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(Chest. 2004;126:1313-1317.)
© 2004 American College of Chest Physicians

New Formula for Predicting Mean Pulmonary Artery Pressure Using Systolic Pulmonary Artery Pressure*

Denis Chemla, MD; Vincent Castelain, MD; Marc Humbert, MD; Jean-Louis Hébert, MD; Gérald Simonneau, MD; Yves Lecarpentier, MD and Philippe Hervé, MD

* From the Service de Physiologie Cardio-Respiratoire (Drs. Chemla, Castelain, Hébert, and Lecarpentier), Hôpital de Bicêtre, Université Paris-Sud 11, Assistance Publique-Hôpitaux de Paris, Le Kremlin-Bicêtre, France; Service de Pneumologie (Drs. Humbert and Simonneau), Hôpital Antoine Béclère, Clamart, France; and Département de Chirurgie Thoracique et Vasculaire (Dr. Hervé), Hôpital Marie Lannelongue, Le Plessis-Robinson, France.

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


   Abstract
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 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: Mean pulmonary artery pressure (MPAP) and systolic pulmonary artery pressure (SPAP) are used interchangeably to define pulmonary hypertension (PH). We tested the hypothesis that the measurement of MPAP and SPAP is redundant in resting humans over a wide pressure range.

Design: Prospective, observational study.

Setting: Catheterization laboratory in a university hospital.

Patients: This study involved 31 patients, as follows: primary PH, nine patients; chronic pulmonary thromboembolism, seven patients; venous PH, six patients; and control subjects with normal pulmonary artery pressure, nine patients.

Interventions: None.

Measurements and results: High-fidelity pulmonary artery pressures were obtained when patients were at rest. Over the wide MPAP range that was under study (10 to 78 mm Hg), MPAP and SPAP were strongly related (r2 = 0.98). Regression analysis performed on the first 16 subjects (test sample) allowed us to propose a formula (MPAP = 0.61 SPAP + 2 mm Hg), the accuracy of which was confirmed in the remaining 15 subjects (validation sample bias, 0 ± 2 mm Hg). If PH was defined by an SPAP in excess of 30 or 40 mm Hg, this corresponded to an MPAP in excess of 20 or 26 mm Hg. If PH was defined by an MPAP of > 25 mm Hg, this corresponded to an SPAP of > 38 mm Hg.

Conclusions: In resting humans, MPAP can be accurately predicted from SPAP over a wide pressure range. The new formula may help to refine the threshold pressure values used in the diagnosis of PH. Further studies are needed to test the hypothesis that our formula may allow the noninvasive prediction of MPAP from Doppler-derived SPAP values.

Key Words: hemodynamic • hypertension • pressure • pulmonary


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Pulmonary hypertension (PH) is characterized by the chronic elevation of pulmonary artery pressure. Cardiac catheterization is currently used to firmly establish the diagnosis, although there is no clear consensus as to what level of pulmonary artery pressure constitutes PH. In most studies, PH is diagnosed on the basis of an increased mean pulmonary artery pressure (MPAP) at rest, and various threshold values have been proposed, namely, 18, 20, or 25 mm Hg,12345 with the latter cutoff value being the one most often used in recent clinical trials. PH also may be defined on the basis of a resting systolic pulmonary artery pressure (SPAP) of > 30 mm Hg, as determined by catheterization.12345 In other studies,67 Doppler-derived SPAP values of > 40 to 50 mm Hg have been used to define PH.

