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Original Research: PULMONARY HYPERTENSION |

High-Resolution Chest CT Findings Do Not Predict the Presence of Pulmonary Hypertension in Advanced Idiopathic Pulmonary Fibrosis* FREE TO VIEW

David A. Zisman, MD, FCCP; Arun S. Karlamangla, PhD, MD; David J. Ross, MD; Michael P. Keane, MD, FCCP; John A. Belperio, MD; Rajan Saggar, MD; Joseph P. Lynch, III, MD, FCCP; Abbas Ardehali, MD; Jonathan Goldin, PhD, MD
Author and Funding Information

*From the Department of Medicine (Drs. Zisman, Ross, Keane, Belperio, Saggar, and Lynch), Division of Pulmonary and Critical Care Medicine; Department of Medicine (Dr. Karlamangla), Division of Geriatrics; Department of Surgery (Dr. Ardehali), Division of Cardiothoracic Surgery; and Department of Radiology (Dr. Goldin), David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA.

Correspondence to: David A. Zisman, MD, FCCP, Interstitial Lung Disease Center, David Geffen School of Medicine at UCLA, 37–131 Center for Health Sciences, Los Angeles, CA 90095; e-mail: dzisman@mednet.ucla.edu



Chest. 2007;132(3):773-779. doi:10.1378/chest.07-0116
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Published online

Background: Reliable, noninvasive approaches to the diagnosis of pulmonary hypertension (PH) in patients with idiopathic pulmonary fibrosis (IPF) are needed. We tested the hypothesis that chest CT-determined extent of pulmonary fibrosis and/or main pulmonary artery diameter (MPAD) can be used to identify the presence of PH in patients with advanced IPF.

Methods: Cross-sectional study of 65 patients with advanced IPF and available right-heart catheterization and high-resolution chest CT. An expert radiologist scored ground-glass opacity, lung fibrosis, and honeycombing in the CT images on a scale of 0 to 4. These scores were also summed into a total profusion score. The main pulmonary artery was measured at its widest dimension on the supine full-chest sequence. At this same level, the widest aorta diameter was measured.

Results: Chest CT-determined fibrosis score, ground-glass opacity score, honeycombing score, total profusion score, diameter of the main pulmonary artery, and the ratio of the pulmonary artery to aorta diameter did not differ between those with and without PH. There was no significant correlation between mean pulmonary artery pressure and any of the chest CT-determined measures.

Conclusions: High-resolution chest CT-determined extent of pulmonary fibrosis and/or MPAD cannot be used to screen for PH in advanced IPF patients.

Figures in this Article

Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic fibrosing interstitial pneumonia associated with the histologic appearance of usual interstitial pneumonia.1Pulmonary hypertension (PH) commonly complicates advanced IPF and is associated with a worse prognosis.26

Right-heart catheterization (RHC) is the “gold standard” test to diagnose PH in patients with IPF. However, RHC is invasive, costly, and associated with complications. Although echocardiography is the most commonly used test to screen for PH in patients with interstitial lung disease, it is not a reliable screening test.5,7 Reliable, noninvasive approaches to the diagnosis of PH in patients with IPF would improve patient safety and reduce cost.

Previous studies812 in patients with pulmonary vascular disease and diverse lung conditions have suggested that chest CT-determined pulmonary artery diameters can be used to predict PH. However, this has not been tested in a homogeneous sample of patients with well-characterized IPF. Mechanistically, the severity of lung fibrosis should correlate with the prevalence and degree of PH. However, the relationships between CT assessments of lung fibrosis and pulmonary artery pressure have not been studied in patients with IPF. Therefore, in this study, we examined whether the CT-determined extent and severity of pulmonary fibrosis and main pulmonary artery diameter (MPAD) could be used to diagnose PH in patients with advanced IPF.

