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doi:10.1378/chest.06-2485
(Chest. 2007; 131:657-663)
© 2007 American College of Chest Physicians
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Pulmonary Hypertension and Pulmonary Function Testing in Idiopathic Pulmonary Fibrosis*

Steven D. Nathan, MD, FCCP; Oksana A. Shlobin, MD; Shahzad Ahmad, MD; Susan Urbanek, RN and Scott D. Barnett, PhD

* From Inova Fairfax Hospital, Falls Church, VA.

Correspondence to: Steven D. Nathan, MD, FCCP, Medical Director, Lung Transplant Program, Inova Heart & Vascular Institute, Inova Fairfax Hospital, 3300 Gallows Rd, Falls Church, VA 22042; e-mail: steven.nathan{at}inova.com

Abstract

Background: Pulmonary hypertension (PH) is commonly seen in patients with idiopathic pulmonary fibrosis (IPF). We sought to examine the relationship between pulmonary function tests (PFTs), including the percentage of predicted FVC (FVC%), percentage of predicted total lung capacity, percentage of predicted diffusing capacity of the lung for carbon monoxide (DLCO%), the composite physiologic index (CPI), and PH. The ability of FVC%, DLCO%, and FVC%/DLCO% ratio to predict underlying PH was assessed.

Methods: Retrospective review of IPF patients seen at a tertiary referral center over an 8-year interval in whom both PFT and right-heart catheterization data were available.

Results: The study cohort consisted of 118 patients, of whom 48 patients (40.7%) had PH. There was no correlation between measures of lung volumes or the CPI with underlying PH. There was a modest association between DLCO% and PH, with DLCO% < 30 having a twofold-higher prevalence of PH (56.4%) compared to DLCO% ≥ 30 (28.6%). Cardiac dysfunction might have played a small role, since 16.1% of the patients had an associated elevated pulmonary capillary wedge pressure. There was a trend to a higher prevalence and greater severity of PH in those patients with FVC% > 70 compared to the group with FVC% < 40.

Conclusion: PH is common in patients with IPF. There is a poor correlation between lung function measures and PH, suggesting that factors other than fibrosis may play a role in the etiology. The unexpected high prevalence and severity of PH in patients with well-maintained lung function have implications for the prognosis and management of the disease.

Key Words: hypertension • pulmonary • pulmonary fibrosis • pulmonary function tests

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic condition associated with a poor prognosis and a median survival of 2.5 to 5 years.123 Predicting the prognosis of patients with IPF remains imprecise. While progressive lung fibrosis plays a major role in disease progression, it has been shown that some patients decline precipitously and succumb to their disease despite well-maintained lung volumes.45 It has also been suggested that pulmonary hypertension (PH) plays an important and underappreciated role in the functional status and prognosis of patients with IPF.67

We sought to characterize the relationship between underlying PH and commonly measured pulmonary function parameters. Specifically, we investigated if lung volumes are predictive of underlying PH. We further determined the relationship between the extent of disease as determined by the composite physiologic index (CPI) and underlying PH.8 In addition, the relationship between the single-breath diffusing capacity of the lung for carbon monoxide (DLCO) and PH was characterized. In patients with diffuse systemic sclerosis, the ratio of FVC to DLCO has been demonstrated to be predictive of PH.91011 We sought to validate this ratio as a predictor of PH in our cohort of IPF patients.

Materials and Methods

The study population consisted of patients with IPF seen at our institution over an 8-year period (from 1997 to 2005) in whom right-heart catheterization (RHC) and pulmonary function studies were available for analysis. Our institution has programs for both interstitial lung disease and lung transplantation. The criteria for performing RHC was age < 65 years in the context of evaluation for lung transplantation. Catheterization in patients > 65 years old was performed at the discretion of the attending physician. All RHCs were performed in the cardiac catheterization laboratory with supplemental oxygen as necessary to maintain oxygen saturation levels > 90%.7 Seventy-nine of these patients were the subject of a prior report7 from our group defining the prevalence and impact of PH in IPF patients. Pulmonary artery pressures were correlated with the PFTs that were closest temporally to the performance of the RHC. The reference equations of Knudson et al12 were used for the PFTs. PH was defined as a mean pulmonary artery pressure (mPAP) > 25 mm Hg.

