Estimation Of Pulmonary Vascular Resistance Research Articles

Kiosk 3R-FA-05 - Estimation of Pulmonary Vascular Resistance of Children with Single Ventricle in Glenn Physiology

Kiosk 3R-FA-05 - Estimation of Pulmonary Vascular Resistance of Children with Single Ventricle in Glenn Physiology

Echocardiographic estimation of pulmonary vascular resistance in advanced lung disease.

Noninvasive assessment of pulmonary hemodynamics is often performed by echocardiographic estimation of the pulmonary artery systolic pressure (ePASP), despite limitations in the advanced lung disease population. Other noninvasive hemodynamic variables, such as echocardiographic pulmonary vascular resistance (ePVR), have not been studied in this population. We performed a retrospective analysis of 147 advanced lung disease patients who received both echocardiography and right heart catheterization for lung transplant evaluation. The ePVR was estimated by four previously described equations. Noninvasive and invasive hemodynamic parameters were compared in terms of correlation, agreement, and accuracy. The ePVR models strongly correlated with invasively determined PVR and had good accuracy with biases of <1 Wood units (WU), although with moderate precision and wide 95% limits of agreement varying from 5.9 to 7.8 Wood units. The ePVR models were accurate to within 1.9 WU in over 75% of patients. In comparison to the ePASP, ePVR models performed similarly in terms of correlation, accuracy, and precision when estimating invasive hemodynamics. In screening for pulmonary hypertension, ePVR models had equivalent testing characteristics to the ePASP. Mid-systolic notching of the right ventricular outflow tract Doppler signal identified a subgroup of 11 patients (7%) with significantly elevated PVR and mean pulmonary artery pressures without relying on the acquisition of a tricuspid regurgitation signal. Analysis of ePVR and determination of the notching pattern of the right ventricular outflow tract Doppler flow velocity envelope provide reliable insights into hemodynamics in advanced lung disease patients, although limitations in precision exist.

A novel echocardiographic estimate of pulmonary vascular resistance employing the hydraulic analogy to Ohm's law.

Assessment of pulmonary vascular resistance (PVR) is critical for accurate diagnosis and optimal pharmacotherapy in pulmonary hypertension. We aimed to test the diagnostic performance of a novel, Doppler-based method to evaluate PVR based on Ohm's law (PVRecho) using pragmatic estimates of pulmonary capillary wedge pressure (PCWP). Simultaneous right heart catheterization (RHC) and echocardiography was performed in a derivation cohort of 111 patients in sinus rhythm referred for PH evaluation and PVRecho independently validated in 238 patients. PVRecho was calculated using pulmonary artery mean pressure estimates (PAMPecho) obtained from peak tricuspid gradient employing a fixed right atrial pressure estimate, PCWPecho was estimated as 10 or 20mmHg using age-related mitral E/A cut-offs and cardiac output from left ventricular outflow. In the derivation cohort, both PAMPecho and PCWPecho estimates demonstrated excellent agreement with catheterization measurements. PVRecho was highly feasible, demonstrated negligible bias and excellent agreement with PVRRHC (Bias=-0.58, SD 2.2mmHg) and outperformed the Abbas method to identify PVRRHC>3WU (AUC=0.85 vs. 0.70; p=0.02). In the validation cohort, PVRecho preserved good invasive agreement with negligible bias, displayed strong diagnostic performance (AUC=0.84) and significant ability to distinguish isolated post-capillary from combined post- and pre-capillary pulmonary hypertension (PH) subgroups (AUC=0.77). PVRecho based on Ohm's law employing pragmatic estimates of PCWPecho demonstrates excellent agreement with invasive reference standard measurements and strong diagnostic ability to identify elevated PVRRHC. This novel approach may be useful during therapy selection to distinguish PH hemodynamic subgroups.

Association between the albumin-bilirubin (ALBI) score and severity of portopulmonary hypertension (PoPH): A data-mining analysis.