Study Sample

We retrospectively reviewed the medical records of all patients with IPF who were seen at our institution between July 1999 and June 2006. During the initial visit, all patients prospectively provided written informed consent (approved by the University of California, Los Angeles institutional review board) to use their clinical and demographic information for research purposes. All patients met accepted diagnostic criteria for IPF, and the majority (74%) had histopathologic evidence of usual interstitial pneumonia.1 Three hundred twenty-two patients with well-documented IPF were seen at the center during this period and were candidates for inclusion in this study. To be included in the study, participants had to have had a high-resolution CT (HRCT) of the chest within 1 month of RHC. RHC was performed as part of the lung transplant evaluation (74%) or for participation in a clinical trial (ClinicalTrials.gov identifier NCT00352482). Sixty-five patients met this entry criterion, and 27 of them had PH.

Measurements

RHC data included measurements of pulmonary arterial pressures with the patient at rest. We defined PH as resting mean pulmonary artery pressure (MPAP) > 25 mm Hg.13After at least 5 min of rest, pulse oxygen saturation (Spo2) was measured on room air. Standard methodology was used when performing pulmonary function tests and 6-min walk distance (6MWD).17

Chest HRCT Scoring System

All HRCTs were performed in the prone position, acquiring 1.0- or 1.5-mm-thick sections at 1 cm throughout the entire thorax and then in the supine position. Full-volume CT scans reconstructed every 3 mm were acquired at suspended inspiration. HRCTs were reconstructed with a sharp kernel (B50; Siemens; Malvern, PA) and field of view of the widest outer rib to outer rib dimension. All studies were scored by an expert thoracic radiologist (J.G.) blinded to clinical and hemodynamic information, using a Likert scale (where 0 = absent, 1 = 1 to 25%, 2 = 26 to 50%, 3 = 51 to 75% and 4 = 76 to 100%) for extent of parenchymal abnormality in three categories: ground-glass opacity, lung fibrosis, and honeycombing. These scores were also summed into a total CT profusion score. This scoring system is based on that reported by Kazerooni et al.18 The following radiographic definitions were employed: ground-glass opacity, hazy parenchymal opacity in the absence of reticular opacity, or architectural distortion; lung fibrosis, reticular opacification, traction bronchiectasis, and bronchiolectasis; and honeycombing, clustered air-filled cysts with dense walls. Each lung lobe was scored separately (upper, lung apex to aortic arch; middle, aortic arch to inferior pulmonary veins; and lower, inferior pulmonary veins to diaphragm), and the mean score over all five lobes was computed for each category of parenchymal abnormality: fibrosis (CT-determined fibrosis score [CT-fib]), ground-glass opacity (CT-determined ground-glass score [CT-alv]), honeycombing (CT-determined honeycomb score [CT-hc]), and total profusion (CT-determined total profusion score [CT-tot] = CT-fib + CT-alv + CT-hc). Lobe scores were also weighted by typical relative size (right upper lobe, 0.0935; right middle lobe, 0.0935; right lower lobe, 0.363; left upper lobe, 0.155; and left lower lobe, 0.297) and summed to create weighted scores for fibrosis (weighted CT-fib [wCT-fib]), ground-glass (weighted CT-alv [wCT-alv]), honeycombing (weighted CT-hc [wCT-hc]), and total profusion (weighted CT-tot [wCT-tot]). We also created a maximum fibrosis score (mCT-fib) based on the most affected lobe.

MPAD was measured at its widest dimension on the supine full-chest sequence. At this same level, the widest aorta diameter (AD) was measured, and the MPAD/AD ratio was calculated. MPAD was also normalized by body surface area (BSA, meters squared), which was calculated according to the following equation: BSA = 0.00718 × W0.425 × H0.725, where W is body weight (kilograms), and H is body height (centimeters).19

Statistical Analysis

We compared mean values of all putative predictors of PH in patients with and without PH using the Student t test. We also examined the Pearson correlation coefficient between MPAP and each of the putative predictors of PH. We then regressed MPAP on CT-fib, wCT-alv, wCT-hc, and MPAD/AD in a multivariable linear regression model. The CT-derived scores chosen for the model were the scores with the highest correlation with MPAP in each category (fibrosis, ground-glass opacity, honeycombing, and pulmonary artery size).

