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Pulmonary vascular disease
Original article
Galectin-3 and aldosterone as potential tandem biomarkers in pulmonary arterial hypertension
Free
  1. Laurent Calvier1,
  2. Ekaterina Legchenko1,
  3. Lena Grimm1,
  4. Hannes Sallmon2,
  5. Adam Hatch3,
  6. Brian D Plouffe3,
  7. Christoph Schroeder4,
  8. Johann Bauersachs5,
  9. Shashi K Murthy3,6,
  10. Georg Hansmann1
  1. 1Department of Pediatric Cardiology and Critical Care, Hannover Medical School, Hannover, Germany
  2. 2Department of Neonatology, Charité University Medical Center, Berlin, Germany
  3. 3Department of Chemical Engineering, Northeastern University, Boston, Massachusetts, USA
  4. 4Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany
  5. 5Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
  6. 6Barnett Institute of Chemical and Biological Analysis, Northeastern University, Boston, Massachusetts, USA
  1. Correspondence to Professor Dr Georg Hansmann, Department of Pediatric Cardiology and Critical Care, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany; hansmann.georg{at}mh-hannover.de, georg.hansmann{at}gmail.com

Abstract

Background Several studies have identified circulating biomarkers to be associated with the presence and severity of pulmonary arterial hypertension (PAH). Recent evidence supports a role for galectin-3 (Gal-3) and the mineralcorticoid aldosterone in left ventricular failure. However, studies on aldosterone together with Gal-3 in PAH are lacking.

Objective We investigated a novel Aldosterone-galectin-3 (Gal-3) tandem and several other potential PAH biomarkers and their association with the disease severity.

Methods A total of 57 patients, 41 with idiopathic PAH. (IPAH) and 16 with PAH associated with connective tissue disease (CTD), and 8 age-matched, non-relative controls were studied. Gal-3, aldosterone and other potential protein plasma concentrations were measured by single ELISA and multi-array MSD (Meso Scale Discovery) technology.

Results Gal-3 values were increased in both patients with IPAH (12.2±0.6 ng/mL; p<0.05) and with PAH-CTD (14.1±1.6 ng/mL; p<0.05) versus control (8.5±0.9 ng/mL), while aldosterone was significantly elevated in IPAH only (248.5±38.8 pg/mL vs control 71.9±18.2 pg/mL; p<0.05). In addition, aldosterone, Gal-3, and N-terminal pro-brain natriuretic peptide (NT-proBNP) values were all higher in patients in WHO functional class II–III versus PAH functional class I or controls. The vascular injury marker intercellular adhesion molecule 1 (ICAM-1) was increased in IPAH and PAH-CTD versus controls (559.5±18.2 pg/mL and 734.1±59.4 pg/mL vs controls 394.8±39.3 pg/mL, p<0.05, p<0.0001, respectively), whereas vascular cell adhesion molecule 1 (VCAM-1) and proinflammatory, anti-angiogenic interleukin-12 (IL-12) were elevated in PAH-CTD only (879.5±110.0 pg/mL and 391.2±70.3 pg/mL vs controls 489.8±44.6 pg/mL, p<0.01, and 102.1±15.2 pg/mL, p<0.01, respectively).

Conclusions Heightened Gal-3 and aldosterone plasma concentrations in PAH patients indicate a role for Gal-3 signalling in the pathobiology of IPAH and PAH-CTD, and may serve as biomarkers for functional status and progression of disease.

https://doi.org/10.1136/heartjnl-2015-308365

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