Portopulmonary hypertension (PoPH) is a severe complication of chronic liver disease. We aimed to investigate the etiology of chronic liver disease and the factors associated with the severity of PoPH. Echocardiography was undergone in 833 patients with chronic liver disease during 2005-2019 and 13 patients (1.6%) were diagnosed with PoPH in this observational study. At the diagnosis of PoPH, liver function was evaluated by albumin-bilirubin (ALBI) score. Severe PoPH was defined as (1) mean pulmonary arterial pressure (mPAP)≥50mmHg or (2) mPAP: 35-49mmHg and pulmonary vascular resistance≥400dyne/s/cm5 . Factors associated with severe PoPH were evaluated by decision-tree analysis. In patients with PoPH, the leading etiology of chronic liver disease was hepatitis C virus (HCV) (46.2% [sustained virological response (SVR): 23.1% and non-SVR: 15.4%]). Severe PoPH was observed in 53.8% of patients and the 5-year survival rate was 48.1%. There was a significant correlation of mPAP with ALBI score (r=0.6456, p=0.0171). In the decision-tree and random forest analyses, the most impacted classifier for severe PoPH was the ALBI score. In patients with ALBI score≥-1.45, all patients showed severe PoPH, while the prevalence of severe PoPH was 25.0% in patients with ALBI score<-1.45. We found that HCV including SVR was the major etiology of chronic liver disease in patients with PoPH. Moreover, we revealed that the ALBI score was the most impacted factor associated with severe PoPH. Thus, ALBI score may be useful for the estimation of pulmonary vascular resistance.

Inaccuracy of a non-invasive estimation of pulmonary vascular resistance assessed by cardiovascular magnetic resonance in heart failure patients

Pulmonary vascular resistance (PVR) is a marker of pulmonary vascular remodeling. A non-invasive model assessed by cardiovascular magnetic resonance (CMR) has been proposed to estimate PVR. However, its accuracy has not yet been evaluated in patients with heart failure. We prospectively included 108 patients admitted with acute heart failure (AHF), in whom a right heart catheterization (RHC) and CMR were performed at the same day. PVR was estimated by CMR applying the model: PVR = 19.38 − [4.62 × Ln pulmonary artery average velocity (in cm/s)] − [0.08 × right ventricle ejection fraction (in %)], and by RHC using standard formulae. The median age of the cohort was 67 years (interquartile range 58–73), and 34% were females. The median of PVR assessed by RHC and CMR were 2.2 WU (1.5–4) and 5 WU (3.4–7), respectively. We found a weak correlation between invasive PVR and PVR assessed by CMR (Spearman r = 0.21, p = 0.02). The area under the ROC curve for PVR assessed by CMR to detect PVR ≥ 3 WU was 0.57, 95% confidence interval (CI): 0.47–0.68. In patients with AHF, the non-invasive estimation of PVR using CMR shows poor accuracy, as well as a limited capacity to discriminate increased PVR values.

Limitations of a non-invasive model of the estimation of pulmonary vascular resistance by magnetic resonance imaging in patients with heart failure

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. Pulmonary vascular resistance (PVR) is a hemodynamic parameter with important diagnostic and prognostic implications in patients with heart failure. Currently the gold standard technique for its quantification is right heart catheterization (RHC). However, cardiovascular magnetic resonance imaging (CMR) has been postulated as a non-invasive alternative for its estimation. The aim of this study is to assess the accuracy of a non-invasive model of PVR estimated by CMR in a specific subgroup of patients with acute heart failure (AHF). Methods. Between January 2014 and December 2018, 108 patients with AHF who underwent RHC and CMR on the same day were prospectively included. PVR was assessed by CMR using the model: 19.38 - [4.62 x Ln mean pulmonary artery velocity - 0.08 x right ventricular ejection fraction (RVEF)]. During RHC, PVR were calculated using the ratio between transpulmonary gradient and cardiac output. We evaluated their correlation using the Spearman correlation coefficient, receiver operating characteristic [ROC] curves, and Bland-Altman analysis. Results. The mean age of our cohort was 65 ± 11 years and 64.8% were male. The median PVR (Wood Units, WU) assessed by CMR and RHC were 5.1 WU (3.4 - 6.8) and 3 WU (1.5 - 3.9); p &amp;lt; 0.001, respectively. A weak correlation was observed between the PVR obtained by RHC and those obtained by CMR in our population (r = 0.21; p = 0.02). On Bland-Altman analysis, the mean bias was -1.7, and the 95% limits of agreement ranged from -10.02 to 6.6 WU. The area under the ROC curve for PVR assessed by CMR to detect PVR ³3 WU was 0.57, 95% confidence interval (CI): 0.47-0.68. Conclusions. In patients with AHF, the non-invasive estimation of PVR using CMR shows poor accuracy, as well as a limited capacity to discriminate increased PVR values.