The mPAP was correlated with the percentage of predicted FVC (FVC%), percentage of predicted total lung capacity (TLC%), percentage of predicted DLCO (DLCO%), and FVC%/DLCO% ratio. The prevalence of PH in those patients with FVC ≥ 50% was defined and compared to the prevalence in those patients below this threshold. This relationship was explored further with an analysis of PH by FVC% decile groups. The ability of the FVC, DLCO, and their ratio to predict underlying PH was assessed via receiver operator characteristic (ROC) curves.

mPAP was correlated with CPI, which is a physiologic correlate of the extent of disease in IPF as assessed by high-resolution CT (HRCT) scan.8 The CPI was calculated by the following equation: 91.0 – (0.65 x DLCO%) – (0.53 x FVC%) + (0.34 x percentage of predicted FEV1).8

The study was approved by the Inova Institutional Review Board. Some of these data have previously been reported at the 2006 American Thoracic Society meeting.13

Statistical Analysis
Continuous data are presented as mean ± SD, and categorical data are presented as frequency and percentage. Statistical testing was accomplished via Student t test or {chi}2 analysis when appropriate. Odds ratios (ORs) and 95% confidence intervals (CIs) were generated via unconditional logistic regression models to evaluate the effect of pulmonary function on the presence or absence of pulmonary hypertension. ROCs were generated to explore the ability of select PFT parameters to discriminate PH patients from non-PH patients. All statistical analysis was performed using statistical software (SAS Version 9.0; SAS Institute; Cary, NC; and GraphPad Prism, Version 4; GraphPad Software; San Diego, CA).

Results

Over an 8-year period, 347 patients with IPF were evaluated. Of these, 118 patients with RHC and PFT data qualified for the analysis. IPF was diagnosed in all patients as per standard guidelines.14 Of the 118 patients, 86 patients (73%) underwent surgical biopsy or had lung explant tissue consistent with the diagnosis. Patient demographics are shown in Table 1 . All but 12 of the patients were ≤ 65 years old. Of the cohort, 48 patients (40.7%) qualified as having PH. The groups with and without PH were well matched for gender, age, and lung function. The mean pulmonary capillary wedge pressure (PCWP) was higher in the PH group (12.2 ± 5.8 mm Hg) compared to the group without PH (8.2 ± 4.6 mm Hg). Of the 118 patients, 19 patients (16.1%) had PCWPs ≥ 15 mm Hg. In this group, 12 patients (63.2%) had PH with a mean mPAP of 30.3 mm Hg. Of these, two patients had transpulmonary gradients < 10 mm Hg.


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  		Table 1. Demographics and Baseline Physiologic Parameters (n = 118)*

 
The median time interval between RHC and PFT measurements was 60 days (range, 1 to 319 days). In 81 of the patients (69.0%), the PFTs were performed before RHC, with a median time interval of 59 days (range, 1 to 305 days). In 37 patients (31.0%), the PFTs were performed after RHC, with a median time interval of 57 days (range, 1 to 319 days). There were 118 patients with FVC%, 102 patients with DLCO%, and 94 patients with TLC% data available for analysis. There were 108, 76, and 35 patients with data within 6 months, 3 months, and 1 month of each other, respectively.

There was no significant correlation between FVC%, DLCO%, and the ratio of the two with mPAP (Fig 1 ). The results of logistic regression suggest similar findings. DLCO% (OR, 0.96; 95% CI, 0.96 to 1.01; C-statistic, 0.53) and FVC% (OR, 1.01; 95% CI, 0.99 to 1.03; C-statistic, 0.52) were not significant predictors of PH.


Figure 1
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  		Figure 1. Correlation of mPAP with FVC% (left, A), DLCO% (center, B), and FVC%/DLCO% ratio (right, C).

 
The prevalence of PH in patients with an FVC > 50% was 41.5%, compared to 39.6% in those with an FVC < 50% (p < 0.985). The FVC% grouped by deciles analysis revealed no difference in the prevalence or severity of PH across groups (Table 2 ). An independent comparison between the highest and lowest decile groups paradoxically demonstrated a trend to a higher prevalence of PH in the former group (62.5% vs 36.4%, p < 0.111). There was also a greater severity of PH in the group with FVC% > 70 compared to the group with FVC% < 40 (p < 0.008). An analysis using the TLC% showed similar results (Table 2), as did an analysis with patients > 65 years old excluded. However, a secondary analysis excluding the patients with an elevated PCWP only demonstrated a trend to a greater severity of PH in the highest vs lowest decile groups (Table 3 ).


