CMR Tissue Mapping Demonstrates Longitudinal Changes in T1, T2, and ECV Mapping in Heart Transplant Recipients

Background: Myocardial tissue characterization by cardiac magnetic resonance (CMR) imaging provides non-invasive measures of fibrosis, inflammation, and edema through T1, T2, and extracellular volume (ECV) mapping.¹ In heart transplant (HTx) recipients, longitudinal changes in these parameters may reflect graft remodeling associated with complications such as acute cellular rejection (ACR) or cardiac allograft vasculopathy (CAV).^2,3 However, clinical and demographic correlates of different trajectories HTx patient (stable vs. chnages over time in tissue parameters) remain poorly understood. We sought to characterize longitudinal changes in tissue mapping indices and to explore their associations with comorbidities and HTx-related features.

Methods: Seventy-five post-HTx recipients underwent baseline and follow-up CMR including CINE imaging (short axis, base to apex) and left ventricular tissue parameter mapping (T2, pre- and post-contrast T1) at least one year apart (minimum time between scans 1.0 years; mean 4.4±2.0 years). 'Total' values were defined as the mean of the three short axis slices (basal, mid, apical), whereas 'Peak' values were the highest pixel value within the ROI. Demographic and clinical variables included age, sex, race, BMI, hypertension, hyperlipidemia, coronary artery disease, diabetes, prior myocardial infarction, and transplant indication (Table 1). Longitudinal changes in tissue parameters were normalized for time (Δ/year) and categorized as increasing, stable, or decreasing using predefined thresholds (T1 ±5 ms/yr, T2 ±1 ms/yr, ECV ±1%/yr). Associations between CMR tissue parameter trajectories and clinical features were assessed using chi-square/Fisher’s exact tests for categorical variables, and Kruskal–Wallis tests for continuous or ordinal variables.

Results: The cohort (75 patients, 47 male, mean age 48±16 years) demonstrated significant longitudinal changes in myocardial tissue parameters (Table 1). As shown in Figure 1, native left ventricular T1 (996.0±76.6 vs. 1027.6±73.9 ms, p=0.005), peak T1 (1076.9±89.9 vs. 1104.6±82.7 ms, p=0.046), and T2 (52.4±5.3 vs. 50.6±4.3 ms, p=0.005) increased significantly between baseline and follow-up. When stratified by peak ECV trajectory, hypertension was significantly associated with stability of values (p=0.007), whereas non-hypertensive patients were more likely to exhibit increasing or decreasing trajectories (Table 2). Associations with age and diabetes were found to be non-significant.

Conclusion: In HTx recipients, CMR tissue-mapping indices showed measurable longitudinal changes, with significant increases in native T1 (total and peak) and total T2 over time. Hypertension was associated with a stable peak-ECV trajectory, suggesting comorbidity-linked patterns of graft remodeling. Next steps will test whether these imaging trajectories are associated with adverse outcomes, specifically ISHLT ACR grade and CAV grade, to determine whether tissue-mapping dynamics reflect histopathologic rejection and vasculopathy.

Baseline characteristics and longitudinal CMR tissue parameter changes in heart transplant recipients.

Panel A. Baseline demographics and clinical characteristics

Variable	Overall (n=75)
Age at MRI, years	48 ± 16
Time between HTx and MRI, years	7.2 ± 5.6
BMI	27.6 ± 5.3
Male sex, n (%)	47 (62.7%)
Race, n (%)	Asian: 4 (5.3%) Black or African American: 14 (18.7%) White: 54 (72%) Unknown: 3 (4%)
Ethnicity, n (%)	Hispanic or Latino: 11 (14.7%) Not Hispanic or Latino: 64 (85.3%)
Transplant indication	Ischemic: 14 (18.7%) Non-ischemic: 61 (81.3%)
Hypertension, n (%)	62 (82.7%)
Hyperlipidemia, n (%)	46 (61.3%
CAD, n (%)	25 (33%)
Prior MI, n (%)	15 (20%)
Diabetes, n (%)	24 (32%)

Panel B. Longitudinal CMR tissue parameter changes.

Tissue Parameter		N	Values			Trajectory (n, %)
			Baseline	Follow-up	p-value	Decreasing / Stable / Increasing
T1 (ms)	Total	75	996.0±76.1	1027.6±73.4	.0045**	19 (25%)	17 (23%)	39 (52%)
	Peak	75	1076.9±89.3	1104.6±82.2	.043**	17 (23%)	19 (25%)	39 (52%)
T2 (ms)	Total	72	52.4± 5.3	50.7± 4.4	.0052**	21 (29%)	46 (64%)	5 (7%)
	Peak	72	59.9±9.9	57.6±7.7	.066	28 (39%)	26 (36%)	18 (25%)
ECV (%)	Total	70	28.7±4.8	29.2± 7.1	.062	13 (19%)	33 (48%)	23 (33%)
	Peak	70	35.2±7.4	35.9± 11.0	0.65	17 (24%)	26 (38%)	26 (38%)

Panel A summarizes demographic and clinical features, reported as mean ± SD or n (%).Panel B shows baseline and follow-up values for T1, T2, and ECV mapping, with patients stratified into decreasing, stable, or increasing trajectories per year (thresholds: T1 ±5 ms/yr, T2 ±1 ms/yr, ECV ±1%/yr). p < 0.01 indicates statistical significance.Association of peak ECV trajectory with clinical variables.

Variable	Decreasing	Stable	Increasing	p-value
Age, yrs (mean ± SD)	48.9 ± 15.2	54.3 ± 14.5	44.3 ± 16.6	0.14
Gender, male (n, %)	17 (37%)	17 (37%)	12 (26%)	.221
Race (white)	13 (26%)	21 (42%)	16 (32%)	.458
BMI	28.4 ± 5.3	27.7 ± 4.7	26.7 ± 5.6	.683
Transplant indication—ischemic	5 (38%)	4 (31%)	4 (31%)	.687
Hypertension	17 (30%)	27 (47%)	13 (23%)	.0068**
Hyperlipidemia	15 (34%)	18 (41%)	11 (25%)	.433
CAD	8	9	7	.904
Prior MI	4	5	5	.93
Diabetes	8	12	4	.199

Distribution of demographic and comorbidity features across ECV change categories. Hypertension was significantly associated with stable peak ECV (p=0.007).Figure 1. Boxplots of tissue parameters at baseline and follow-up. Native T1 total, T1 peak, and total T2 values demonstrated significant increases between baseline and follow-up, indicating progressive myocardial remodeling.