Pulmonary arterial wave reflection as a novel estimate of pulmonary vascular resistance

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): International Medical Research and Development Fund Background Measuring pulmonary vascular resistance (PVR) is essential for diagnosing pulmonary hypertension. PVR can be estimated from a simple ratio of tricuspid regurgitation velocity (TRV) to time-velocity integral of flow through right ventricular outflow tract (RVOT) (Abbas equation), but this relationship has been shown to be unreliable in patients with high PVR. Once PVR is elevated, there is an increased pressure wave reflected from the peripheral of pulmonary artery (PA). We tested the hypothesis that assessing PA wave reflection could be an alternative method for estimating PVR. Methods This study recruited 83 patients (69 ± 14 years old, 44 men), including 41 patients with left-sided heart disease, 23 patients with pulmonary arterial hypertension and 19 patients with chronic thromboembolic pulmonary hypertension. PA wave reflection was assessed by separating PA pressure waveform derived from a Doppler tracing of TRV into forward and backward pressure (Pf and Pb), using a velocity profile at RVOT. This separation was based on the concept of wave intensity. PVR was estimated using Abbas equation. Pb and PVR by Abbas equation were compared for the correlations with direct measurement of PVR by right heart catheterisation within 48 hours after echocardiography. Results Figure A illustrates Pb and Pf waveforms obtained from a patient with chronic thromboembolic pulmonary hypertension. Pb increased from mid systole and formed a late peak of PA pressure waveform. Pb correlated strongly with PVR by catheter (figure B), whereas PVR by Abbas equation underestimated PVR especially when PVR was high, resulting in a moderate correlation (figure C). Receiver-operator characteristic curves showed a higher accuracy of Pb for identifying PVR &amp;gt; 3WU as well as 6WU, compared with PVR by Abbas equation (figure D and E). Conclusions This novel echocardiographic method for assessing PA wave reflection helps diagnose the severity of pulmonary hypertension. Abstract Figure.

Noninvasive estimation of pulmonary vascular resistance improves portopulmonary hypertension screening in liver transplant candidates.

Despite limitations in sensitivity and specificity, estimation of the pulmonary artery systolic pressure (ePASP) on echocardiography is used for portopulmonary hypertension (PoPH) screening in liver transplant (LT) candidates. We proposed that alternative echocardiographic models, such as estimated pulmonary vascular resistance (ePVR), may provide improved testing characteristics in PoPH screening. In a retrospective analysis of 100 LT candidates, we found that the formula ePVR=ePASP/VTIRVOT +3 if MSN (VTIRVOT =right ventricular outflow tract time velocity integral; MSN=mid-systolic notching of the VTIRVOT Doppler signal) significantly improves accuracy of PoPH screening compared to ePASP. We determined the optimal ePVR cutoff for PoPH screening to be 2.76 Wood units, as this cutoff provided 100% sensitivity and 73% specificity in screening for clinically significant PoPH. Comparatively, ePASP at a cutoff of 40mmHg provided 91% sensitivity and 48% specificity. We devised a new screening algorithm based on the use of ePVR at intermediate ePASP values (35-54mmHg), and we confirmed the testing characteristics of this algorithm in a separate validation cohort of 50 LT candidates. In screening LT candidates for PoPH, the ePASP lacks accuracy, leading to unnecessary RHCs and undiagnosed cases of PoPH. A screening algorithm which incorporates the ePVR may be more reliable.

Analysis of Biphasic Right Ventricular Outflow Doppler Waveform in Patients with Pulmonary Hypertension.