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  		Table 2. Deciles of Physiologic Parameters Compared to Pulmonary Artery Pressures (n = 118)

 

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  		Table 3. Deciles of Physiologic Parameters Compared to Pulmonary Artery Pressures in Patients With Normal PCWP (n = 99)

 
An analysis by decile of the DLCO% with PH is shown in Table 2. There appeared to be a closer association between DLCO% and PH. For example, 22 of 39 patients (56.4%) patients with DLCO% < 30 had PH, compared to 18 of 63 patients (28.6%) with DLCO% ≥ 30 (p < 0.008). We investigated whether there was an association between FVC%/DLCO% ratio and PH. An analysis of various cut points of this ratio is also shown in Table 2. A ratio of ≥ 1.5 was associated with an almost twofold-higher risk of associated PH (43.1% vs 27.0%, p < 0.015).

The ability of FVC%, DLCO%, and their ratio as predictors of underlying PH was also assessed via ROCs (Fig 2 ). The performance characteristics of the FVC were very poor, with an area under the curve (AUC) of 0.517, while that of DLCO% and FVC%/DLCO% ratio performed slightly better, with AUCs of 0.643 and 0.613, respectively.


Figure 2
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  		Figure 2. ROCs of FVC% (left, A), DLCO% (center, B), and FVC%/DLCO% ratio (right, C). Sens = sensitivity; Spec = specificity; AUC = area under the curve.

 
The CPI has been shown to correlate closely with the extent of disease as assessed by HRCT in patients with IPF.8 PFT measurements for the calculation of the CPI were available in 101 patients. However, as shown in Figure 3 , we failed to demonstrate any correlation of the CPI with the mPAP.


Figure 3
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  		Figure 3. Correlation of CPI with mPAP.

 
Discussion

PH is a common accompaniment of IPF and has a significant impact on outcomes.67 A possible explanation for the development of PH is that of progressive fibrosis resulting in destruction of the pulmonary vasculature. If the PH of IPF is due to progressive fibrosis, then one might expect to see a relationship between measures of fibrosis and the prevalence and severity of PH. We sought to test the hypothesis that progressive fibrosis is mostly responsible for the PH of IPF by assessing the relationship between physiologic measures of fibrosis and PH. Contrary to our hypothesis, we failed to demonstrate any such correlations.

FVC% is commonly used to define severity and to follow the course of patients with IPF. FVC% is believed to be a physiologic correlate of the extent of fibrosis. If fibrosis played a major role in the genesis of PH in IPF, and if FVC% was an adequate correlate of the extent of fibrosis, then one might expect a correlation between FVC% and PH. Again, we failed to demonstrate any such relationship between FVC% and either the prevalence or severity of PH. Moreover, TLC% did not show any significant correlation with either the prevalence or severity of PH. Paradoxically, there appeared to be a trend toward a higher prevalence and greater severity of PH in the group of patients with FVC% (and TLC%) > 70 as compared to the groups with FVC% (and TLC%) < 40. However, this apparent paradox was lost when patients with an elevated PCWP were excluded. Nonetheless, this lack of a relationship between lung volumes and PH raises issues about both the FVC% and TLC% as surrogates for fibrosis and/or the role of fibrosis in the etiology of PH in IPF.

The finding of a relatively high prevalence of PH in patients with well-preserved lung function should be confirmed by others, ideally in the form of a prospectively designed study. If it is, then this might have implications with regards to outcomes in this group. One might speculate that the etiology of demise in IPF patients is bimodal with underlying, and perhaps occult PH playing a greater role in patients with well-maintained lung function. In patients with lower levels of lung function, fibrosis likely plays a more prominent role with a mortality bias that precludes patients with a greater propensity for PH from this group.