Because MPAP and SPAP are used interchangeably to define PH, it is currently accepted that MPAP and SPAP provide a redundant estimate of the state of pulmonary circulation. This point remains to be confirmed experimentally and may appear to be counterintuitive. Indeed, MPAP reflects the steady component of flow and the functional status of the distal (resistive) pulmonary vasculature, while SPAP is expected to encompass the pulsatile component of arterial load, which includes the characteristics of right ventricular ejection and the characteristics of the proximal (elastic) pulmonary arteries and wave reflections.89 In the present study, we tested the hypothesis that MPAP could be accurately predicted from SPAP over a wide pressure range.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
The prospective study was approved by the ethics board of Paris-Sud 11 University, and informed consent was obtained for all patients. The study involved 31 patients (23 men and 8 women) who had been referred to our catheterization laboratory either for severe PH or for the investigation of chest pain, heart failure, or other cardiovascular disorders. PH was defined by an MPAP of > 25 mm Hg at rest while the patient was breathing room air. Precapillary (ie, arterial) and postcapillary (ie, venous) PH were defined on the basis of a mean pulmonary artery occlusion pressure of < 15 mm Hg or ≥ 15 mm Hg, respectively. The final diagnoses were as follows: pulmonary arterial hypertension, 16 patients (primary PH [PPH], 9 patients; chronic pulmonary thromboembolism [CPTE], 7 patients); pulmonary venous hypertension, 6 patients (comprising patients with left heart diseases, namely, idiopathic dilated cardiomyopathy or coronary artery disease); and normal pulmonary artery pressures, 9 patients. PPH was diagnosed according to the criteria of the National Institutes of Health Patient Registry for the Catheterization of PPH.10 CPTE diagnosis was based on the existence of multiple perfusion defects seen on the perfusion lung scan and a typical angiographic pattern (ie, pouchings, webs, stenosis, parietal irregularities, abrupt narrowing, and vascular amputations).11 All PPH and CPTE patients were treated with anticoagulants. No patient was undergoing vasodilator treatment at the time of the study. Patients with right-to-left interatrial shunting or with significant tricuspid insufficiency on echocardiography were excluded from the study. Part of the study population has been described elsewhere.1213

Catheterization Technique and Measurements
Hemodynamic evaluation was carried out on supine patients who were breathing room air, according to our routine protocol.121314 Right heart catheterization was performed using the Seldinger technique with an 8F sheath via the jugular or basilic vein in patients with PPH and CPTE, and via the femoral vein in other subjects. The right heart catheter was a 7.5F, two-lumen, thermodilution pressure-measuring tipped catheter with a high-fidelity transducer (Cordis/Sentron; Roden, the Netherlands).15 The catheter was placed into either the right or left pulmonary artery. Pressure data were computed (model 3200 SX; Toshiba; Tokyo, Japan), and we used a sampling frequency of 1,000 Hz, without filtering of the analog signal, as has been previously recommended.15 Pulmonary artery occlusion pressure was determined according to standard procedures. Cardiac output was measured in triplicate using the thermodilution technique. Cardiac index and stroke volume index were calculated according to standard formulas. Pulmonary vascular resistance index was calculated as follows: MPAP – pulmonary artery occlusion pressure/cardiac index.

The MPAP was defined as the area under the pressure curve divided by the pulse interval. The SPAP was determined automatically by the computer analysis. The onset of pressure pulse and the corresponding diastolic pulmonary artery pressure (DPAP) were identified as the time when the pressure derivative increased steeply. The intraobserver and interobserver variabilities for DPAP measurements were 6 ± 4% and 1 ± 1%, respectively. We calculated pulmonary artery pulse pressure (SPAP – DPAP). The characteristics of the study population are given in Table 1 .


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  		Table 1.. Characteristics of the Study Population*

 
Data Analysis and Statistics
The consecutive patients were divided into two successive samples. The test sample was used to test the link between MPAP and SPAP, and to propose a formula linearly relating the two pressures. The test sample (16 patients) comprised four PPH patients, four CPTE patients, three patients with venous PH, and five normotensive subjects. The next 15 patients entered the validation sample, in which we tested the accuracy of the MPAP vs SPAP formula previously obtained in the test sample. The data are presented as the mean ± SD. Pressure and time parameters were averaged out over > 10 consecutive cardiac cycles. Linear regressions were performed using the least-squares method. A p value of < 0.05 was considered to be statistically significant.


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
In the overall population (31 patients), there was a positive linear relationship between MPAP and SPAP (r2 = 0.982), DPAP (r2 = 0.958), and pulmonary artery pulse pressure (r2 = 0.900). Individual pressure values are given in Table 2 . When SPAP was considered as the independent variable in the test sample, MPAP and SPAP were linearly related according to the following equation: MPAP = 0.61 SPAP + 2 mm Hg (r2 = 0.979; 16 patients) [Fig 1 ].


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  		Table 2.. Individual Values for SPAP, DPAP, and MPAP (n = 31)

 


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  		Figure 1.. Linear relationship between MPAP and SPAP in the test sample (MPAP = 0.61 SPAP + 2 mm Hg; 16 patients; r2 = 0,979; p < 0.001). {blacksquare} = control subjects; {square} = patients with venous PH; • = patients with CPTE; {circ} = patients with PPH.

 
When the MPAP formula that was obtained in the test sample was applied to the validation sample, a pressure bias (formula – true MPAP) equal to 0 ± 2 mm Hg was obtained. The bias was not related to MPAP (Fig 2 ).