Pulmonary hypertension (PH) with pulmonary vascular disease (PVD) is a progressive and debilitating disease associated with increased pulmonary vascular resistance (PVR). Biphasic right ventricular outflow tract (RVOT) Doppler flow is frequently seen in severe PH patients with PVD. In association with hemodynamics, the precise analysis of biphasic RVOT Doppler flow (RVDF) has not been fully elucidated. Therefore, the purpose of the present study is to analyze the relation between the hemodynamics and indices of biphasic RVDF in PH patients with PVD.Seventy PH patients with biphasic RVDF were analyzed. All patients underwent transthoracic echocardiography and right heart catheterization. For the analysis of biphasic RVDF, the early waveform was determined as P1 while the late waveform was determined as P2. For each P1 and P2, the duration (D, seconds) and peak flow velocity (PFV, in m/second) were measured.P1D and P2PFV were significantly correlated with PVR (P1D: r = -0.542, P < 0.0001, P2PFV: r = -0.513, P < 0.0001). Therefore, we propose a novel RVDF formula for estimation of PVR, as follows. PVR = 26 - 77 × P1D - 14 × P2PFV. The PVR could be estimated by this proposed formula (r = 0.649, P < 0.0001), which is derived from one Doppler image only unlike previously used PVR prediction formula.P1D and P2PFV were associated with PVR. Moreover, this simple RVDF formula proposed herein can estimate PVR in PH patients with PVD.

Reliability of Doppler echocardiography in the assessment of high pulmonary vascular resistance in patients with severe pulmonary arterial hypertension

BackgroundThe objective is to assess whether the squaring of tricuspid regurgitation velocity (TRV) gives an improved estimate of pulmonary vascular resistance (PVR) or is equivalent to the ratio of TRV and time velocity integral of right ventricular outflow tract (TVIRVOT) (TRV/TVIRVOT) for assessing PVR in patients with high PVR values. MethodsThirty patients predicted to have PVR >6 WU by Doppler were included in the present study. TRV and TVIRVOT were measured by echo Doppler. TRV/TVIRVOT and TRV2/TVIRVOT were calculated. PVRCATH was estimated within 2 h of Doppler study. Regression equations for calculating PVR from TRV/TVIRVOT (PVRECHO1) and TRV2/TVIRVOT (PVRECHO2) were developed. Bland–Altman analysis for agreement between PVRCATH and PVRECHO1, PVRECHO2 was carried out. ResultsThe mean value of PVRCATH was found to be 15.08 ± 7.03 WU. The calculated values of PVRECHO1 and PVRECHO2 were found to be 15.08 ± 6.34 WU and 15.05 ± 6.08 WU, respectively. The linear regression analysis carried out for PVRCATH and TRV/TVIRVOT showed good correlation (R = 0.84). Bland–Altman analysis showed excellent agreement between the two Doppler methods and invasive PVR with negligible bias. ConclusionNoninvasive estimation of PVR by Doppler is reliable even in patients with high PVR (>6 WU) and, squaring TRV is not superior to TRV alone.

O44-4 - A Simple Non-invasive Method of Estimating Pulmonary Vascular Resistance by Doppler Echocardiography in Patients without Acute Exacerbated Left Heart Failure

Background: Assessment of pulmonary vascular resistance (PVR) plays an important role in managing patients with elevated pulmonary artery pressure. To date, several formulae for estimating PVR with echocardiography have been proposed. The problem is, however, most of them contain values not always measured in routine echocardiographic examination, which makes it difficult to assess one's PVR retrospectively. The aim of this study is to investigate feasibility of a new simple echocardiographic measurement of PVR (PVRecho), peak tricuspid regurgitation pressure gradient divided by three times of left ventricular cardiac output derived from Doppler echocardiography (TRPG/3LVCO), in patients without acute exacerbated left-sided heart failure. Method: From July 2014 to May 2017, PVR calculated by right heart catheterization (PVRcath), and TRPG and LVCO by echocardiography were available in 57 patients. Patients with cardiac shunt, atrial fibrillation, severe mitral regurgitation, or emergency catheterization were excluded. Among these patients, PVRecho and PVRcath were compared using linear progression and Bland-Altman analysis. Result: Mean PVRcath was 2.2 ± 1.8 WU. PVRecho had a good correlation with PVRcath (r = 0.66, P < .001). On Bland-Altman analysis, the mean difference was 0.1 ± 1.3WU, which is comparable with other formulae previously reported. Patients with lower pulmonary capillary wedge pressure showed better correlation between PVRecho and PVRcath. Conclusion: The new simple formula for estimation of PVR showed comparable correlation with previously reported formulae.