All tests were two tailed, and p values < 0.05 were required for statistical significance. All statistical analyses were performed using statistical software (SAS version 9.1; SAS Institute; Cary, NC).

Power Calculations

Our study was designed to have 80% power to detect ≥ 0.75σ differences in putative predictors between the PH and no-PH groups (where σ is the common SD in the two groups) and to detect correlations ≥ 0.34 between MPAP and putative predictors.

The study sample (n = 65) had more advanced pulmonary disease (with lower FVC, diffusing capacity of the lung for carbon monoxide [Dlco], and room air Spo2) than the rest of the cohort (n = 257) but was representative of the cohort with respect to age, gender, and race (Table 1 ). MPAP in the study sample was similar to the MPAP in the 56 patients with RHC data who were excluded from the study because their RHC was > 1 month distant from their HRCT.

Comparisons of Patients With and Without PH

Patients with and without PH did not differ with respect to age, gender, race, and BSA (Table 2 ). As expected, those with PH had significantly lower Dlco, 6MWD, and resting room air Spo2 and significantly higher FVC/Dlco and MPAP than those without PH, but they did not perform significantly worse on FVC or Dlco/alveolar volume (VA) and had similar CT-derived scores for extent and severity of parenchymal disease and CT-derived MPAD, MPAD/AD, and MPAD/BSA. Similarly, CT scores weighted by relative lobar size and the maximum CT–fib over all lobes did not differ between those with or without PH.

Correlation Between MPAP and Putative PH Predictors

As shown in Table 3 , there were strong and statistically significant correlations in the expected directions between MPAP and both 6MWD and resting, room air Spo2. We observed a modest and significant correlation between MPAP and Dlco, Dlco/VA percentage and FVC percentage of predicted/Dlco percentage of predicted. However, there was no correlation between MPAP and FVC, CT-fib, CT-alv, CT-hc, CT-tot, MPAD, AD, MPAD/AD, or the MPAD/BSA ratio (Fig 1, 2 ). Similarly, there was no correlation between MPAP and CT scores weighted by relative lobar size or the maximum CT-fib. Furthermore, we found no correlation between other RHC-derived measurements (right atrial pressure, pulmonary vascular resistance, cardiac output, cardiac index) and any of the chest CT-determined measures (data not shown).

Multivariable Linear Regression of MPAP on CT-Derived Predictors

We regressed the MPAP on the CT scores (one from each category) with the highest correlation with MPAP (namely, CT-fib, wCT-alv, wCT-hc, and MPAD/AD) in a multivariable linear regression model. The model-adjusted R2 was 0.008 (p = 0.35).

PH is common in patients with advanced IPF, and its presence has a significant adverse impact on survival.23 Noninvasive approaches to the diagnosis of PH in patients with IPF are needed. In this study, we found that the CT-determined extent and severity of pulmonary fibrosis and MPAD do not help in identifying PH in advanced IPF patients.

