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Serial galectin-3 and future cardiovascular disease in the general population
  1. A Rogier van der Velde1,
  2. Wouter C Meijers1,
  3. Jennifer E Ho2,
  4. Frank P Brouwers1,
  5. Michiel Rienstra1,
  6. Stephan J L Bakker3,
  7. Anneke C Muller Kobold4,
  8. Dirk J van Veldhuisen1,
  9. Wiek H van Gilst1,
  10. Pim van der Harst1,
  11. Rudolf A de Boer1
  1. 1Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  2. 2Cardiovascular Medicine Section, Department of Medicine, Boston University School of Medicine, Boston, USA
  3. 3Department of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  4. 4Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  1. Correspondence to Dr Rudolf A de Boer, Department of Cardiology, University of Groningen, Medical Center Groningen, P. O. Box 30.001, Groningen 9700 RB, The Netherlands; r.a.de.boer{at}umcg.nl

Abstract

Background Lifetime risk for cardiovascular (CV) disease is high but predicting incident events on an individual level remains difficult. Single measurements of galectin-3, a marker of tissue fibrosis, predict mortality and new-onset heart failure (HF). Persistently elevated levels may indicate a clinically silent disease process.

Objectives Our aim was to establish the value of serial galectin-3 measurements to predict CV outcomes in the general population.

Methods Plasma galectin-3 was measured in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study at baseline and after ∼4 years. Changes in serial galectin-3 were expressed as categorical changes or absolute change from baseline and were related to subsequent outcome.

Results Serial galectin-3 was measured in 5958 subjects (mean age 49±12 years; 49% female). The median duration of follow-up was 8.3 years. Persistently elevated galectin-3 (defined as highest quartile at baseline and highest quartile during visit 2, n=757 subjects) was associated with a higher risk for new-onset HF, CV mortality, all-cause mortality, new-onset atrial fibrillation and CV events, compared with subjects with non-persistently elevated galectin-3. After multivariable adjustments for baseline characteristics, serial galectin-3 remained an independent predictor of new-onset HF (HR 1.85 (1.10–3.13); p=0.02) but not for other outcomes. Serial measurements provided more accurate prognostic value to predict new-onset HF, compared with a single baseline measurement (Harrell's C: 0.72 (0.68–0.75) vs 0.68 (0.65–0.72); p=0.002, respectively) with significant net reclassification.

Conclusions Persistently elevated galectin-3 predicts new-onset HF after adjustment for covariates, and serial measurements provide more accurate prognostic information compared with single determination of galectin-3. This may help to identify individuals who are at risk for incident HF and might provide a measure to monitor interventions.

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