Abstract

BackgroundThe repair surgery of congenital heart disease (CHD) associated with the right ventricular (RV)-pulmonary artery (PA) pathophysiology often left patients with critical post-operative lesions, leading to regurgitation and obstruction in the PAs. These lesions need longitudinal (with time) assessment for monitoring the RV function, in order for patients to have appropriate treatment before irreversible RV dysfunction occurs. In this research, we computed energy loss in the branch PAs using blood flow and pressure drop data obtained from 4D phase contrast (PC) MRI, to non-invasively quantify the RV-PA pathophysiology.Methods4D PC MRI was acquired for a CHD patient with abnormal RV-PA physiology, including pulmonary regurgitation and PA stenosis, and a subject with normal RV-PA physiology. The blood velocity, flow rate, and pressure drop data, obtained from 4D PC MRI, were used to compute and compare the energy loss values between the patient and normal subjects.ResultsThe pressure drop in the branch PAs for the patient was −1.3 mmHg/s and −0.2 mmHg/s for the RPA and LPA, respectively, and was larger (one order of magnitude) than that for the control. Similarly, the total energy loss in the branch PAs for the patient, -96.9 mJ/s and −16.4 mJ/s, for the RPA and LPA, respectively, was larger than that for the control.ConclusionsThe amount of energy loss in the pulmonary blood flow for the patient was considerably larger than the normal subject due to PA regurgitation and PA stenosis. Thus, we believe that the status of RV-PA pathophysiology for CHD patients can be evaluated non-invasively using energy loss endpoint.

Highlights

  • The repair surgery of congenital heart disease (CHD) associated with the right ventricular (RV)-pulmonary artery (PA) pathophysiology often left patients with critical post-operative lesions, leading to regurgitation and obstruction in the pulmonary arteries (PAs)

  • RV-PA physiology, normal pulmonary valve function, and no stenosis was seen in the PAs

  • The pressure drop and energy loss in the branch PAs versus time curves for both subjects are shown in Figures 7 and 8, respectively

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Summary

Introduction

The repair surgery of congenital heart disease (CHD) associated with the right ventricular (RV)-pulmonary artery (PA) pathophysiology often left patients with critical post-operative lesions, leading to regurgitation and obstruction in the PAs. Patients with right ventricular (RV) or pulmonary valve lesions, such as tetralogy of Fallot (TOF), aortic valve disease requiring the Ross procedure (aortic autograft with RV-PA homograft), or complex transposition of the great arteries (TGA), are often left with pulmonary insufficiency (PI) leading to progressive RV dilatation and occasionally resulting in pressure overload due to residual pulmonary stenosis. Those sequelae can result in progressive RV myocardial dysfunction, increasing the risk of sudden death [3,4,5,6]. Used metrics include body-surface-area (BSA) indexed RV end-diastolic and end-systolic volumes (EDVI and ESVI, respectively), ejection fraction, and RV end-systolic pressure (ESP)

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