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(Circulation. 2004;110:1091-1096.)
© 2004 American Heart Association, Inc.

Original Articles

Plasma Surfactant Protein-B

A Novel Biomarker in Chronic Heart Failure

Carmine G. De Pasquale, BMBS; Leonard F. Arnolda, MBBS PhD; Ian R. Doyle, PhD; Philip E. Aylward, MBBS PhD; Derek P. Chew, MBBS; Andrew D. Bersten, MBBS MD

From Cardiac Services (C.G.D.P., P.E.A., D.P.C.) and the Critical Care Unit (A.D.B.), Flinders Medical Centre, Adelaide, Australia; the Cardiology Department (L.F.A.), Royal Perth Hospital and West Australian Institute of Medical Research, Perth, Australia; and the Physiology Department (I.R.D.), Flinders University of South Australia, Adelaide, Australia.

Correspondence to Carmine G. De Pasquale, Cardiac Services, Flinders Medical Centre, Flinders Drive, Bedford Park, 5042, Adelaide, South Australia, Australia. E-mail carmine.depasquale{at}fmc.sa.gov.au

Received August 27, 2003; de novo received January 5, 2004; revision received April 13, 2004; accepted April 14, 2004.

Background— In chronic heart failure (CHF), elevated pulmonary microvascular pressure (P_mv) results in pulmonary edema. Because elevated P_mv may alter the integrity of the alveolocapillary barrier, allowing leakage of surfactant protein-B (SP-B) from the alveoli into the circulation, we aimed to determine plasma levels of SP-B in CHF and their relation to clinical status.

Methods and Results— Fifty-three outpatients with CHF had plasma SP-B and N-terminal proBNP (NT-proBNP) assayed, in addition to a formalized clinical assessment at each clinic review over a period of 18 months. The control group comprised 19 normal volunteers. Plasma SP-B was elevated in CHF (P<0.001), and levels increased with New York Heart Association classification (P<0.001). SP-B correlated with objective clinical status parameters and NT-proBNP. During follow-up, major cardiovascular events occurred in patients with higher plasma SP-B (P<0.01) and NT-proBNP (P<0.05). Furthermore, on conditional logistic regression analysis, only SP-B was independently associated with CHF hospitalization (P=0.005). The 53 patients underwent a total of 210 outpatient visits. When the diuretic dosage was increased on clinical grounds, SP-B had increased 39% (P<0.001) and NT-proBNP had increased 32% (P<0.001). Conversely, at the next visit, SP-B fell 12% (P<0.001), whereas NT-proBNP fell 39% (P<0.001).

Conclusions— Plasma SP-B is increased in CHF, and levels are related to clinical severity. Furthermore, within individual patients, SP-B levels vary with dynamic clinical status and NT-proBNP levels. Because plasma SP-B is independently associated with CHF hospitalization, it may, by virtue of its differing release mechanism to NT-proBNP, be a clinically useful biomarker of the pulmonary consequences of raised P_mv.

Key Words: edema • heart failure • lung • natriuretic peptides • proteins

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