Non-invasive estimation of pulmonary vascular resistance in patients of pulmonary hypertension in congenital heart disease with unobstructed pulmonary flow
Abstract:Context:Pulmonary vascular resistance (PVR) is a critical and essential parameter during the assessment and selection of modality of treatment in patients with congenital heart disease accompanied by pulmonary arterial hypertension.Aim:The present study was planned to evaluate non-invasive echocardiographic parameters to assess pulmonary vascular resistance.Settings and Design:This prospective observational study included 44 patients admitted in the cardiology and pediatric cardiology ward of our institution f… Show more
“…However, their measurement required two sets of Doppler recording: (1) during tricuspid regurgitation and (2) systolic pulmonary flow. In fact, all Doppler based methods have yielded similar results (21-26) with the same major limitation: the need to measure tricuspid regurgitation hemodynamics. Measurable tricuspid regurgitation Doppler envelopes may not be present in normotensive patients, PH patients with modestly elevated pressures, or in patients with poor acoustic windows due to body habitus.…”
Purpose
To develop an estimate of pulmonary vascular resistance (PVR) using blood flow measurements from 3-dimensional velocity-encoded phase contract magnetic resonance imaging (here termed 4D MRI).
Materials and Method
17 patients with pulmonary hypertension (PH) and 5 controls underwent right heart catheterization (RHC), 4D and 2D Cine MRI (1.5T) within 24 hours. MRI was used to compute maximum spatial peak systolic vorticity in the main pulmonary artery (MPA) and right pulmonary artery (RPA), cardiac output, and relative area change in the MPA. These parameters were combined in a 4-parameter multivariate linear regression model to arrive at an estimate of PVR. Agreement between model predicted and measured PVR was also evaluated using Bland-Altman plots. Finally, model accuracy was tested by randomly withholding a patient from regression analysis and using them to validate the multivariate equation.
Results
A decrease in vorticity in the MPA and RPA were correlated with an increase in PVR (MPA: R2 = 0.54, P < 0.05; RPA: R2 = 0.75, P < 0.05). Expanding on this finding, we identified a multivariate regression equation that accurately estimates PVR (R2 = 0.94, P < 0.05) across severe PH and normotensive populations. Bland-Altman plots showed 95% of the differences between predicted and measured PVR to lie within 1.49 Wood units. Model accuracy testing revealed a prediction error of approximately 20%.
Conclusion
A multivariate model that includes MPA relative area change and flow characteristics, measured using 4D and 2D Cine MRI, offers a promising technique for non-invasively estimating PVR in PH patients.
“…However, their measurement required two sets of Doppler recording: (1) during tricuspid regurgitation and (2) systolic pulmonary flow. In fact, all Doppler based methods have yielded similar results (21-26) with the same major limitation: the need to measure tricuspid regurgitation hemodynamics. Measurable tricuspid regurgitation Doppler envelopes may not be present in normotensive patients, PH patients with modestly elevated pressures, or in patients with poor acoustic windows due to body habitus.…”
Purpose
To develop an estimate of pulmonary vascular resistance (PVR) using blood flow measurements from 3-dimensional velocity-encoded phase contract magnetic resonance imaging (here termed 4D MRI).
Materials and Method
17 patients with pulmonary hypertension (PH) and 5 controls underwent right heart catheterization (RHC), 4D and 2D Cine MRI (1.5T) within 24 hours. MRI was used to compute maximum spatial peak systolic vorticity in the main pulmonary artery (MPA) and right pulmonary artery (RPA), cardiac output, and relative area change in the MPA. These parameters were combined in a 4-parameter multivariate linear regression model to arrive at an estimate of PVR. Agreement between model predicted and measured PVR was also evaluated using Bland-Altman plots. Finally, model accuracy was tested by randomly withholding a patient from regression analysis and using them to validate the multivariate equation.