An interesting finding in our study was the prevalence of a higher-than-normal PCWP in 16.1% of the patients. It is possible that passive congestion or diastolic dysfunction could have contributed to the genesis of PH in some of these patients. However, of those patients with an elevated PCWP and PH, the transpulmonary gradient was < 10 mm Hg in only two patients, suggesting that cardiac dysfunction as the sole cause of PH is quite rare (2 of 48 cases, or 4.2%). DLCO% has been shown to correlate with underlying PH in IPF as well as other forms of fibrotic lung disease such as scleroderma.710 We confirmed a modest relationship between the two; 56.4% of our patients with DLCO% < 30 had a component of PH vs 28.6% of those with DLCO% above this threshold. However, as demonstrated by our ROC analysis (AUC, 0.671), the association was not sufficiently robust for DLCO% to suffice as a stand-alone surrogate for underlying PH. The FVC%/DLCO% ratio has been touted in other patient groups, specifically diffuse systemic sclerosis, as a predictor of PH.91011 We attempted to see if there was a similar association in IPF and if this ratio had better prediction capabilities than its individual composite components. However, the AUC of the ROC for this ratio was slightly less than that of the DLCO% alone, and therefore did not provide improved performance characteristics as a predictor of PH. A FVC%/DLCO% ratio > 1.5 was associated with a nearly twofold-increased risk of PH; however, as noted, a DLCO% < 30 was also associated with a similar increased risk of PH.

FVC% might not be the best parameter to define the extent of the underlying parenchymal disease in patients with IPF. A significant number of patients with IPF are either current or ex-smokers, which can confound the correlation between lung volumes and the degree of fibrosis. IPF has been shown to coexist with emphysema in a number of case series.15161718 The CPI is an index that incorporates FVC, FEV1, and DLCO% in one score that has been shown to correlate more closely with the extent of disease as determined by HRCT. An advantage of this index is that it accounts for any associated emphysema. We therefore performed an analysis comparing PH to the CPI (n = 101) in patients for whom all PFT parameters were available. Once again, there was no relationship demonstrated between this measure of fibrosis and either the presence or severity of PH. In any event, associated concomitant emphysema should also have been accounted for in the analysis of total lung capacity (TLC), which also failed to show a relationship to PH.

Our study is subject to a number of limitations. First, because of its retrospective design, there was a variable time period between pulmonary function measurements and RHC. However, an analysis of those patients with data measurements within 90 days (n = 76) and within 30 days (n = 35) showed similar results. We do not believe that this time lapse between the two studies detracts significantly from one surprising aspect of our study: the trend to the higher prevalence and greater severity of PH in the patients with the least restriction (FVC% > 70) compared to the group with the worst restriction (FVC% < 40). In the latter group of 22 patients, the average interval between the PFTs and RHC was 84 days; but in most of them (16 of 22 patients), PFTs were performed before RHC. It is very unlikely that these patients would have reverted to a higher decile of lung function if more contemporaneous PFT results were available. In the former group, most PFTs (59%) were performed within 3 months of RHC measures; for the 10 patients with PH, all but 2 patients had PFTs within this time frame or after RHC measurement.

Our patient selection is subject to some bias since RHC was mostly performed in the context of lung transplantation evaluation. However, due to the unpredictable disease course in patients with IPF, it is the policy of our program to evaluate all age-appropriate patients for transplantation at the time of initial presentation. Therefore, our patient population was not skewed to those with more severe disease. An attestation to this is the relatively high numbers of patients with well-preserved lung function. However, because patients > 65 years old are generally not regarded as potential transplant candidates, there is an associated age bias with only 12 patients > 65 years old included in the analysis.

Finally, we did not have HRCT correlations of the extent of disease or fibrosis for comparison to our PFT and hemodynamic measurements. Despite these limitations, our study represents the largest single series of pulmonary artery measurements correlated with lung function across a wide range of disease severity based on FVC%.

In conclusion, our study failed to demonstrate a significant relationship between various physiologic measures of lung fibrosis, including FVC%, TLC%, and CPI. There did appear to be a relationship between a reduced DLCO and PH, with a DLCO% < 30 having a high likelihood of associated PH. Factors other than the extent of fibrosis appear to play a significant role in the genesis of PH in patients with IPF. These might include, but are not necessarily limited to, local or systemic hypoxemia, pulmonary thromboembolism, cardiac dysfunction, genetic predisposition, and variable cytokine or chemokine expression. The etiology and course of PH in IPF warrants further study, as do therapies directed at preventing or treating this common complicating comorbidity.

Footnotes

Abbreviations: AUC = area under the curve; CI = confidence interval; CPI = composite physiologic index; DLCO = diffusing capacity of the lung for carbon monoxide; DLCO% = percentage of predicted diffusing capacity of the lung for carbon monoxide; FVC% = percentage of predicted FVC; HRCT = high-resolution CT; IPF = idiopathic pulmonary fibrosis; mPAP = mean pulmonary artery pressure; OR = odds ratio; PCWP = pulmonary capillary wedge pressure; PFT = pulmonary function test; PH = pulmonary hypertension; RHC = right-heart catheterization; ROC = receiver operator characteristic; TLC = total lung capacity; TLC% = percentage of predicted total lung capacity

This research was not funded, and none of the authors have any potential or actual conflicts of interest.

