We would like to thank JASE for publishing our recent report regarding noninvasive estimation of pulmonary vascular resistance (PVR). We are humbled by the kind words of Opotowsky et al . in their letter to the editor.
In reference to Opotowsky et al .’s letter, first, we agree that adding an algorithm may carry a slight chance of limiting the clinical applicability of our method. However, the reason we steered away from pulmonary arterial systolic pressure (used in their equation), compared with tricuspid regurgitation velocity (TRV), for the transpulmonary pressure correlate, is the inherent difficulty in accurately assessing right atrial pressure by echocardiography. Right atrial pressure would add a third variable to PVR assessment, which carries a risk for increasing the inaccuracy and the interobserver variability. TRV, on the other hand, is attractive because it is a single value.
Second, omitting an estimate of right atrial pressure also appears to balance out, to some extent, the omission of a correlate for left atrial pressure in either of our equations. The importance of left atrial pressure was elegantly highlighted in a recent editorial by Sorajja and Nishimura.
Third, in our study and other observations of the time-velocity integral of the right ventricular outflow tract (TVI RVOT ), we note that the notching mentioned by Opotowsky et al . does vary. Furthermore, in its extreme forms, notching will lead to a decrease in the total systolic duration and time-velocity integral of the TVI RVOT waveform. In those cases, there will be no notch, albeit an elevated PVR, with no accounting for the extra 3 in their proposed equation.
Since our first publication in 2003, our main goal has been to provide a simple, noninvasive means to differentiate patients with normal versus elevated PVR, a goal that TRV/TVI RVOT and TRV 2 /TVI RVOT achieve. TRV/TVI RVOT has been further validated by other groups and was found to provide prognostic information in patients with different disease subsets (>2,000 patients collectively). We agree that TRV/TVI RVOT × 10 (in patients with TRV/TVI RVOT < 0.275 and/or PVR < 6 Wood units) and TRV 2 /TVI RVOT × 5 (in patients with PVR < 12 Wood units regardless of TRV/TVI RVOT ) provide a reasonable, albeit not perfect, noninvasive estimate of PVR. We concede that for higher PVR values, the noninvasive techniques have not been studied and may fall short.
For now, right heart catheterization will remain the gold standard for the evaluation of pulmonary hemodynamics in all patients with pulmonary hypertension, especially before the initiation of therapy, as stated by the American College of Cardiology guidelines. Noninvasive measures, such as TRV/TVI RVOT and TRV 2 /TVI RVOT , may act as gatekeepers in a similar fashion as stress tests, in some patients, before cardiac catheterization.