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Role of T1 mapping as a complementary tool to T2* for non-invasive cardiac iron overload assessment.

ABSTRACT: Iron overload-related heart failure is the principal cause of death in transfusion dependent patients, including those with Thalassemia Major. Linking cardiac siderosis measured by T2* to therapy improves outcomes. T1 mapping can also measure iron; preliminary data suggests it may have higher sensitivity for iron, particularly for early overload (the conventional cut-point for no iron by T2* is 20ms, but this is believed insensitive). We compared T1 mapping to T2* in cardiac iron overload.In a prospectively large single centre study of 138 Thalassemia Major patients and 32 healthy controls, we compared T1 mapping to dark blood and bright blood T2* acquired at 1.5T. Linear regression analysis was used to assess the association of T2* and T1. A "moving window" approach was taken to understand the strength of the association at different levels of iron overload.The relationship between T2* (here dark blood) and T1 is described by a log-log linear regression, which can be split in three different slopes: 1) T2* low, <20ms, r2 = 0.92; 2) T2* = 20-30ms, r2 = 0.48; 3) T2*>30ms, weak relationship. All subjects with T2*<20ms had low T1; among those with T2*>20ms, 38% had low T1 with most of the subjects in the T2* range 20-30ms having a low T1.In established cardiac iron overload, T1 and T2* are concordant. However, in the 20-30ms T2* range, T1 mapping appears to detect iron. These data support previous suggestions that T1 detects missed iron in 1 out of 3 subjects with normal T2*, and that T1 mapping is complementary to T2*. The clinical significance of a low T1 with normal T2* should be further investigated.

SUBMITTER: Torlasco C

PROVIDER: S-EPMC5821344 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Role of T1 mapping as a complementary tool to T2* for non-invasive cardiac iron overload assessment.

Torlasco Camilla C Cassinerio Elena E Roghi Alberto A Faini Andrea A Capecchi Marco M Abdel-Gadir Amna A Giannattasio Cristina C Parati Gianfranco G Moon James C JC Cappellini Maria D MD Pedrotti Patrizia P

PloS one 20180221 2

<h4>Background</h4>Iron overload-related heart failure is the principal cause of death in transfusion dependent patients, including those with Thalassemia Major. Linking cardiac siderosis measured by T2* to therapy improves outcomes. T1 mapping can also measure iron; preliminary data suggests it may have higher sensitivity for iron, particularly for early overload (the conventional cut-point for no iron by T2* is 20ms, but this is believed insensitive). We compared T1 mapping to T2* in cardiac i ...[more]

PMID: 29466447

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Project description:AIMS:The purpose of this retrospective single-centre study was to evaluate the non-invasive detection of endomyocardial biopsy (EMB)-established chronic myocardial inflammation in patients with heart failure with reduced ejection fraction (HFrEF) using T1 and T2 mapping. METHODS AND RESULTS:The study population consisted of 52 retrospectively identified HFrEF patients who underwent EMB and cardiac magnetic resonance imaging at 3 Tesla. EMB was defined according to the position statement of the European Society of Cardiology and served as reference to identify inflammation in all patients. A control group of healthy volunteers with prior cardiac magnetic resonance imaging studies (n = 58) was also identified. Global and segmental T1 and T2 values as well as septal measurements and tissue heterogeneity parameters were calculated. Out of the 52 patients with HFrEF, 33 patients had myocardial inflammation detected by EMB, while 19 patients were EMB negative for inflammation. Mean left ventricular ejection fraction was 31% in both groups (P = 0.97). Global T1 and T2 values in HFrEF patients were significantly higher compared with healthy controls (T1 1275 ± 69 ms vs. 1,175 ± 44 ms, P < 0.001; T2 40.0 ± 3.4 ms vs. 37.9 ± 1.6 ms, P < 0.001). The distribution of T1 and T2 values between patients with and without EMB-proven chronic myocardial inflammation was not statistically different when regarding global (T1 1292 ± 71 ms vs. 1266 ± 67 ms, P = 0.26; T2 40.0 ± 2.6 ms vs. 40.0 ± 3.9 ms, P = 1.0), septal (T1 1299 ± 63 ms vs. 1289 ± 76 ms, P = 0.76; T2 40.1 ± 3.5 ms vs 40.0 ± 6.4 ms, P = 0.49) or maximum segmental values (T1 1414 ± 111 ms vs. 1363 ± 88 ms, P = 0.15; T2 47.3 ± 5.2 ms vs. 48.8 ± 11.8 ms, P = 0.53). Mean absolute deviation of segmental T1 and T2 values and log-transformed pixel-wise standard deviation as parameters of tissue heterogeneity did not reveal statistical significant differences between inflammation-positive and inflammation-negative HFrEF patients (all P > 0.4). CONCLUSIONS:Conventionally performed quantitative T1 and T2 mapping values significantly correlated with prevalence of HFrEF but did not discriminate HFrEF patients with or without chronic myocardial inflammation in our cohort. This suggests that EMB is the preferred method to detect chronic myocardial inflammation in HFrEF.

Project description:Stress and rest T1-mapping may assess for myocardial ischemia and extracellular volume (ECV). However, the stress T1 response is method-dependent, and underestimation may lead to misdiagnosis. Further, ECV quantification may be affected by time, as well as the number and dosage of gadolinium (Gd) contrast administered. We compared two commonly available T1-mapping approaches in their stress T1 response and ECV measurement stability. Healthy subjects (n = 10, 50% female, 35 ± 8 years) underwent regadenoson stress CMR (1.5 T) on two separate days. Prototype ShMOLLI 5(1)1(1)1 sequence was used to acquire consecutive mid-ventricular T1-maps at rest, stress and post-Gd contrast to track the T1 time evolution. For comparison, standard MOLLI sequences were used: MOLLI 5(3)3 Low (256 matrix) & High (192 matrix) Heart Rate (HR) to acquire rest and stress T1-maps, and MOLLI 4(1)3(1)2 Low & High HR for post-contrast T1-maps. Stress and rest myocardial blood flow (MBF) maps were acquired after IV Gd contrast (0.05 mmol/kg each). Stress T1 reactivity (delta T1) was defined as the relative percentage increase in native T1 between rest and stress. Myocardial T1 values for delta T1 (dT1) and ECV were calculated. Residuals from the identified time dependencies were used to assess intra-method variability. ShMOLLI achieved a greater stress T1 response compared to MOLLI Low and High HR (peak dT1 = 6.4 ± 1.7% vs. 4.8 ± 1.3% vs. 3.8 ± 1.0%, respectively; both p < 0.0001). ShMOLLI dT1 correlated strongly with stress MBF (r = 0.77, p < 0.001), compared to MOLLI Low HR (r = 0.65, p < 0.01) and MOLLI High HR (r = 0.43, p = 0.07). ShMOLLI ECV was more stable to gadolinium dose with less time drift (0.006-0.04% per minute) than MOLLI variants. Overall, ShMOLLI demonstrated less intra-individual variability than MOLLI variants for stress T1 and ECV quantification. Power calculations indicate up to a fourfold (stress T1) and 7.5-fold (ECV) advantage in sample-size reduction using ShMOLLI. Our results indicate that ShMOLLI correlates strongly with increased MBF during regadenoson stress and achieves a significantly higher stress T1 response, greater effect size, and greater ECV measurement stability compared with the MOLLI variants tested.

Dataset Information

Role of T1 mapping as a complementary tool to T2* for non-invasive cardiac iron overload assessment.

Publications

Role of T1 mapping as a complementary tool to T2* for non-invasive cardiac iron overload assessment.

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