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  		Figure 2.. Lack of influence of the true MPAP on the bias (ie, predicted MPAP – true MPAP) in the validation sample (15 patients; r2 = 0.07; p = 0.65). MPAP was predicted according to the following formula: MPAP = 0.61 SPAP + 2 mm Hg.

 
The formula was used to evaluate the pressure thresholds currently used to define PH. According to our formula, if PH was defined by an SPAP of > 30 or 40 mm Hg, this corresponded to an MPAP threshold of 20 or 26 mm Hg, respectively. Another formula (not shown) indicated that if PH was defined by an MPAP of > 20 or 25 mm Hg, this corresponded to an SPAP threshold of 30 or 38 mm Hg, respectively. Although the mean bias was 0 mm Hg using the latter formula, individual SPAP could not be reasonably predicted from MPAP, given the large 95% confidence interval for the bias (ie, –8 to 8 mm Hg).


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The present prospective study demonstrates that MPAP can be accurately predicted from SPAP according to the following formula:

In their pioneer study, Laskey et al9 provided individual high-fidelity pressure values in 10 normotensive subjects and 8 PPH patients (see Tables 1 and 2 in Laskey et al9). The MPAP vs SPAP relationship that we have calculated from their data9 is as follows: MPAP = 0.61 SPAP + 1 mm Hg (r2 = 0.99; MPAP range, 9 to 67 mm Hg). The equation calculated from the data of Laskey et al9 was nearly identical to the equation obtained in our subjects, and this strengthens the relevance of the new formula that we have proposed (ie, the test sample) and validated (ie, the validation sample).

The present study demonstrates that MPAP and SPAP were strongly related over an MPAP range of 10 to 78 mm Hg (r2 = 0.98 in our subjects; 31 patients). This unusually high r2 value was consistent with the 0.99 r2 value obtained with retrospective analysis of the 18 subjects studied by Laskey et al.9 Thus, the new, provocative finding of our study is that if one knows the SPAP, the MPAP was essentially redundant, if one assumes that the pressure bias was small enough to be negligible (ie, 0 ± 2 mm Hg). This must be viewed as a specific property of pulmonary artery hemodynamics as the same is not observed at the aortic level.16 MPAP and SPAP are expected to reflect the steady and pulsatile components of pulmonary arterial load, respectively.1289 Although our finding that MPAP and SPAP were strongly related may appear to be counterintuitive, some studies1718 have suggested that changes in elasticity and pulsatile pressure are primarily due to an increase in MPAP in PH patients. Furthermore, in our study, pulmonary artery pulse pressure was less strongly related to MPAP than was SPAP, and therefore pulse pressure may give a more reliable estimate of pulmonary artery pulsatile load.913

The main implication of our results is that the threshold pressure values used in PH patients could be refined. If PH was defined by an SPAP of > 30 or 40 mm Hg, this corresponded to an MPAP of > 20 or 26 mm Hg, respectively. If PH was defined by an MPAP of > 25 mm Hg, this corresponded to an SPAP threshold of 38 mm Hg, a value that appears to be more realistic than the 30 mm Hg value currently used in catheterization studies. This may bring the pressure threshold used in catheterization laboratories closer to that used in Doppler studies (SPAP, > 40 mm Hg).67 Finally, further studies are need to test the hypothesis that our formula may allow the noninvasive prediction of MPAP from Doppler-derived SPAP.

For an invasive study, and bearing in mind that high-fidelity catheters were used, it should be pointed out that the number of subjects studied (31 patients) was likely to be sufficient to sustain the conclusions drawn from the data. The data were clear-cut, and the retrospective analysis of a previous study9 furnished fairly consistent results. High-fidelity pressure catheters are the "gold standard" when attempting to obtain reliable insight into pulmonary artery pathophysiology.819 Signal distortions are unavoidable when using fluid-filled catheters, especially when pulsatile pressure is documented.819 Thus, we cannot exclude the possibility that another formula applies in patients studied with fluid-filled catheters. One strength of the study was that our formula was applied over a wide pressure range, but we cannot exclude the possibility that more accurate formulas apply in specific subgroups studied over narrow pressure ranges. Finally, only patients with chronic PH were studied, and our results may not apply to acute PH.20

The present prospective study demonstrates that MPAP can be accurately predicted from SPAP in resting humans over a wide pressure range. Further studies are needed to test the hypothesis that our formula may allow the noninvasive prediction of MPAP from Doppler-derived SPAP.