Intuitively, the severity of lung fibrosis should correlate with the prevalence and degree of PH. It seems logical that as IPF progresses and the lungs become more fibrotic, the cross-sectional area of the pulmonary vascular bed is reduced, the pulmonary vascular resistance rises, and PH ensues; however, in this study, MPAP did not correlate with CT-based measurements of lung fibrosis, and these variables did not differ between those with and without PH. Previously, we and others25,20have shown that MPAP does not correlate with the degree of restrictive physiology (FVC, total lung capacity) in IPF. PH is also disproportionate to the degree of restrictive ventilatory impairment (FVC) in patients with sarcoidosis and pulmonary Langerhan cell histiocytosis.2122 This study provides the first radiographic confirmation of the notion that the loss of pulmonary vascular conductance in IPF is not proportional to the extent of fibrosis. Vascular remodeling in IPF has been the subject of intense investigation over the last few years.2327 There is evidence of regional heterogeneity, with some areas demonstrating increased vascularity, and other areas demonstrating decreased vascularity.2327 While fibroblastic foci are notable for the absence of blood vessels, they are surrounded by a rich network of vessels.28That is probably why there is little correlation between extent of fibrosis and MPAP. Although a higher extent of lung fibrosis on CT has been associated with worse outcome in IPF patients,2931 our findings suggest that it is unlikely that a higher CT fibrosis portends poor prognosis in connection with PH in IPF patients. By contrast, hypoxemia is an independent predictor of mortality in IPF,3234 and it is also strongly linked to PH. This study and previous studies by us and others25 have consistently observed a strong association between high MPAP and low Spo2, suggesting that vasoconstriction in response to hypoxia is an important factor in the development of PH in patients with IPF. Although initially reversible, pathologic changes induced by hypoxia-induced vasoconstriction ultimately result in irreversible vascular remodeling.,3536

Previous studies of the association between pulmonary artery size and pulmonary artery pressure have been inconsistent, with some investigators9,11,3739 finding correlations in the expected direction, and others4042 reporting no correlation. Our results support the previous studies4042 that have found no correlation between pulmonary arterial diameter and pulmonary artery pressure. It should be emphasized that our study population consisted of a homogeneous group of well-characterized IPF patients, whereas other investigators9,12,40,42 have focused on a wide spectrum of cardiopulmonary diseases, with a large proportion of patients with pulmonary vascular disease (PVD) such as idiopathic pulmonary arterial hypertension or chronic thromboembolism.1011,39,4142 Although we cannot explain these disparate findings with certainty, it is quite possible that pulmonary artery size and pressure are correlated only in PVD and not in IPF. It is also possible that PH in our patients was not severe enough to cause increase in MPAD. In previous studies8,11 that have found associations between pulmonary artery size and PH, the PH cases were predominantly composed of patients with PVD with greater pulmonary artery pressures than our IPF patients with PH. Haimovici et al9 observed that when the severe PH cases were omitted by excluding patients with idiopathic pulmonary artery hypertension and patients with Eisenmenger syndrome, the correlation between CT-measured pulmonary artery size and MPAP dropped. In a separate study, inclusion of PVD patients increased the MPAP of the PH group from 35.1 to 45.3 mm Hg. In that study, MPAD increased from 33 to 35 mm when PVD patients were included in the PH group,42 and the sensitivity and specificity of MPAD in predicting PH was lower in the subgroup of patients with parenchymal lung disease when compared to patients with PVD.42 Our study is consistent with these findings, and together they suggest that PH due to IPF may not increase MPAD. It is also conceivable that the restrictive lung physiology in IPF may result in a traction effect on the mediastinal vascular structures, distending the pulmonary artery independent of the underlying pulmonary artery pressure; this effect may dampen the influence of the pulmonary artery pressure on the MPAD in patients with IPF. Ng et al12 showed in multivariable analysis that total lung capacity, a marker of traction on mediastinal structures, independently contributed to MPAD. Consistent with this hypothesis, the pulmonary artery diameter in our control group (IPF patients without PH) was greater (31.3 ± 4 mm) than the values reported by others in their control subjects without cardiopulmonary disease: 24.2 ± 2 mm,11 and 27.2 ± 3 mm.8

