Advanced lung disease—medical aspects
Pro-brain natriuretic peptide as marker of cardiovascular or pulmonary causes of dyspnea in patients with terminal parenchymal lung disease

https://doi.org/10.1016/S1053-2498(03)00060-3Get rights and content

Abstract

Background

Increased plasma concentrations of pro-atrial natriuretic peptide (proANP) and pro-brain natriuretic peptide (proBNP) are features of left ventricular impairment. However, concentrations of proANP and proBNP in patients with isolated terminal parenchymal lung disease are not known. Therefore, we measured the plasma concentrations of natriuretic precursor peptides in patients with terminal parenchymal lung disease who had normal left ventricular function and who were referred for evaluation for lung transplantation.

Methods

We measured plasma N-terminal proANP and proBNP in patients undergoing right heart catheterization (n = 50) and related results to hemodynamic variables obtained during catheterization.

Results

Plasma proBNP concentrations were unaffected in patients with terminal parenchymal lung disease and normal left ventricular function (median, 2.5 pmol/liter; range, 0–22; upper reference limit, 15 pmol/liter). In contrast, patients with primary pulmonary hypertension displayed more than a 40-fold increase in plasma proBNP concentrations (median, 107 pmol/liter vs 2.5 pmol/liter, p < 0.0001). Plasma N-terminal proANP increased moderately (median, 664 pmol/liter; range, 36–1,620; upper reference limit, 600 pmol/liter) but correlated to plasma proBNP concentrations (r = 0.47, p < 0.0001). Finally, regional vascular proBNP concentrations revealed the heart as the secretory site.

Conclusions

Our findings strongly support the contention that natriuretic peptide measurements are efficient markers for cardiovascular causes of dyspnea. Moreover, our results eliminate natriuretic peptides as markers of moderate pulmonary hypertension in patients with terminal parenchymal lung disease.

Section snippets

Patients

We enrolled consecutive patients with a diagnosis of terminal parenchymal lung disease who had been referred for lung transplantation evaluation between February 2000 and April 2001. In this study, patients were required to fulfil the following criteria: to have 1) normal left ventricular function as assessed by 2-dimensional echocardiography; 2) no significant coronary artery disease using angiography; 3) no renal impairment (serum creatinine concentration ≤130 μmol/liter); and 4) no sustained

Results

Table I lists the characteristics of the 44 patients with terminal parenchymal lung disease, divided into sub-groups, and the characteristics of the 6 patients with PPH.

Discussion

The main finding in this study is that patients with terminal parenchymal lung disease and normal left ventricular function who were referred for lung transplantation had no increase in plasma proBNP concentrations. Moreover, we found no relation between mean PAP and plasma peptide concentrations in these patients. In contrast, the group of patients with PPH displayed increased plasma concentrations of N-terminal proANP (2-fold) and plasma proBNP (40-fold). We demonstrated an association

Acknowledgements

The authors thank Lone Olsen and Mette Groos for their expert technical assistance.

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