   Footnotes
 
Abbreviations: CPTE = chronic pulmonary thromboembolism; DPAP = diastolic pulmonary pressure; MPAP = mean pulmonary pressure; PH = pulmonary hypertension; PPH = primary pulmonary hypertension; SPAP = systolic pulmonary artery pressure

Received for publication December 18, 2003. Accepted for publication March 31, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Davidson, CJ, Fishman, RF, Bonow, RO (1997) Cardiac catheterization. Braunwald, E eds. Heart disease: a textbook of cardiovascular medicine. 5th ed. ,177-203 WB Saunders. Philadelphia, PA:
  2. Weir, EK, Michelakis, ED, Archer, SL, et al Pulmonary hypertension. Willerson, JT Cohn, JN eds. Cardiovascular medicine 2nd ed. 2000,1856-1884 Churchill Livingstone. Philadelphia, PA:
  3. Rich, S, Braunwald, E, Grossman, W Pulmonary hypertension. Braunwald, E eds. Heart disease: a textbook of cardiovascular medicine. 5th ed. 1997,780-806 WB Saunders. Philadelphia, PA:
  4. Moraes, D, Loscalzo, J Pulmonary hypertension: newer concepts in diagnosis and management. Clin Cardiol 1997;20,676-682[ISI][Medline]
  5. Chemla, D, Castelain, V, Hervé, P, et al Haemodynamic evaluation of pulmonary hypertension. Eur Respir J 2002;20,1314-1331[Abstract/Free Full Text]
  6. World Health Organization. Executive summary from the World Symposium on Primary Pulmonary Hypertension 1998. Evian, France, September 6–10, 1998. Available at: http:/who.int/ncd/cvd/pph.html. Accessed November 21, 2000
  7. McQuillan, BM, Picard, MH, Leavitt, M, et al Clinical correlates and reference intervals for pulmonary artery systolic pressure among echocardiographically normal subjects. Circulation 2001;104,2797-2802[Abstract/Free Full Text]
  8. Milnor, WR Hemodynamics. 1982 William & Wilkins. Baltimore, MD:
  9. Laskey, WK, Ferrari, VA, Palevsky, HI, et al Pulmonary artery hemodynamics in primary pulmonary hypertension. J Am Coll Cardiol 1993;21,406-412[Abstract]
  10. Rich, SD, Dantzker, R, Ayres, SM, et al Primary pulmonary hypertension: a national prospective study. Ann Intern Med 1987;107,216-223[CrossRef][ISI][Medline]
  11. Auger, WR, Fedullo, PF, Moser, KM, et al Chronic major-vessel thromboembolic pulmonary artery obstruction: appearance at angiography. Radiology 1992;182,393-398[Abstract/Free Full Text]
  12. Chemla, D, Hébert, JL, Coirault, C, et al Matching dicrotic notch and mean pulmonary artery pressure: implications for effective arterial elastance. Am J Physiol 1996;271,H1287-H1295
  13. Castelain, V, Hervé, P, Lecarpentier, Y, et al Pulmonary artery pulse pressure and wave reflection in chronic pulmonary thromboembolism and primary pulmonary hypertension. J Am Coll Cardiol 2001;37,1085-1092[Abstract/Free Full Text]
  14. Castelain, V, Chemla, D, Humbert, M, et al Pulmonary artery pressure-flow relations after prostacyclin in primary pulmonary hypertension. Am J Respir Crit Care Med 2002;165,338-340[Abstract/Free Full Text]
  15. Aubert, AE, Vrolix, M, de Geest, H, et al In vivo comparison between two tip pressure transducer systems. Int J Clin Monit Comput 1995;12,77-83[CrossRef][ISI][Medline]
  16. Chemla, D, Hébert, JL, Aptecar, E, et al Empirical estimates of mean aortic pressure: advantages, drawbacks and implications for pressure redundancy. Clin Sci (Lond) 2002;103,7-13[Medline]
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  19. Chemla, D, Castelain, V, Simonneau, G, et al Pulse wave reflection in pulmonary hypertension. J Am Coll Cardiol 2002;39,743[Free Full Text]
  20. Aguston, MH, Arcilla, RA, Gasul, RM The diagnosis of bilateral stenosis of the primary pulmonary artery branches based on the characteristic pulmonary trunk pressure curves. Circulation 1962;26,421-427[Abstract/Free Full Text]



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