Received for publication October 13, 2006. Accepted for publication November 30, 2006.

References

  1. Bjoraker, JA, Ryu, JH, Edwin, MK, et al (1998) Prognostic significance of histopathologic subsets in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med 157,199-203
  2. Latsi, PI, du Bois, RM, Nicholson, AG, et al Fibrotic idiopathic interstitial pneumonia: the prognostic value of longitudinal functional trends. Am J Respir Crit Care Med 2003;168,531-537[Abstract/Free Full Text]
  3. King, TE, Jr, Tooze, JA, Schwarz, MI, et al Predicting survival in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med 2001;164,1171-1181[Abstract/Free Full Text]
  4. Martinez, FJ, Safrin, S, Weycker, D, et al The clinical course of patients with idiopathic pulmonary fibrosis. Ann Intern Med 2005;142,963-967[Abstract/Free Full Text]
  5. King, TE, Jr, Safrin, S, Starko, KM, et al Analyses of efficacy end points in a controlled trial of interferon-{gamma} 1b for idiopathic pulmonary fibrosis. Chest 2005;127,171-177[Abstract/Free Full Text]
  6. Nadrous, HF, Pellikka, PA, Krowka, MJ, et al Pulmonary hypertension in patients with idiopathic pulmonary fibrosis. Chest 2005;128,2393-2399[Abstract/Free Full Text]
  7. Lettieri, CJ, Nathan, SD, Barnett, SD, et al Prevalence and outcomes of pulmonary arterial hypertension in idiopathic pulmonary fibrosis. Chest 2006;129,746-752[Abstract/Free Full Text]
  8. Wells, AU, Desai, SR, Rubens, MB, et al Idiopathic pulmonary fibrosis: a composite physiologic index derived from disease extent observed by computed tomography. Am J Respir Crit Care Med 2003;167,962-969[Abstract/Free Full Text]
  9. Steen, VD The lung in systemic sclerosis. J Clin Rheum 2005;11,40-46
  10. Steen, VD, Graham, G, Conte, C, et al Isolated diffusing capacity reduction in systemic sclerosis. Arthritis Rheum 1992;35,765-767[ISI][Medline]
  11. Trad, S, Amoura, Z, Beigelman, C, et al Pulmonary arterial hypertension is a major mortality factor in diffuse systemic sclerosis, independent of interstitial lung disease. Arthritis Rheum 2006;54,184-191[CrossRef][ISI][Medline]
  12. Knudson, RJ, Leboowitz, MD, Holberg, CJ, et al Changes in the normal maximal expiratory flow-volume curve with growth and aging. Am Rev Respir Dis 1983;127,725-734[ISI][Medline]
  13. Nathan, SD, Ahmad, S, Shlobin, OA, et al Correlation of pulmonary function testing with pulmonary arterial hypertension (PAH) in patients with idiopathic pulmonary fibrosis (IPF) [abstract].Am J Respir Crit Care Med 2006;3,S103
  14. American Thoracic Society.. Idiopathic pulmonary fibrosis: diagnosis and treatment; international consensus statement, American Thoracic Society (ATS), and the European Respiratory Society (ERS). Am J Respir Crit Care Med 2000;161,646-664[Free Full Text]
  15. Wiggins, J, Strickland, B, Turner-Warwick, M Combined cryptogenic fibrosing alveolitis and emphysema. Respir Med 1990;84,365-369[ISI][Medline]
  16. Hiwatari, N, Shimura, S, Takishima, T Pulmonary emphysema followed by pulmonary fibrosis of undetermined cause. Respiration 1993;60,354-358[ISI][Medline]
  17. Doherty, MJ, Pearson, MG, O’Grady, EA, et al Cryptogenic fibrosing alveolitis with preserved lung volumes. Thorax 1997;52,998-1002[Abstract]
  18. Cottin, V, Nunes, H, Brillet, PY, et al Combined pulmonary fibrosis and emphysema: a distinct underrecognised entity. Eur Respir J 2005;26,586-593[Abstract/Free Full Text]

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