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Communications to the Editor |

New Formula for Predicting Mean Pulmonary Artery Pressure FREE TO VIEW

Denis Chemla, MD; Vincent Castelain, MD; Yves Lecarpentier, MD; Marc Humbert, MD; Gérald Simonneau, MD; Philippe Hervé, MD
Author and Funding Information

Affiliations: CHU de Bicêtre, Le Kremlin-Bicêtre, France,  Hôpital Antoine Béclère, Clamart, France,  Hôpital Marie Lannelongue, le Plessis-Robinson, France

Correspondence to: Prof. Denis Chemla, MD, Service EFCR, Broca 7, Hôpital de Bicêtre, 78 rue du Général Leclerc, 94 275 Le Kremlin Bicêtre, France; e-mail: denis.chemla@bct.ap-hop-paris.fr



Chest. 2005;128(1):467. doi:10.1378/chest.128.1.467
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To the Editor:

We appreciate the interest of Drs. Fisher and Hassoun in our recent study (October 2004).1 In their first comment, they suggest that a more appropriate evaluation of our formula would have been obtained by determining the mean difference between the calculated mean pulmonary artery pressure (mPAP) and the measured mPAP (bias). This important methodologic issue was in fact taken into account in our article, where the bias value was presented in the validation sample.1 We feel that obtaining a predictive formula in the test sample and calculating the bias in the validation sample only is appropriate from a statistical point of view. Nevertheless, in an attempt to comply with their comment, we have calculated the bias in the overall population from raw pressure data. We obtain a – 0.2 mm Hg bias (95% limits of agreement from – 5.6 to + 5.2 mm Hg), and the slight discrepancies between their calculations and ours may be explained as follows. In our study, high-fidelity pressures were automatically calculated with a 0.1 mm Hg precision, and values were averaged out over > 10 consecutive cycles.1However, for sake of simplicity for the reader, the pressures presented in both text and tables have been corrected to the nearest whole number, which makes more clinical sense. Finally, as far as the validity of our new formula is concerned, namely mPAP = 0.61 sPAP + 2 mm Hg (where sPAP is systolic PAP), our retrospective analysis of the data by Laskey et al2 led to an essentially similar relationship.

In their further comment, Drs. Fisher and Hassoun have calculated mPAP by using the standard formula (mPAP = 2/3 dPAP + 1/3 sPAP; where dPAP is diastolic PAP), and we obtain roughly similar results (bias = − 1.4 mm Hg; 95% limits of agreement, – 4.1 to 1.3 mm Hg). They conclude that “the standard formula is easier and arguably more accurate,” and our reply will discriminate practical from physiologic considerations. From a practical point of view, there is no need of any formula in the catheterization laboratory, as mPAP is automatically integrated over time by the computer system. Conversely, we feel that our formula is easier to use than the standard one in the echo-Doppler laboratory, where precise measurements of dPAP are not always available, whereas more reliable measurements of sPAP are often obtained. Furthermore, our formula was less biased (and thus more accurate) than the empirical formula, which was, however, more precise as evidenced by the narrower 95% limits of agreement.

From a physiologic point of view, the principle that underlies scientific modeling caution against favoring the complex models over the simple ones. This logical principle is attributed to the medieval philosopher William of Occam (1285 to 1349) who stated that plurality should not be posited without necessity (Occam’s razor). The standard formula (two-pressure model) implies that mPAP is twice as sensitive to dPAP as it is to sPAP. Although we agree that the standard formula is accurate and precise, we suspect that this model is essentially redundant, as sPAP explained 98% of the mPAP variance in our study1and 99% in our retrospective analysis of the study by Laskey et al.2 This strengthens the validity of an alternative, single-pressure model in which sPAP reasonably predicts mPAP.

In their final comment, Drs Fisher and Hassoun caution against the use of our formula to diagnose pulmonary hypertension from Doppler-derived sPAP estimates given the “significant inaccuracy” of sPAP estimates. This was not the aim of our study to test this point, and we were very cautious in our conclusions. Although we are fully aware of studies reporting discrepancies between invasive and noninvasive sPAP,3 we feel that both the careful estimation of right atrial pressure and the correction for confounding factors (eg, demographic ones) may help improve the reliability of sPAP Doppler measurements, especially when performed by experienced teams. Finally, further technical improvements of Doppler devices may well help obtain even more reliable sPAP estimates in the near future.

Chemla, D, Castelain, V, Humbert, M, et al (2004) New formula for predicting mean pulmonary artery pressure using systolic pulmonary artery pressure.Chest126,1313-1317. [CrossRef] [PubMed]
 
Laskey, WK, Ferrari, VA, Palevsky, HI, et al Pulmonary artery hemodynamics in primary pulmonary hypertension.J Am Coll Cardiol1993;21,406-412. [CrossRef] [PubMed]
 
Chemla, D, Castelain, V, Hervé, P, et al Haemodynamic evaluation of pulmonary hypertension.Eur Respir J2002;20,1314-1331. [CrossRef] [PubMed]
 

Figures

Tables

References

Chemla, D, Castelain, V, Humbert, M, et al (2004) New formula for predicting mean pulmonary artery pressure using systolic pulmonary artery pressure.Chest126,1313-1317. [CrossRef] [PubMed]
 
Laskey, WK, Ferrari, VA, Palevsky, HI, et al Pulmonary artery hemodynamics in primary pulmonary hypertension.J Am Coll Cardiol1993;21,406-412. [CrossRef] [PubMed]
 
Chemla, D, Castelain, V, Hervé, P, et al Haemodynamic evaluation of pulmonary hypertension.Eur Respir J2002;20,1314-1331. [CrossRef] [PubMed]
 
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