Key result
Heart-transplant patients with nonspecific graft dysfunction demonstrated significantly decreased stress myocardial perfusion and a trend toward increased activated T cells compared to normal heart-transplant patients.
Why the study?
The study investigated myocardial perfusion differences and changes in immune cell response in heart-transplant patients with nonspecific graft dysfunction compared with CAV patients and normal heart-transplant patients.
Does regadenoson stress CMR and immune cell profiling identify differences in myocardial perfusion and T-cell activation in heart-transplant patients with nonspecific graft dysfunction compared to normal graft function and CAV?
Observational (n=17)
Single-blind
Yes
Does regadenoson stress CMR and immune cell profiling identify differences in myocardial perfusion and T-cell activation in heart-transplant patients with nonspecific graft dysfunction compared to normal graft function and CAV?
Nonspecific graft dysfunction in heart-transplant patients is associated with decreased stress myocardial perfusion and increased activated T cells, suggesting an immune-mediated microvascular allograft vasculopathy.
May support immune-mediated microvascular vasculopathy in nonspecific graft dysfunction; hypothesis-generating and requires prospective validation before clinical use.
Background We investigated the myocardial perfusion differences and changes in immune cell response in heart-transplant patients with nonspecific graft dysfunction (NGD) compared to cardiac allograft vasculopathy (CAV) patients and normal heart-transplant patients. Methods and Results We prospectively studied 17 heart-transplant patients (59.8±14.1 years, 78% male) from January to June 2016. Regadenoson stress cardiac MRI was performed in the patients and peripheral blood obtained contemporaneously to isolate peripheral blood mononuclear cells (PBMCs). Stress myocardial perfusion showed significantly decreased myocardial perfusion using maximum upslope method in NGD and CAV patients compared to normal heart-transplant patients. Myocardial scar by late gadolinium enhancement also was significantly increased in nonspecific graft dysfunction patients compared to normal. Evaluation of PBMCs by flow cytometry showed a trend towards increased activated HLA-DR + T cells in NGD patients compared to normal. Clinical outcomes for cardiac hospitalization, allograft loss/retransplant, death were assessed at 8 years. Conclusions NGD shows decreased stress myocardial perfusion by cardiac MRI and a trend towards increased activated T cells in PBMCs, suggestive of an immune-mediated cause for allograft dysfunction.
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Kim et al. (2020) conducted an observational in Cardiac Allograft Dysfunction (n=17). Nonspecific graft dysfunction (NGD) vs. Normal heart-transplant patients was evaluated on Stress myocardial perfusion by cardiac MRI. Heart-transplant patients with nonspecific graft dysfunction demonstrated significantly decreased stress myocardial perfusion and a trend toward increased activated T cells compared to normal heart-transplant patients.
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