Why the study?
Myocardial perfusion impacts cardiac function after surgical repair of critical congenital heart disease, but the feasibility and physiologic validity of noninvasive perioperative transthoracic ultrafast power Doppler assessment remained unproven.
Can ultrafast power Doppler (UPD) noninvasively assess physiologic changes in myocardial perfusion in neonates with critical congenital heart disease?
Can ultrafast power Doppler (UPD) noninvasively assess physiologic changes in myocardial perfusion in neonates with critical congenital heart disease?
Ultrafast power Doppler is a feasible noninvasive technique to quantify myocardial perfusion changes in neonates with critical congenital heart disease undergoing surgery.
Perioperative UPD may enable noninvasive myocardial perfusion monitoring in CCHD; leaves open clinical utility pending validation.
Aims Myocardial perfusion impacts cardiac function following surgical repair of critical congenital heart disease (CCHD). Temporal variation assessment of myocardial blood volume throughout the cardiac cycle can be a surrogate for perfusion. Ultrafast power Doppler (UPD) is an ultrasound imaging technique capable of noninvasively quantifying myocardial blood volume changes. The objective of this study is to demonstrate the feasibility of perioperative transthoracic UPD assessment and to determine if UPD reflects physiologic changes in myocardial perfusion. Methods and results Five neonatal transposition of the great arteries (TGA) undergoing arterial switch operation (ASO), five hypoplastic left heart syndrome (HLHS) undergoing Stage 1 palliation (S1P), and five age/weight-matched controls were prospectively recruited. Transthoracic UPD acquisitions were performed before/after operations. Segmental perfusion in right/left ventricles (RV/LV) was assessed. The controls’ myocardial perfusion patterns are visually similar to published human references for both ventricles. Systolic/diastolic myocardial perfusion differences were modified by ASO in the RV (P = 0.03) but not for LV (P = 0.99). For HLHS patients, no difference after S1P was observed in either the RV (P = 0.16) nor the LV (P = 0.51). Conclusion For TGA patients, the perfusion profile of the myocardium seems to be directly influenced by the intracavitary pressure (directly driving coronary perfusion pressure), namely if it was the systemic or sub-pulmonary ventricle. Our data suggests that UPD could noninvasively quantify myocardial perfusion variation. Myocardial perfusion patterns change in CCHD according to their haemodynamic and surgical status. Correlation with clinical outcomes requires further study.
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Nguyen et al. (2025) studied this question.
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