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Comparative Study
. 2019 Aug;12(8 Pt 2):1659-1669.
doi: 10.1016/j.jcmg.2018.08.021. Epub 2018 Nov 15.

Comparing CMR Mapping Methods and Myocardial Patterns Toward Heart Failure Outcomes in Nonischemic Dilated Cardiomyopathy

Affiliations
Comparative Study

Comparing CMR Mapping Methods and Myocardial Patterns Toward Heart Failure Outcomes in Nonischemic Dilated Cardiomyopathy

Tomas Vita et al. JACC Cardiovasc Imaging. 2019 Aug.

Abstract

Objectives: In patients with nonischemic dilated cardiomyopathy (NIDCM), native T1, partition coefficient (λGd), and extracellular volume fraction (ECV) mapping may offer prognostic values beyond late gadolinium enhancement (LGE), by scaling the range of myocardial changes.

Background: In patients with NIDCM, LGE is seen in 30% of patients and it indicates adverse prognosis.

Methods: The study mapped 6 anatomical locations using all 4 cardiac magnetic resonance (CMR) tissue-characterizing methods and associated with outcome. The authors performed T1 mapping of the myocardium and the blood pool, before and serially after contrast injection, using a Look-Locker cine gradient-echo technique to obtain T1 and the corresponding reciprocal R1 values. λGd values were derived from the slopes of the least-squares regression lines for myocardial versus blood R1, then adjusted to serum hematocrit to yield ECV.

Results: Consecutive 240 NIDCM patients (49 ± 16 years of age; 38% women) underwent CMR for cardiac function, LGE, native T1, λGd, and ECV. After a median of 3.8 years, 36 (15%) experienced major adverse cardiac events (MACE), including 22 heart failure hospitalizations and 14 deaths. Nonischemic LGE was detected in 34%, whereas ECV was elevated (≥1 location) in 58%. Comparing the 4 methods, mean ECV and λGd both demonstrated strong association with MACE (both p < 0.001). In contrast to native T1 and LGE, ECV values from all 6 locations were associated with MACE and death, with the anteroseptum being the most significant (p < 0.0001). The number of abnormal ECV locations correlated linearly with annual MACE rates (p = 0.0003). Mean ECV was the only predictor to enter a prognostic model that contained age, sex, New York Heart Association functional class, and left ventricular ejection fraction. For every 10% increase, mean ECV portended to a 2.8-fold adjusted increase risk to MACE (p < 0.001).

Conclusions: In this study of patients with NIDCM, mapping the myocardial extent of abnormality using ECV offers prognostication toward heart failure outcomes incremental to LGE or native T1 mapping.

Keywords: ECV; NIDCM; dilated cardiomyopathy; native T1; partition coefficient.

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Figures

Figure 1.
Figure 1.. Image Processing of Look-Locker T1 Imaging
Look-Locker T1 imaging using a low flip-angle segmented gradient echo pulse sequence (flip=10°, TR/TE=5.5/2.8 ms). Images for a total of 17 times after inversion (TI) were acquired and every second one is displayed in this montage (a). Three short-axis cuts were imaged for 1 pre- and 3 post-contrast T1 measurements. Bullseye view representing color-encoded T1 values for mid ring locations by Look-Locker imaging as shown in (b). The average signal intensity for each of the 18 segments was used, with IR phase restoration, for fitting to a parametrized representation of the inversion recovery, A + B∙exp(−TI/T1*), where A, B, and T1* are adjustable parameters, and TI the time after application of the adiabatic inversion pulse. T1 was calculated from A, B, and T1 * to correct for radio-frequency pulse effects during the Look-Locker read-outs. The data and best fit IR curve are shown in magnitude mode (c). A total of four T1 measurements were used for estimation of ECV by least-squares linear regression (d). ECV corresponds to the slope of the regression line, multiplied by (1-hematocrit). ECV values estimated as shown in (e) are color-encoded and displayed in the 6 anatomical locations.
Figure 2.
Figure 2.. Kaplan-Meier Curve Stratified by ECV Tertiles.
Kaplan–Meier survival curves demonstrating progressive reduction of MACE-free survival from the lowest to the highest ECV tertiles.
Figure 3.
Figure 3.. Annualized Event Rates of MACE stratified by LVEF < 30% and ECV Tertiles.
There was progressive increase in the annual MACE rates across the escalating ECV tertiles, regardless of patients’ status of LVEF <30%.
Figure 4.
Figure 4.. Univariable Associations of the Anatomical Locations Across the Tissue Characterization Methods with MACE.
Mean ECV values in all 6 anatomical locations had robust association with MACE, which is in contrast to native T1 mapping and LGE presence. Abnormalities in anteroseptal and inferoseptal locations were more closely linked with MACE.
Figure 5.
Figure 5.. Annualized Event-Rates Based on the extent of Abnormal Anatomical locations in LGE, native T1 and ECV.
The total number of abnormal anatomical locations by LGE (panel a) and λGd(panel b) were not significantly associated with MACE. In panel c, the extent of abnormal ECV locations showed a linear trend towards the risk of MACE (p<0.01 for trend). This suggests the diffuse myocardial pattern mapped by ECV characterized the risk to MACE more closely than LGE or native T1. For every additional abnormal ECV myocardial location, the risk increases by 18% (HR 1.18, 95%CI: 1.01-1-39, p=0.0003 for trend).
Figure 6.
Figure 6.. Univariable Analysis Associations of the Anatomical Locations Across the Tissue Characterization Methods with MACE, in Patients with no LGE
In LGE negative patients, all locations by ECV maintained robust prognostic association with MACE. In comparison, locations by native T1, λGd, and LGE were not associated with MACE regardless of the anatomical location of abnormality.

Comment in

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