Comparison of stroke work between repaired tetralogy of Fallot and normal right ventricular physiologies

Mechanical Engineering, School of Dynamics Systems, University of Cincinnati, 593 Rhodes Hall, ML 0072, Cincinnati, OH, 45221, USA.
Heart and Vessels (Impact Factor: 2.07). 12/2011; 28(1). DOI: 10.1007/s00380-011-0212-7
Source: PubMed


Adult patients who underwent tetralogy of Fallot repair surgery (rTOF) confront life-threatening ailments due to right ventricular (RV) myocardial dysfunction. Pulmonary valve replacement (PVR) needs to be performed to restore the deteriorating RV function. Determination of correct timing to perform PVR in an rTOF patient remains subjective, due to the unavailability of quantifiable clinical diagnostic parameters. The objective of this study is to evaluate the possibility of using RV body surface area (BSA)-indexed stroke work (SW(I)) to quantify RV inefficiency in TOF patients. We hypothesized that RV SW(I) required to push blood to the lungs in rTOF patients is significantly higher than that of normal subjects. Seven patients with rTOF pathophysiology and eight controls with normal RV physiology were registered for this study. Right ventricular volume and pressure were measured using cardiac magnetic resonance imaging and catheterization, respectively. Statistical analysis was performed to quantify the difference in SW(I) between the RV of the rTOF and control groups. Right ventricular SW(I) in rTOF patients (0.176 ± 0.055 J/m(2)) was significantly higher by 93.4% (P = 0.0026) than that of controls (0.091 ± 0.030 J/m(2)). Further, rTOF patients were found to have significantly higher (P < 0.05) BSA normalized RV end-systolic volume, end-systolic pressure, and regurgitation fraction than control subjects. Ejection fraction and peak ejection rate of rTOF patients were significantly lower (P < 0.05) than those of controls. Patients with rTOF pathophysiology had significantly higher RV SW(I) compared with subjects with normal RV physiology. Therefore, RV SW(I) may be useful to quantify RV inefficiency in rTOF patients along with currently used clinical end points such as RV volume, pressure, regurgitation fraction, and ejection fraction.

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Available from: Namheon Lee, Aug 01, 2014
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    • "(Eq. 5a) can be rewritten in terms of pressure drop, flow rate, and velocity at the PAs. The right-hand side of Eq. 5b, 5c, and 5d, i.e., the rate of the pressure-flow and kinetic energy terms at the PAs [9], RPA, LPA and MPA, respectively, can be substituted into Eq. 5a while maintaining flow balance at the PAs (Q MPA  = Q RPA  + Q LPA ). "
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    ABSTRACT: The repair surgery of congenital heart disease (CHD) associated with the right ventricular (RV)-pulmonary artery pathophysiology often left patients with critical post-operative lesions, leading to regurgitation and obstruction in the pulmonary arteries (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. 4D 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 normal and abnormal subjects. The 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. The 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-based endpoint, such as energy loss in the branch PAs.
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