Published Online
on March 30, 2009

A more recent version of this article appeared on May 1, 2009

This Article Full Text (PDF) All Versions of this Article: 2/3/175    most recent CIRCHEARTFAILURE.108.819607v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Magrì, D. Articles by Agostoni, P. Search for Related Content PubMed PubMed Citation Articles by Magrì, D. Articles by Agostoni, P. Related Collections Congestive

Original Article

Circulating Plasma Surfactant Protein Type B as Biological Marker of Alveolar-Capillary Barrier Damage in Chronic Heart Failure

Damiano Magrì¹; Maura Brioschi²; Cristina Banfi²; JeanPaul Schmid³; Pietro Palermo²; Mauro Contini²; Anna Apostolo²; Maurizio Bussotti²; Elena Tremoli²; Susanna Sciomer⁴; Gaia Cattadori²; Cesare Fiorentini² and Piergiuseppe Agostoni^5,6

¹ University of Milan and University of Rome "La Sapienza," Italy;
² University of Milan, Italy;
³ Bern University Hospital, and University of Bern, Switzerland;
⁴ University of Rome "La Sapienza," Italy;
⁵ University of Milan, Italy; University of Washington, Seattle, WA

⁶ E-mail: piergiuseppe.agostoni{at}cardiologicomonzino.it

Background—Surfactant protein B (SPB) is needed for alveolar gas exchange. SPB is increased in the plasma of heart failure (HF) patients with a concentration that is higher when HF severity is highest. The aim of the current study was to evaluate the relationship between plasma SPB and both alveolar-capillary diffusion at rest and ventilation vs. carbon dioxide production (VE/VCO₂) during exercise.

Methods and Results—Eighty chronic consecutive HF patients and 20 healthy controls were evaluated but the required quality for procedures was only reached by 71 HF patients and 19 healthy controls. Each subject underwent pulmonary function measurements, including lung diffusion (DL_CO) and membrane diffusion (D_M), and maximal cardiopulmonary exercise test. Plasma SPB was measured by immunoblotting. In HF patients SPB values were higher [4.5(11.1) vs 1.6(2.9), p= 0.0006, median and 25-75th interquartile], while DL_CO (19.7±4.5 vs 24.6±6.8 mL/mmHg/min, p< 0.0001, mean±SD) and D_M (28.9±7.4 vs 38.7±14.8, p< 0.0001) were lower. Peak oxygen consumption (VO₂) and VE/VCO₂ slope were 16.2±4.3 vs 26.8±6.2 ml/kg/min (p< 0.0001) and 29.7±5.9 and 24.5±3.2 (p< 0.0001) in HF and controls, respectively. In the HF population, univariate analysis showed a significant relationship between plasma SPB and DL_CO, D_M, peak VO₂ and VE/VCO₂ slope (p< 0.0001 for all). On multivariable logistic regression analysis D_M (beta: –0.54, SE: 0.018, p< 0.0001), peak VO₂ (beta: –0.53, SE: 0.036, p= 0.004) and VE/VCO₂ slope (beta: 0.25, SE: 0.026, p= 0.034) were independently associated with SPB.

Conclusion—Circulating plasma SPB levels are related to alveolar gas diffusion, overall exercise performance and efficiency of ventilation showing a link between alveolar-capillary barrier damage, gas exchange abnormalities and exercise performance in HF.

Key Words: heart failure • alveolar capillary barrier • cardiopulmonary exercise test • lung diffusion • surfactant protein B