Certain limitations of our study need to be acknowledged. This was a retrospective review of patients evaluated at a single center. Most of our patients underwent evaluation for lung transplantation, reflecting the presence of patients with more advanced IPF; hence, our results may not apply to the general population of IPF patients. However, we and others26 have shown that PH is more prevalent in patients with severe IPF (defined by reduced Dlco and/or Spo2); hence, this population is the one in whom identification of PH is more critical. Similar to other studies,37,3941 on this topic, CT scores were read by a single radiologist; however, since interobserver accuracy in measuring MPAD and extent of pulmonary fibrosis has been shown to be good,8,12,18 we do not believe that the lack of additional readings by more than one expert radiologist biased our findings. Ours is a cross-sectional study of the association between CT-derived measures and PH in IPF patients. Hence, we cannot conclude that PH secondary to IPF is causally unrelated to changes in CT. That would require a longitudinal study. However, we can say that CT-derived measures of parenchymal disease and MPAD cannot be used to screen for PH in advanced IPF patients. Finally, our sample size may have limited our ability to find a real underlying association between CT-derived measures and PH. Since our study was powered to find correlations ≥ 0.34, we can infer only that if there are undetected correlations between MPAP and one or more of the CT-derived measures, they are likely to be < 0.34. Since this and previous studies45 have found correlations between MPAP and simple measurements (such as 6MWD, Spo2, and Pao2) of the order of 0.5 and 0.7, we can conclude that HRCT-derived measures cannot distinguish between PH and no PH as well as simple clinical measurements such as oxygenation and the 6MWD. In summary, HRCT-determined severity and extent of pulmonary fibrosis and pulmonary artery size cannot be used to screen for PH in advanced IPF patients.

Abbreviations: AD = aorta diameter; BSA = body surface area; CT-alv = CT-determined ground-glass score; CT-fib = CT-determined fibrosis score; CT-hc = CT-determined honeycomb score; CT-tot = CT-determined total profusion score; Dlco = diffusing capacity of the lung for carbon monoxide; HRCT = high-resolution CT; IPF = idiopathic pulmonary fibrosis; mCT-fib = maximum CT-derived fibrosis score over all lobes; MPAD = main pulmonary artery diameter; MPAP = mean pulmonary artery pressure; 6MWD = 6-min walk distance; PH = pulmonary hypertension; PVD = pulmonary vascular disease; RHC = right-heart catheterization; Spo2 = pulse oxygen saturation; wCT-alv = weighted CT-determined ground-glass score; wCT-fib = weighted CT-determined fibrosis score; wCT-hc = weighted CT-determined honeycomb score; wCT-tot = weighted CT-determined total profusion score; VA = alveolar volume

All work was performed at the David Geffen School of Medicine.

Dr. Zisman received research grants from Actelion Pharmaceuticals and Cotherix Pharmaceuticals to do multicenter studies. Dr. Zisman is funded by the National Institutes of Health IPF Clinical Research Network, which includes participation in a pulmonary hypertension study with sildenafil.

This work was supported, in part, by grants from the National Institutes of Health: 5U10HL080411 and 5P50HL67665 to Dr. Zisman, HL080206 and HL086491 to Dr. Belperio, and AR055075 to Dr. Keane.

The authors have no other conflicts of interest to disclose.

Table Graphic Jump Location
Table 1. Descriptive Statistics for Major Characteristics*
* 

Data are presented as mean (SD) or %. Age and gender are available in all 322 patients; race is available in 320 of 322 patients; FVC (absolute and percentage of predicted) is available in 304 of 322 patients; Dlco (absolute and percentage of predicted) is available in 293 of 322 patients; resting room air Spo2 is available in 266 of 322 patients; and MPAP is available in 121 of 322 patients.

 

Includes Asian and African-American patients.

§ 

These 56 patients had RHC data but were excluded because their RHC were not performed within 1 month of HRCT.

Table Graphic Jump Location
Table 2. Patient Characteristics Based on the Presence or Absence of PH by RHC*
* 

Data are presented as mean (SD) or %.

 

Includes Asian and African-American patients.

Table Graphic Jump Location
Table 3. Pearson Correlation Coefficients Between MPAP and Putative Predictors of PH
* 

Test of zero correlation.

