SCMR 22nd Annual Scientific Sessions
Background: In pediatric heart transplant (PHT) patients, cardiac catheterization is used to monitor for coronary allograft vasculopathy (CAV) by angiography of epicardial vessels. Cardiac catheterization has no safe and consistent method for measuring the burden of microvascular disease. Cardiac MRI (CMR) with quantitative adenosine perfusion testing offers safe, non-invasive estimates of myocardial perfusion. Our study investigated the myocardial perfusion reserve index (MPR) in pediatric heart transplant (PHT) recipients with and without angiographic evidence of CAV.
Methods: All patients with CAV followed at our institution who received their transplant before age 18 were asked to participate. A group of age and sex matched PHT controls without angiographic CAV was also recruited. Patients underwent CMR with adenosine stress perfusion testing. Global T1 (GT1) and extracellular volume (ECV), additional markers of microvascular disease, were also obtained. Normal myocardial structure and function data were measured as well. Myocardial perfusion was evaluated by administering a gadolinium bolus and then quantifying signal intensity over time at both rest and stress. MPR is the ratio of estimated myocardial blood flow during stress to that during rest. Adequate stress was measured by changes in heart rate and blood pressure as well as monitoring for splenic switch off.
There were 15 PHT patients, age 12-22, who underwent CMR with adenosine stress perfusion testing. 8 patients had CAV by previously seen by angiography and 7 had no CAV diagnosis. No heart block or other significant complications occurred during the study. The mean MPR for the full cohort was decreased at 1.645 (±0.505). The mean MPR for patients with CAV demonstrated a trend of being lower at 1.584 (±0.540) compared to 1.645 (±0.427) for control patients (p=0.34). The GT1 (1016 ± 84) and ECV (30.4% ± 4.4) for the cohort were also abnormal.
The cohort was also analyzed for time after transplant and the number of rejection episodes. The patients within six years of heart transplantation had trends towards higher MPR (1.662 ± 0.431) than those who had their transplants for greater than six years (1.569 ± 0.589;p=0.19). MPR and ECV showed strong correlation across the cohort (R=0.75; p=0.004), but MPR and GT1 did not (R=0.09;p=0.4).
Conclusion: MPR is a safe and feasible method for estimating myocardial perfusion in PHT patients. Our results showed a diminished MPR in the whole cohort, indicating some degree of microvascular disease in most patients. There was a trend toward worse perfusion in patients with angiographic evidence of CAV, and in patients further out from heart transplant. ECV showed strong correlation with MPR, but GT1 did not. Currently there is no reliable way to monitor microvascular disease in pediatric patients, but MPR and ECV show potential and deserve investigation in a larger cohort.