DOES LUNG VOLUME REDUCTION SURGERY COMPROMISE THE PULMONARY CIRCULATION?

To the Editor:

We read with great interest the article by Weg and colleagues (1) reporting the development of pulmonary hypertension (PH) after lung volume reduction surgery (LVRS). We were quite surprised by the outcomes of this study since they are in contradiction with our own results, which show the absence of impairment of pulmonary hemodynamics after LVRS, either at rest or during exercise, in most cases (2).

First of all, the percentage of patients exhibiting PH (i.e., mean pulmonary artery pressure > 20 mm Hg) at initial evaluation, before LVRS was done, seems unexpectedly high. Indeed, PH was present in 8 out of 9 patients in the study of Weg and coworkers (1). Consequently, the mean pulmonary artery pressure () of the whole group was 25.8 ± 4.6 mm Hg. In our own study (2), only 3 out of 9 patients showed mild to moderate PH with a for the group of 20.1 ± 5.7 mm Hg. Thurnheer and coworkers (3) reported in an abstract that PH was present in only 5 of 21 patients before LVRS with a of 17.8 ± 0.7 mm Hg. It is well known that the major cause of secondary pulmonary hypertension in patients with chronic obstructive pulmonary disease (COPD) is alveolar hypoxia. Moreover, it has been shown that in patients with COPD, the pulmonary artery pressure was not correlated with the severity of emphysema but a negative correlation was found between the Ppa and the Pa_O2 (4). The mean Pa_O2 in the patients of Weg and coworkers (1) was 67.7 ± 9.9 mm Hg, demonstrating only mild hypoxemia, and thus the was higher than expected.

The second point of the paper of Weg and coworkers (1) concerns the results of the pulmonary artery occlusion pressure (PAOP). Indeed, the PAOP was abnormally increased in 7 of the 9 patients with a mean of 14.1 ± 4.8 mm Hg for the whole group. In our experience, in COPD patients, even those who follow the "emphysematous" pattern, PAOP was generally found to be in the normal range; this is in agreement with the results published by Butler and coworkers (5). These authors have shown that the wedge pressure was normal at rest (6 ± 3 mm Hg) in a group of 32 COPD patients with a mean Pa_O2 of 59 ± 10 mm Hg and a of 22 ± 6 mm Hg. During exercise, they demonstrated an increased wedge pressure in some patients, and explained this by pulmonary hyperinflation due to lower lobe gas trapping. Accordingly, the increased PAOP at rest in the study of Weg and coworkers (1) is surprising and could perhaps be explained by left ventricular impairment, especially left diastolic dysfunction, which was not assessed in the patients before LVRS. Moreover, the correlation which was found by Weg and coworkers (1), between the Mahler dyspnea score and the PAOP before LVRS is also in favor of left cardiac dysfunction since in COPD patients, arterial pulmonary pressures and the degree of dyspnea are not, or are only weakly, correlated. It must be emphasized that in our study (2), patients were excluded for LVRS if they demonstrated left cardiac insufficiency, whether by cardiac echography, or by dipyridamole-thallium scintigraphy, and, if necessary, by coronary angiography. In our opinion, thallium perfusion scanning with treadmill stress is rather useless in these patients with severe exercise limitations due to their respiratory impairment.

As a third point, we think that kinking of the pulmonary vessels as a result of surgery is less likely to occur. Indeed, it has been shown that the diffusing capacity is not impaired after LVRS (2, 3) and it has even been reported to increase (6) suggesting that the alveolocapillary gas exchange surface is not impaired.

The study by Weg and coworkers investigated (1), as did our own study (2), pulmonary hemodynamics in only a limited number of patients. However, the effects of LVRS on the pulmonary circulation might have important consequences in terms of either mortality or morbidity. Thus, careful pulmonary hemodynamic evaluation should be performed in larger series of patients before, but also after, LVRS in order to clarify what happens to the pulmonary circulation. Moreover, these pulmonary hemodynamic studies should be performed not only at rest, but especially during exercise, as the latter condition considerably enhances dynamic hyperinflation.

Service de Pneumologie et Service des ExplorationsFonctionnelles Respiratoires et de l'ExerciceHôpitaux UniversitairesStrasbourg, France

1. Weg, I. L., L. Rossoff, K. McKeon, L. M. Graver, and S. M. Scharf. 1999. Development of pulmonary hypertension after lung volume reduction surgery. Am. J. Respir. Crit. Care Med. 159: 552-556 [Abstract/Free Full Text].

2. Oswald-Mammosser, M., R. Kessler, G. Massard, J. M. Wihlm, E. Weitzenblum, and J. Lonsdorfer. 1998. Effect of lung volume reduction surgery on gas exchange and pulmonary hemodynamics at rest and during exercise. Am. J. Respir. Crit. Care Med. 158: 1020-1025 [Abstract/Free Full Text].