Figure Jump LinkFigure 1. Relationship between CT-fib and measured MPAP. NS = not significant.Grahic Jump Location
Figure Jump LinkFigure 2. Relationship between CT-determined MPAD and measured MPAP. See Figure 1 legend for expansion of abbreviation.Grahic Jump Location
. American Thoracic Society. (2000) Idiopathic pulmonary fibrosis: diagnosis and treatment; international consensus statement.Am J Respir Crit Care Med161,646-664. [PubMed]
 
Lettieri, CJ, Nathan, SD, Barnett, SD, et al Prevalence and outcomes of pulmonary arterial hypertension in advanced idiopathic pulmonary fibrosis.Chest2006;129,746-752. [PubMed] [CrossRef]
 
Nadrous, HF, Pellikka, PA, Krowka, MJ, et al Pulmonary hypertension in patients with idiopathic pulmonary fibrosis.Chest2005;128,2393-2399. [PubMed]
 
Weitzenblum, E, Ehrhart, M, Rasaholinjanahary, J, et al Pulmonary hemodynamics in idiopathic pulmonary fibrosis and other interstitial pulmonary diseases.Respiration1983;44,118-127. [PubMed]
 
Zisman DA, Ross DJ, Belperio JA, et al. Prediction of pulmonary hypertension in idiopathic pulmonary fibrosis. Respir Med 2007; [Epub ahead of print].
 
Hamada, K, Nagai, S, Tanaka, S, et al Significance of pulmonary arterial pressure and diffusion capacity of the lung as prognosticator in patients with idiopathic pulmonary fibrosis.Chest2007;131,650-656. [PubMed]
 
Arcasoy, SM, Christie, JD, Ferrari, VA, et al Echocardiographic assessment of pulmonary hypertension in patients with advanced lung disease.Am J Respir Crit Care Med2003;167,735-740. [PubMed]
 
Edwards, PD, Bull, RK, Coulden, R CT measurement of main pulmonary artery diameter.Br J Radiol1998;71,1018-1020. [PubMed]
 
Haimovici, JB, Trotman-Dickenson, B, Halpern, EF, et al Relationship between pulmonary artery diameter at computed tomography and pulmonary artery pressures at right-sided heart catheterization: Massachusetts General Hospital Lung Transplantation Program.Acad Radiol1997;4,327-334. [PubMed]
 
Heinrich, M, Uder, M, Tscholl, D, et al CT scan findings in chronic thromboembolic pulmonary hypertension: predictors of hemodynamic improvement after pulmonary thromboendarterectomy.Chest2005;127,1606-1613. [PubMed]
 
Kuriyama, K, Gamsu, G, Stern, RG, et al CT-determined pulmonary artery diameters in predicting pulmonary hypertension.Invest Radiol1984;19,16-22. [PubMed]
 
Ng, CS, Wells, AU, Padley, SP A CT sign of chronic pulmonary arterial hypertension: the ratio of main pulmonary artery to aortic diameter.J Thorac Imaging1999;14,270-278. [PubMed]
 
Rich, S, Dantzker, DR, Ayres, SM, et al Primary pulmonary hypertension: a national prospective study.Ann Intern Med1987;107,216-223. [PubMed]
 
Crapo, RO, Morris, AH, Gardner, RM Reference spirometric values using techniques and equipment that meet ATS recommendations.Am Rev Respir Dis1981;123,659-664. [PubMed]
 
Miller, A, Thornton, JC, Warshaw, R, et al Single breath diffusing capacity in a representative sample of the population of Michigan, a large industrial state: predicted values, lower limits of normal, and frequencies of abnormality by smoking history.Am Rev Respir Dis1983;127,270-277. [PubMed]
 
Macintyre, N, Crapo, RO, Viegi, G, et al Standardisation of the single-breath determination of carbon monoxide uptake in the lung.Eur Respir J2005;26,720-735. [PubMed]
 
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Kazerooni, EA, Martinez, FJ, Flint, A, et al Thin-section CT obtained at 10-mm increments versus limited three-level thin-section CT for idiopathic pulmonary fibrosis: correlation with pathologic scoring.AJR Am J Roentgenol1997;169,977-983. [PubMed]
 
