Abstract

BackgroundPulmonary hypertension is definitively diagnosed by the measurement of mean pulmonary artery (PA) pressure (mPAP) using right heart catheterization. Cardiovascular magnetic resonance (CMR) four-dimensional (4D) flow analysis can estimate mPAP from blood flow vortex duration in the PA, with excellent results. Moreover, the peak systolic tricuspid regurgitation (TR) pressure gradient (TRPG) measured by Doppler echocardiography is commonly used in clinical routine to estimate systolic PA pressure. This study aimed to compare CMR and echocardiography with regards to quantitative and categorical agreement, and diagnostic yield for detecting increased PA pressure.MethodsConsecutive clinically referred patients (n = 60, median [interquartile range] age 60 [48–68] years, 33% female) underwent echocardiography and CMR at 1.5 T (n = 43) or 3 T (n = 17). PA vortex duration was used to estimate mPAP using a commercially available time-resolved multiple 2D slice phase contrast three-directional velocity encoded sequence covering the main PA. Transthoracic Doppler echocardiography was performed to measure TR and derive TRPG. Diagnostic yield was defined as the fraction of cases in which CMR or echocardiography detected an increased PA pressure, defined as vortex duration ≥15% of the cardiac cycle (mPAP ≥25 mmHg) or TR velocity > 2.8 m/s (TRPG > 31 mmHg).ResultsBoth CMR and echocardiography showed normal PA pressure in 39/60 (65%) patients and increased PA pressure in 9/60 (15%) patients, overall agreement in 48/60 (80%) patients, kappa 0.49 (95% confidence interval 0.27–0.71). CMR had a higher diagnostic yield for detecting increased PA pressure compared to echocardiography (21/60 (35%) vs 9/60 (15%), p < 0.001). In cases with both an observable PA vortex and measurable TR velocity (34/60, 56%), TRPG was correlated with mPAP (R2 = 0.65, p < 0.001).ConclusionsThere is good quantitative and fair categorical agreement between estimated mPAP from CMR and TRPG from echocardiography. CMR has higher diagnostic yield for detecting increased PA pressure compared to echocardiography, potentially due to a lower sensitivity of echocardiography in detecting increased PA pressure compared to CMR, related to limitations in the ability to adequately visualize and measure the TR jet by echocardiography. Future comparison between echocardiography, CMR and invasive measurements are justified to definitively confirm these findings.

Highlights

  • Pulmonary hypertension is definitively diagnosed by the measurement of mean pulmonary artery (PA) pressure using right heart catheterization

  • Cardiovascular magnetic resonance (CMR) has higher diagnostic yield for detecting increased PA pressure compared to echocardiography, potentially due to a lower sensitivity of echocardiography in detecting increased PA pressure compared to CMR, related to limitations in the ability to adequately visualize and measure the tricuspid regurgitation (TR) jet by echocardiography

  • Mean values of vortex duration in the pulmonary artery were 9.5 ± 9.7% corresponding to an mean pulmonary artery (PA) pressure (mPAP) of 22.0 ± 6.1 mmHg for reader 1 and 10.8 ± 9.8% corresponding to an mPAP of 22.8 ± 6.2 mmHg for reader 2, with an average measurement between both readers of 10.1 ± 9.4% corresponding to an mPAP of 22.4 ± 5.9 mmHg

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Summary

Introduction

Pulmonary hypertension is definitively diagnosed by the measurement of mean pulmonary artery (PA) pressure (mPAP) using right heart catheterization. Pulmonary hypertension is defined as a mean pulmonary artery (PA) pressure (mPAP) equal to or greater than 25 mmHg assessed invasively by right heart catheterization (RHC) [1]. It affects approximately 1% of adults and is associated with high morbidity and mortality [2]. MPAP can be estimated with echocardiography by adding mean right atrial pressure to TRPG, and a calibration factor [4] These parameters tend to over- or underestimate pulmonary pressure compared with invasive measurements [5, 6]. The usefulness of echocardiography for follow-up and monitoring of treatment in pulmonary hypertension has been shown to be limited [7]

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