Noninvasive Estimation of Pulmonary Vascular Resistance in Pulmonary Hypertension
Article first published online: 24 NOV 2008
© 2008, the Authors Journal compilation © 2008, Wiley Periodicals, Inc.
Volume 26, Issue 5, pages 489–494, May 2009
How to Cite
Rajagopalan, N., Simon, M. A., Suffoletto, M. S., Shah, H., Edelman, K., Mathier, M. A. and López-Candales, A. (2009), Noninvasive Estimation of Pulmonary Vascular Resistance in Pulmonary Hypertension. Echocardiography, 26: 489–494. doi: 10.1111/j.1540-8175.2008.00837.x
- Issue published online: 27 APR 2009
- Article first published online: 24 NOV 2008
- Doppler echocardiography;
- pulmonary hypertension;
- tricuspid regurgitation
Background: Determination of pulmonary vascular resistance (PVR) in patients with suspected or known pulmonary hypertension (PH) requires right heart catheterization. Our purpose was to use Doppler echocardiography to estimate PVR in patients with PH. Methods: Patient population consisted of 52 patients (53 ± 12 years; 35 females) who underwent Doppler echocardiography and right heart catheterization within 24 hours of each other. The ratio of peak tricuspid regurgitation velocity (TRV) and right ventricular outflow time-velocity integral (VTIRVOT) was measured via transthoracic echocardiography and correlated to invasively determined PVR. A linear regression equation was generated to determine PVR by echocardiography based upon the TRV/VTIRVOT ratio. PVR by echocardiography was compared to invasive PVR using Bland-Altman analysis. Results: Significant correlation was demonstrated between TRV/VTIRVOT and PVR by catheterization (r = 0.73; P < 0.001). However, Bland-Altman analysis showed that agreement between PVR determined by echocardiography and invasive PVR was poor (bias = 0; standard deviation = 4.3 Wood units). In a subset of patients with invasive PVR < 8 Wood units (26 patients), correlation between TRV/VTIRVOT and invasive PVR was strong (r = 0.94; P < 0.001). In these patients, agreement between PVR by echocardiography and invasive PVR was satisfactory (bias = 0; standard deviation = 0.5 Wood units). There was no correlation between TRV/VTIRVOT and invasive PVR in patients with PVR > 8 Wood units (n = 26; r = 0.17). Conclusion: While TRV/VTIRVOT correlates significantly with PVR, using it to estimate PVR in a PH patient population cannot be recommended.