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Figures

Figure Jump LinkFigure 1. Relationship between CT-fib and measured MPAP. NS = not significant.Grahic Jump Location
Figure Jump LinkFigure 2. Relationship between CT-determined MPAD and measured MPAP. See Figure 1 legend for expansion of abbreviation.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Descriptive Statistics for Major Characteristics*
* 

Data are presented as mean (SD) or %. Age and gender are available in all 322 patients; race is available in 320 of 322 patients; FVC (absolute and percentage of predicted) is available in 304 of 322 patients; Dlco (absolute and percentage of predicted) is available in 293 of 322 patients; resting room air Spo2 is available in 266 of 322 patients; and MPAP is available in 121 of 322 patients.

 

Includes Asian and African-American patients.

§ 

These 56 patients had RHC data but were excluded because their RHC were not performed within 1 month of HRCT.

Table Graphic Jump Location
Table 2. Patient Characteristics Based on the Presence or Absence of PH by RHC*
* 

Data are presented as mean (SD) or %.

 

Includes Asian and African-American patients.

Table Graphic Jump Location
Table 3. Pearson Correlation Coefficients Between MPAP and Putative Predictors of PH
* 

Test of zero correlation.

References

. American Thoracic Society. (2000) Idiopathic pulmonary fibrosis: diagnosis and treatment; international consensus statement.Am J Respir Crit Care Med161,646-664. [PubMed]
 
Lettieri, CJ, Nathan, SD, Barnett, SD, et al Prevalence and outcomes of pulmonary arterial hypertension in advanced idiopathic pulmonary fibrosis.Chest2006;129,746-752. [PubMed] [CrossRef]
 
Nadrous, HF, Pellikka, PA, Krowka, MJ, et al Pulmonary hypertension in patients with idiopathic pulmonary fibrosis.Chest2005;128,2393-2399. [PubMed]
 
Weitzenblum, E, Ehrhart, M, Rasaholinjanahary, J, et al Pulmonary hemodynamics in idiopathic pulmonary fibrosis and other interstitial pulmonary diseases.Respiration1983;44,118-127. [PubMed]
 
Zisman DA, Ross DJ, Belperio JA, et al. Prediction of pulmonary hypertension in idiopathic pulmonary fibrosis. Respir Med 2007; [Epub ahead of print].
 
Hamada, K, Nagai, S, Tanaka, S, et al Significance of pulmonary arterial pressure and diffusion capacity of the lung as prognosticator in patients with idiopathic pulmonary fibrosis.Chest2007;131,650-656. [PubMed]
 
Arcasoy, SM, Christie, JD, Ferrari, VA, et al Echocardiographic assessment of pulmonary hypertension in patients with advanced lung disease.Am J Respir Crit Care Med2003;167,735-740. [PubMed]
 
Edwards, PD, Bull, RK, Coulden, R CT measurement of main pulmonary artery diameter.Br J Radiol1998;71,1018-1020. [PubMed]
 
Haimovici, JB, Trotman-Dickenson, B, Halpern, EF, et al Relationship between pulmonary artery diameter at computed tomography and pulmonary artery pressures at right-sided heart catheterization: Massachusetts General Hospital Lung Transplantation Program.Acad Radiol1997;4,327-334. [PubMed]
 
Heinrich, M, Uder, M, Tscholl, D, et al CT scan findings in chronic thromboembolic pulmonary hypertension: predictors of hemodynamic improvement after pulmonary thromboendarterectomy.Chest2005;127,1606-1613. [PubMed]
 
Kuriyama, K, Gamsu, G, Stern, RG, et al CT-determined pulmonary artery diameters in predicting pulmonary hypertension.Invest Radiol1984;19,16-22. [PubMed]
 
Ng, CS, Wells, AU, Padley, SP A CT sign of chronic pulmonary arterial hypertension: the ratio of main pulmonary artery to aortic diameter.J Thorac Imaging1999;14,270-278. [PubMed]
 
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    Print ISSN: 0012-3692
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