Abstract
BackgroundMyocardial 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.MethodsConsecutive 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.ResultsBlood [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.ConclusionsCorrecting 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.
Highlights
Myocardial native T1 measurements are likely influenced by intramyocardial blood
There was no difference in characteristics between the derivation and validation cohorts, except for left ventricle (LV) stroke volume (SV) and indexed LVSV (LVSVI), which was lower in the derivation cohort, albeit with a small magnitude of difference
We have demonstrated that correcting for blood characteristics decreases the variability of native myocardial T1 in a clinical population, and reduces gender differences in healthy volunteers
Summary
Myocardial native T1 measurements are likely influenced by intramyocardial blood. Native myocardial T1 mapping has shown diagnostic promise for differentiating healthy myocardium from various pathologies including acute myocardial infarction [2], myocarditis [3, 4], amyloidosis [5], edema [6], Anderson-Fabry disease [7] and other non-ischemic diseases [8, 9]. The T1 values of blood have been shown to vary due to a number of factors like hematocrit [18], sex [10], age [19], and oxygen pressure [18, 20] and variations in these factors may influence the interpretation of myocardial T1 values, and obscure the true T1 value of the myocardium
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