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Le Kremlin-Bicêtre, France
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
It is widely admitted that mean pulmonary artery pressure (mPAP) may be accurately estimated by using the standard formula: mPAP = 2/3 dPAP + 1/3 sPAP, where dPAP is diastolic pulmonary artery pressure, and sPAP is systolic pulmonary artery pressure. This rule of thumb implies that knowing the minimal and maximal values of the pressure signal allows a precise estimation of the mean pressure, as also documented at the systemic counterpart. Accordingly, it is admitted that mPAP is twice as sensitive to dPAP as it is to sPAP. The prominent role of dPAP in the formula implies that dPAP may reflect vascular tone more accurately than sPAP, which depends on pulmonary artery compliance, wave reflections, and characteristics of right ventricular ejection.
An invasive study by our team1 has challenged this model by reporting that sPAP accounts for 98% of mPAP variability in resting humans studied over à range of 10 to 78 mm Hg, and that a new formula (mPAP = 0.61 sPAP + 2) reasonably predicts mPAP, with a 0 ± 2 mm Hg bias (mean ± SD). Our retrospective analysis1 of the pressure data previously published by Laskey et al2 led to similar conclusion. The principle that underlies scientific modeling cautions against favoring the complex models over the simple ones,3 and this favors the use of sPAP only to estimate mPAP, without the need to include dPAP in the model. Although initially challenged,4 our findings have been confirmed in children free of congenital heart diseases,5 and have proved useful to estimate mPAP in large-scale studies performed in both adults6 and children7 for whom only Doppler-derived sPAP data are available. Finally, a linear relationship between mPAP and sPAP has also been documented in pulmonary arterial hypertension patients performing graded, submaximal supine exercise both before and after a 6-week prostacyclin treatment.8
In the present issue of CHEST (see page 633), Syyed et al9 studied pulmonary hemodynamics in control subjects and in patients with pulmonary hypertension. The authors confirm that mPAP and sPAP are linearly related under resting supine conditions (r2 = 0.98), with the two pressures being related by an empirical formula essentially similar to ours. The newness of their excellent study9 is the following: (1) the strong mPAP vs sPAP linear relationship is extended to changes in posture and activity; (2) the relationship is documented irrespective of potential differences in heart rate, cardiac output, gender, and age; and (3) the retrospective analysis of data obtained in freely moving rats and horses suggests similar relationship between the two pressures. Because mPAP (invasive) and sPAP (noninvasive) are used interchangeably to define pulmonary hypertension in humans, it is currently accepted that mPAP and sPAP provide an essentially redundant estimate of the state of pulmonary circulation. Although this point may appear counterintuitive from a physiologic point of view, it is now confirmed.159
The limitations of the present study9 may be discussed. First, data were averaged over several minutes. This may explain a certain amount of scattering and implies caution for the generalizability of the data in patients studied either in the catheterization laboratory or by using Doppler echocardiography. Second, the limited number of chronic pulmonary thromboembolism and idiopathic pulmonary artery hypertension patients prevented any comparison of potential differences in the relationship between the steady and pulsatile component of their pulmonary arterial load, a point that is still under discussion and may have practical implications.10 Third, an important question still awaiting an answer is what is the sensitivity and specificity of various sPAP thresholds to estimate the degree of pulmonary hypertension, as defined by using mPAP? Further large-scale studies are especially needed to answer this practical question. Fourth, the classic formula may be slightly more precise.34 However, its "pay off" appears essentially similar to that of our formula, at the price of doubling the number of independent variables, and this is out the norms of standard rules of modeling.3 Finally, if there were a tight and constant relationship between systolic, diastolic, and mean pulmonary artery pressures,9 pulmonary circulation could be characterized by any single pressure. This viewpoint may appear questionable because mPAP is less strongly related to dPAP than to sPAP,19 and is weakly related to pulse pressure (sPAP – dPAP).1 Thus, while mPAP is accurately predicted by the single sPAP, it is likely that two pressures remain necessary to fully characterize pulmonary hemodynamics.
What can be inferred from these observations, and does it really matter? For physiologists, the present study9 appears to confirm the hypothesis that the functional adaptation of the pulmonary circulation to the disease process is rather monotonous because changes in pulmonary artery elasticity mainly depend on mPAP.1101112 Experimental data have suggested that changes in pulmonary artery compliant properties and pulsatile pressure are primarily due to increases in mPAP under pulmonary hypertension states.11 Furthermore, using both a theoretical model of the pulmonary circulation, and pressure and MRI flow data in humans, is has been reported that the time constant (resistance x compliance) of the large pulmonary arteries remains unchanged in pulmonary hypertension, with pulmonary resistance and compliance being related by an inverse, curvilinear relationship.12
For the clinician, the estimation of sPAP at rest and with exercise by using Doppler echocardiography has gained increasing importance over standard right-heart catheterization in the diagnosis and prognosis of pulmonary hypertension. Although the applicability of noninvasively estimating mPAP from sPAP may be carefully drawn,134 the new formula may be clinically useful for the following: (1) to cross-check the mPAP value estimated by using other Doppler methods; and (2) to improve the noninvasive estimation of pulmonary vascular resistance both before and after treatment, which may have implications for the prognosis and management of pulmonary hypertension.
Footnotes
Dr. Chemla is Director, EA4046, Université Paris Sud and Professor of Medicine, Service de Physiologie Explorations Fonctionnelles, CHU de Bicêtre, AP-HP. Dr. Hervé is Chairman of the Department of Respiratory Physiology, Département de Chirurgie Thoracique et Vasculaire, Hôpital Marie Lannelongue.
The authors have no conflicts of interest to disclose.
References
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