the amount of correction and the optimal blood T1 variables to correct with are unknown. We hypothesized that an appropriate correction would reduce the standard deviation (SD) of native myocardial T1.
  
  
  METHODS
  Consecutive patients (n = 400) referred for CMR with known or suspected heart disease were split into a derivation cohort for model construction (n = 200, age 51 ± 18 years, 50% male) and a validation cohort for assessing model performance (n = 200, age 48 ± 17 years, 50% male). Exclusion criteria included focal septal abnormalities. A Modified Look-Locker inversion recovery sequence (MOLLI, 1.5 T Siemens Aera) was used to acquire T1 and T1* maps. T1 and T1* maps were used to measure native myocardial T1, and blood T1 and T1*. A multivariate linear regression correction model was implemented using blood measurement of R1 (1/T1), R1* (1/T1*) or hematocrit. The correction model from the derivation cohort was applied to the validation cohort, and assessed for reduction in variability with the F-test.
  
  
  RESULTS
  Blood [LV + RV] mean R1, mean R1* and hematocrit correlated with myocardial T1 (Pearson's r, range 0.37 to 0.45, p < 0.05 for all) in both the derivation and validation cohorts respectively, suggesting that myocardial T1 measurements are influenced by intramyocardial blood. Mean myocardial native T1 did not differ between the derivation and validation cohorts (1030 ± 42.6 ms and 1023 ± 45.2 ms respectively, p = 0.07). In the derivation cohort, correction using blood mean R1 and mean R1* yielded a decrease in myocardial T1 SD (45.2 ms to 36.6 ms, p = 0.03). When the model from the derivation cohort was applied to the validation cohort, the SD reduction was maintained (39.3 ms, p = 0.049). This 13% reduction in measurement variability leads to a 23% reduction in sample size to detect a 50 ms difference in native myocardial T1.
  
  
  CONCLUSIONS
  Correcting native myocardial T1 for R1 and R1* of blood improves the precision of myocardial T1 measurement by ~13%, and could consequently improve disease detection and reduce sample size needs for clinical research.
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Jannike
authors.initials: J
authors.lastname: Nickander
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Magnus
authors.initials: M
authors.lastname: Lundin
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Goran
authors.initials: G
authors.lastname: Abdula
authors.affiliation: Department of Medicine, Unit of Cardiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Peder
authors.initials: P
authors.lastname: Sörensson
authors.affiliation: Institute of Cardiovascular Science, University College London, London, UK.
authors.forename: Stefania
authors.initials: S
authors.lastname: Rosmini
authors.affiliation: Institute of Cardiovascular Science, University College London, London, UK.
authors.forename: James C
authors.initials: JC
authors.lastname: Moon
authors.affiliation: National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
authors.forename: Peter
authors.initials: P
authors.lastname: Kellman
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
authors.forename: Andreas
authors.initials: A
authors.lastname: Sigfridsson
authors.affiliation: Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. martin.ugander@gmail.com.
authors.forename: Martin
authors.initials: M
authors.lastname: Ugander
mesh_terms: D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity; D003287:Contrast Media / Q000008:administration & dosage; D005260:Female; D006331:Heart Diseases / Q000097:blood / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D006400:Hematocrit; D006801:Humans; D016014:Linear Models; D019028:Magnetic Resonance Imaging, Cine / Q000379:methods*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009206:Myocardium / Q000473:pathology; D011237:Predictive Value of Tests; D011446:Prospective Studies; D015203:Reproducibility of Results; D012189:Retrospective Studies; D012737:Sex Factors; D013318:Stroke Volume; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right
chemical_list: D003287:Contrast Media
keywords: Native T1; Post-processing; Precision; Quantification; T1 Mapping