4D magnetic resonance flow imaging for estimating pulmonary vascular resistance in pulmonary hypertension.

To develop an estimate of pulmonary vascular resistance (PVR) using blood flow measurements from 3D velocity-encoded phase contract magnetic resonance imaging (here termed 4D MRI). In all, 17 patients with pulmonary hypertension (PH) and five 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 four-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. A decrease in vorticity in the MPA and RPA were correlated with an increase in PVR (MPA: R(2) = 0.54, P < 0.05; RPA: R(2) = 0.75, P < 0.05). Expanding on this finding, we identified a multivariate regression equation that accurately estimates PVR (R(2) = 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 ∼20%. A multivariate model that includes MPA relative area change and flow characteristics, measured using 4D and 2D Cine MRI, offers a promising technique for noninvasively estimating PVR in PH patients. J. MAGN. RESON. IMAGING 2016;44:914-922.

Assessment of N-terminal prohormone B-type natriuretic peptide as a measure of vascular and ventricular function in pediatric pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a progressive disease that puts excessive mechanical loads on the ventricle due to a gradual increase in pulmonary vascular impedance. We hypothesize that the increase in right ventricular (RV) afterload is reflected in the concentration of circulating biochemical markers of ventricular strain and stress (B-type natriuretic peptide [BNP] and N-terminal prohormone BNP [NT-proBNP]). We retrospectively analyzed right heart catheterization (RHC) and serum biochemical analysis data ([Formula: see text]) for a pediatric PAH cohort with no sign of left ventricular dysfunction. Using RHC data, we computed an estimate of pulmonary vascular resistance (PVR), compliance, and ventricular-vascular coupling. We also compared how the early onset of interventricular decoupling (characterized as septal flattening) impacts serum NT-proBNP concentrations. Our data revealed correlated NT-proBNP expression with both the resistive and reactive components of RV afterload, an estimate of ventricular-vascular coupling, and a significant increase in biomarker expression in patients with a flattened interventricular septum. Furthermore, the strong correlation between PVR and NT-proBNP appears to break down under flat septum morphology. Over 80% of resistive RV afterload variance is reflected in serum NT-proBNP concentration in pediatric patients with PAH with no sign of left ventricular dysfunction. Reactive afterload appears to contribute to myocardial NT-proBNP release at advanced stages of PAH. Therefore, in mild-to-moderate PAH, resistive afterload is likely the greatest contributor to RV wall stress. These findings could also be used to estimate invasive RHC measurements from serum biochemical analysis, but more work is needed to improve correlations and overcome the issue of interventricular decoupling.

Pulmonary Haemodynamics in Sickle Cell Disease Are Driven Predominantly by a High-Output State Rather Than Elevated Pulmonary Vascular Resistance: A Prospective 3-Dimensional Echocardiography/Doppler Study.

AimsPatients with sickle cell disease have significant morbidity and mortality. Pulmonary hypertension is suggested to be an important contributor but its nature and severity in these patients and how best to non-invasively assess it are controversial. We hypothesised that a high-output state rather than primary pulmonary vascular pathology may be the major abnormality in sickle cell disease. This study aimed to evaluate the characteristics and severity of pulmonary hypertension in patients with sickle cell disease using detailed echocardiography.Methods and ResultsWe undertook a prospective study in 122 consecutive stable outpatients with sickle cell disease and 30 age, gender and ethnicity-matched healthy controls. Echocardiographic evaluation included 3D ventricular volumes, sphericity, tissue Doppler, and non-invasive estimation of pulmonary vascular resistance. 36% of patients had a tricuspid regurgitant velocity ≥2.5 m.s-1 but only 2% had elevated pulmonary vascular resistance and the prevalence of right ventricular dysfunction was very low. Patients with raised tricuspid regurgitant velocity had significantly elevated biventricular volumes and globular left ventricular remodelling, related primarily to anaemia. In a subgroup of patients who underwent cardiac catheterization, invasive pulmonary haemodynamics confirmed the echocardiographic findings.ConclusionsElevated cardiac output and left ventricular volume overload secondary to chronic anaemia may be the dominant factor responsible for abnormal cardiopulmonary haemodynamics in patients with sickle cell disease. 3D echocardiography with non-invasive estimation of pulmonary vascular resistance represents a valuable approach for initial evaluation of cardiopulmonary haemodynamics in sickle cell disease.