Results
A decrease in vorticity in the MPA and RPA were correlated with an increase in PVR (MPA: R2 = 0.54, P < 0.05; RPA: R2 = 0.75, P < 0.05). Expanding on this finding, we identified a multivariate regression equation that accurately estimates PVR (R2 = 0.94, P < 0.05) across severe PH and normotensive populations. Bland-Altman plots showed 95% of the differences between predicted and measured PVR to lie within 1.49 Wood units. Model accuracy testing revealed a prediction error of approximately 20%.
Conclusion
A multivariate model that includes MPA relative area change and flow characteristics, measured using 4D and 2D Cine MRI, offers a promising technique for non-invasively estimating PVR in PH patients.
“…The TRV/RVOT VTI ratio has recently been shown to correlate well with PVR measured at catheterization in pediatric PH patients. 44 Pande et al 44 showed that, in this pediatric cohort (mean age: 9.7 years), the TRV/RVOT VTI ratio value of 0.14 provided a sensitivity of 96% and a specificity of 93% for a PVR of 6 Wood units. Normative pediatric RVOT VTI values were recently published.…”
Section: Trv/rvot Velocity Time Integral (Vti) Ratiomentioning
Transthoracic echocardiography (TTE) is the most accessible noninvasive diagnostic procedure for the initial assessment of pediatric pulmonary hypertension (PH). This review focuses on principles and use of TTE to determine morphologic and functional parameters that are also useful for follow-up investigations in pediatric PH patients. A basic echocardiographic study of a patient with PH commonly includes the hemodynamic calculation of the systolic pulmonary artery pressure (PAP), the mean and diastolic PAP, the pulmonary artery acceleration time, and the presence of a pericardial effusion. A more detailed TTE investigation of the right ventricle (RV) includes assessment of its size and function. RV function can be evaluated by RV longitudinal systolic performance (e.g., tricuspid annular plane systolic excursion), the tricuspid regurgitation velocity/right ventricular outflow tract velocity time integral ratio, the fractional area change, tissue Doppler imaging-derived parameters, strain measurements, the systolic-to-diastolic duration ratio, the myocardial performance (Tei) index, the RV/left ventricle (LV) diameter ratio, the LV eccentricity index, determination of an enlarged right atrium and RV size, and RV volume determination by 3-dimensional echocardiography. Here, we discuss the potential use and limitations of TTE techniques in children with PH and/or ventricular dysfunction. We suggest a protocol for TTE assessment of PH and myocardial function that helps to identify PH patients and their response to pharmacotherapy. The outlined protocol focuses on the detailed assessment of the hypertensive RV; RV-LV crosstalk must be analyzed separately in the evaluation of different pathologies that account for pediatric PH.
“…TRV:VTI [RVOT] ratio have been shown to correlate well with PVR in children and a cut off value of 0.14 provided high predictive values. 34 However, neonatal studies are lacking.…”
Pulmonary hypertension contributes to morbidity and mortality in both the term newborn infant, referred to as persistent pulmonary hypertension of the newborn (PPHN), and the premature infant, in the setting of abnormal pulmonary vasculature development and arrested growth. In the term infant, PPHN is characterized by the failure of the physiological postnatal decrease in pulmonary vascular resistance that results in impaired oxygenation, right ventricular failure, and pulmonary-to-systemic shunting. The pulmonary vasculature is either maladapted, maldeveloped, or underdeveloped. In the premature infant, the mechanisms are similar in that the early onset pulmonary hypertension (PH) is due to pulmonary vascular immaturity and its underdevelopment, while late onset PH is due to the maladaptation of the pulmonary circulation that is seen with severe bronchopulmonary dysplasia. This may lead to cor-pulmonale if left undiagnosed and untreated. Neonatologist performed echocardiography (NPE) should be considered in any preterm or term neonate that presents with risk factors suggesting PPHN. In this review, we discuss the risk factors for PPHN in term and preterm infants, the etiologies, and the pathophysiological mechanisms as they relate to growth and development of the pulmonary vasculature. We explore the applications of NPE techniques that aid in the correct diagnostic and pathophysiological assessment of the most common neonatal etiologies of PPHN and provide guidelines for using these techniques to optimize the management of the neonate with PPHN.
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