3. Thurnheer, R., U. Stammberger, A. Zollinger, K. E. Bloch, E. W. Russi, and W. Weder. 1998. Pulmonary artery pressures before and 6 months after bilateral thoracoscopic lung volume reduction surgery. 11th Annual Meeting of the EACTS, P156.

4. Biernacki, W., G. A. Gould, K. F. Whyte, and D. C. Flenley. 1989. Pulmonary hemodynamics, gas exchange, and the severity of emphysema as assessed by quantitative CT scan in chronic bronchitis and emphysema. Am. Rev. Respir. Dis. 139: 1509-1515 [Medline].

5. Butler, J., F. Schrijen, A. Henriquez, J. M. Polu, and R. K. Albert. 1988. Cause of raised wedge pressure on exercise in chronic obstructive pulmonary disease. Am. Rev. Respir. Dis. 138: 350-354 [Medline].

6. Gelb, A. F., N. Zamel, R. J. McKenna, and M. Brenner. 1996. Mechanism of short-term improvement in lung function after emphysema resection. Am. J. Respir. Crit. Care Med. 154: 945-951 [Abstract].

From the Authors:

We thank Drs. Kessler and Oswald-Mammosser for their interest in our work and for their comments. Their data on lung volume reduction surgery (1) were reported after our article was submitted for publication. However, rather than concluding that the data are contradictory, we feel that there are lessons to be learned by comparison of the patients studied in these reports.

Our patients were excluded for pulmonary artery systolic (PA) pressure greater than 40 mm Hg and mean pulmonary artery (PA_m) pressure greater than 35 mm Hg. Indeed, our patients had a fairly high PA_m but they were not hypoxic at the time of the right heart catheterization; oxygen was administered under continuous pulse oximetry to ensure that saturations remained above 90%. As indicated, our patients maintained preoperative and postoperative PO₂ higher than 67 mm Hg. The diffusion capacity in our patients (2) was less (25% of predicted, data not presented) than in Oswald-Mammosser and coworkers' study (50% of predicted). We suspect that these findings indicate a greater initial obliteration of the pulmonary vascular bed in our patients.

Although we did not formally study the patients for diastolic dysfunction, in five of our nine patients radionuclide angiography was performed immediately after the right heart catheterization, and overall there was no evidence of systolic dysfunction or of a correlation with time to peak filling in the early diastolic phase. In one patient, findings of apparent congestive heart failure developed after surgery in a patient with normal systolic function, and diastolic dysfunction was suspected on clinical grounds. It seems unlikely that diastolic dysfunction is so prevalent in our population. Rather, the characterization of the pulmonary artery occlusion pressure (PAOP) as an accurate measurement of the left atrial pressure has been questioned in the patient with a scarred, nonhomogeneous lung. Although Butler and colleagues (3) explained the increased PAOP pressure as indicative of air trapping in the lower lobes, we did not demonstrate a decrease in the PAOP after surgery, when, as a result of the removal of lung tissue, the juxtacardiac pressure might have been decreased; however, in our patients paramediastinal lung tissue was not removed. We attempted to exclude ischemic heart disease in our patients with pharmacologic stress testing rather than exercise perfusion imaging, for the reason indicated by Kessler and Oswald-Mammosser. Finally, we reported a correlation of the Mahler dyspnea scale with the PA, rather than the PAOP, as cited by Kessler and Oswald-Mammosser.

We agree that kinking of the pulmonary vasculature after surgery is not a highly likely cause of pulmonary hypertension postoperatively, but it cannot be excluded in the absence of visualization of the arteries. More likely, in our opinion, is an altered balance of pulmonary vasomotor reactivity in the postoperative period. The role of exercise is interesting. Hemodynamics were measured in several of our patients during upright exercise conditions and this data is being analyzed.

Fortunately, a large scale study is underway in the United States to attempt to clarify these issues. The multi-center National Emphysema Therapy Trial, in which we are a participating center, is studying these issues in a large population of patients in an organized manner.

Department of MedicineLong Island Jewish Medical CenterNew Hyde Park, New York

1. Oswald-Mammosser, M., R. Kessler, G. Massard, J. M. Wihlm, E. Weitzenblum, and J. Lonsdorfer. 1998. Effect of lung volume reduction surgery on gas exchange and pulmonary hemodynamics at rest and during exercise. Am. J. Respir. Crit. Care Med. 158: 1020-1025 .

2. Weg, I. L., L. Rossoff, K. McKeon, L. M. Graver, and S. M. Scharf. 1999. Development of pulmonary hypertension after lung volume reduction surgery. Am. J. Respir. Crit. Care Med. 159: 552-556 .

3. Butler, J., F. Schrijen, A. Henriquez, J.-M. Polu, and R. K. Albert. 1988. Cause of raised wedge pressure on exercise in chronic obstructive pulmonary disease. Am. Rev. Respir. Dis. 138: 350-354 .