A feasible method for non-invasive measurement of pulmonary vascular resistance in pulmonary arterial hypertension: Combined use of transthoracic Doppler-echocardiography and cardiac magnetic resonance. Non-invasive estimation of pulmonary vascular resistance

BackgroundTransthoracic Doppler-echocardiography (TTE) can estimate mean pulmonary arterial pressure (MPAP) and pulmonary capillary wedge pressure (PCWP) reliably, and cardiac magnetic resonance (CMR) is the best modality for non-invasive measurement of cardiac output (CO). We speculated that the combined use of TTE and CMR could provide a feasible method for non-invasive measurement of pulmonary vascular resistance (PVR) in pulmonary arterial hypertension (PAH). Methods and resultsRight heart catheterization (RHC) was undertaken in 77 patients (17M/60F) with PAH, and simultaneous TTE was carried out to evaluate MPAP, PCWP and CO. Within 2days, CO was measured again with CMR in similar physiological status. Then, PVR was calculated with the integrated non-invasive method: TTE-derived (MPAP–PCWP)/CMR-derived CO and the isolated TTE method: TTE-derived (MPAP–PCWP)/TTE-derived CO, respectively. The PVR calculated with integrated non-invasive method correlated well with RHC-calculated PVR (r=0.931, 95% confidence interval 0.893 to 0.956). Between the integrated non-invasive PVR and RHC-calculated PVR, the Bland–Altman analysis showed the satisfactory limits of agreement (mean value: −0.89±2.59). In comparison, the limits of agreement were less satisfactory between TTE-calculated PVR and RHC-calculated PVR (mean value: −1.80±3.33). Furthermore, there were excellent intra- and inter-observer correlations for the measurements of TTE and CMR (P<0.001 for all). ConclusionsThe combined use of TTE and CMR provides a clinically reliable method to determine PVR non-invasively. In comparison with RHC, the integrated method shows good accuracy and repeatability, which suggests the potential for the evaluation and serial follow-up in patients with PAH. Translational perspectiveIn PAH, the non-invasive measurement of PVR is very important in clinical practice. Up to now, however, the widely accepted non-invasive method is still unavailable. Since TTE can estimate (MPAP–PCWP) reliably and CMR is the best image modality for the measurement of CO, the combined use of two modalities has the potential to determine PVR non-invasively. In this research, the integrated non-invasive method showed good diagnostic accuracy and repeatability compared with RHC. Therefore, it might be a feasible method for non-invasive measurement of PVR in patients with PAH.

(955) - Right Ventricular Outflow Tract Doppler Envelope Mid-Systolic Notching Predicts Pulmonary Vascular Disease in Patients With Advanced Lung Disease

Mid-systolic notching of the right ventricular outflow tract (RVOT) Doppler flow velocity envelope (FVERVOT) correlates with high pulmonary vascular resistance (PVR) in patients with diverse etiologies of pulmonary hypertension (PH). The ratio of peak tricuspid regurgitant velocity (TRV) and time-velocity integral of the RVOT (TVIRVOT) provides a reliable non-invasive estimate of PVR. We investigated whether PVR can be predicted by the shape of FVERVOT or TRV/TVIRVOT in pts with advanced lung disease (ALD) undergoing lung transplant evaluation.

Noninvasive estimation of pulmonary vascular resistance in patients of pulmonary hypertension in unclassified congenital heart disease with unobstructed pulmonary flow

Noninvasive estimation of pulmonary vascular resistance in patients of pulmonary hypertension in unclassified congenital heart disease with unobstructed pulmonary flow

Estimation of cardiac output and pulmonary vascular resistance by contrast echocardiography transit time measurement: a prospective pilot study.

BackgroundStudies with other imaging modalities have demonstrated a relationship between contrast transit and cardiac output (CO) and pulmonary vascular resistance (PVR). We tested the hypothesis that the transit time during contrast echocardiography could accurately estimate both CO and PVR compared to right heart catheterization (RHC).Methods27 patients scheduled for RHC had 2D-echocardiogram immediately prior to RHC. 3 ml of DEFINITY contrast followed by a 10 ml saline flush was injected, and a multi-cycle echo clip was acquired from the beginning of injection to opacification of the left ventricle. 2D-echo based calculations of CO and PVR along with the DEFINITY-based transit time calculations were subsequently correlated with the RHC-determined CO and PVR.ResultsThe transit time from full opacification of the right ventricle to full opacification of the left ventricle inversely correlated with CO (r = -0.61, p < 0.001). The transit time from peak opacification of the right ventricle to first appearance in the left ventricle moderately correlated with PVR (r = 0.46, p < 0.01). Previously described echocardiographic methods for the determination of CO (Huntsman method) and PVR (Abbas and Haddad methods) did not correlate with RHC-determined values (p = 0.20 for CO, p = 0.18 and p = 0.22 for PVR, respectively). The contrast transit time method demonstrated reliable intra- (p < 0.0001) and inter-observer correlation (p < 0.001).ConclusionsWe describe a novel method for the quantification of CO and estimation of PVR using contrast echocardiography transit time. This technique adds to the methodologies used for noninvasive hemodynamic assessment, but requires further validation to determine overall applicability.

Reliability of Doppler-Based Measurement of Pulmonary Vascular Resistance in Congenital Heart Disease with Left-to-Right Shunt Lesions.

Pulmonary vascular resistance (PVR) is a crucial parameter in the management of patients with left-to-right shunt lesions. Cardiac catheterization (Cath) is the gold standard test to assess PVR (PVRcath ), but it is invasive and hence, risky in children with pulmonary arterial hypertension (PAH). A noninvasive tool to assess PVR is desirable. Ratio of tricuspid regurgitation velocity (TRV) and time-velocity integral of right ventricular outflow tract (TVIRVOT ) by Doppler was previously shown to be a reliable noninvasive method for estimation of PVR in acquired PAH. Peak TR velocity and TVIRVOT were recorded from 63 prospective patients with various congenital shunt lesions. Subsequently, the patients were subjected to cath in less than 2hours. The patients were subdivided into four subsets based on age and pulmonary arterial mean pressure (PAMP). A regression equation was developed for calculation of PVR from TRV/TVIRVOT (PVREcho ) which was indexed for BSA (PVRIEcho ). Bland-Altman analysis was done for agreement between PVRIcath and PVRIEcho . Receiver operating characteristic (ROC) curves were plotted to test the identity of the two methods and also the applicability of PVRIEcho across a wide range of Wood units. Receiver operating characteristic curve plotted between the two methods showed good identity. Bland-Altman analysis showed excellent agreement between the two methods with negligible bias. ROC curves showed that PVRIEcho was accurate in distinguishing different cutoff values of PVR in each of the 4 groups. Noninvasive Doppler estimation of PVR is reliable in patients with shunt lesions over a wide range of PVR.

Prognostic value of pulmonary vascular resistance estimated by cardiac magnetic resonance in patients with chronic heart failure.

Pulmonary arterial hypertension is known to be related to worse prognosis in patients with heart failure (HF). Quantification of pulmonary vascular resistance (PVR) still requires invasive right heart catheterization. Recent studies have shown an accurate method for non-invasive estimation of PVR by cardiac magnetic resonance (CMR). Our aim was to evaluate the prognostic value of PVR calculated by CMR in patients with congestive HF. We calculated PVR by CMR in 132 patients [age 65.6 ± 13.1 years, left ventricular ejection fraction (LVEF) 35.1 ± 16.4%, ischaemic aetiology 40%] recently admitted for decompensated HF and derived to our cardiac imaging unit for diagnosis. Patients with cardiac events (readmission for HF or all-cause death) had higher values of PVR [6.77 ± 1.9 vs. 4.1 ± 1.6 Wood units (Wu), P < 0.001] during follow-up [mean 10.3 (1-31) months]. In multivariable Cox regression analysis, only a PVR ≥5.2 Wu [hazard ratio (HR) 4.27; 95% confidence interval (CI) 1.75-10.42; P < 0.001) and the presence of late gadolinium enhancement (LGE) on CMR (HR 2.24; 95% CI 1.03-4.86; P = 0.04) were independent predictors for adverse events at follow-up. Non-invasive estimation of PVR by CMR might be useful for risk stratification of patients with chronic HF, irrespective of aetiology or LVEF.