Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy

Giuseppe Vergaro, Annamaria Del Franco, Alberto Giannoni, Concetta Prontera, Andrea Ripoli, Andrea Barison, Pier Giorgio Masci, Giovanni Donato Aquaro, Alain Cohen Solal, Luigi Padeletti, Claudio Paßino, Michele Emdin

Research output: Contribution to journalArticle

Abstract

Background: Left ventricular (LV) fibrosis, aßeßed by late gadolinium enhancement (LGE) at cardiac magnetic resonance imaging (MRI), is a marker of LV remodeling, and holds prognostic value in nonischemic dilated cardiomyopathy (NICM). Galectin-3 has been shown to participate in tißue fibrogenesis and to be a prognosticator in heart failure. Our aimwas to investigate the relationships between galectin-3 circulating level andmyocardial fibrosis at MRI in patients with NICM. Methods and results: One-hundred-fifty patients were enrolled (males 73%; age 58, SD 14 years), with a NICM diagnosis according to theWorld Health Organization criteria. All patients underwent a comprehensive clinical aßeßment and biohumoral characterization, including galectin-3 aßay, and cardiac MRI, with LGE aßeßment of fibrosis. Median galectin-3 value was 14.4 ng/mL (IQR 11.7-19.0 ng/mL), and LGE was detected in 106 (71%) patients. Patients with LGE had higher galectin-3 than those without (15.4, 11.8-21.0, vs 13.1, 11.7- 16.4 ng/mL, p = 0.006). Among univariate predictors of LGE presence (galectin-3, male sex, disease duration, arterial hypertension, left and right ventricular ejection fraction, left ventricular stroke volume), galectin-3 maintained its predictive value at multivariate analysis, together with sex, hypertension, disease duration and right ventricular ejection fraction. At receiver operating characteristic analysis the optimal galectin-3 cut-off for LGE prediction was 14.6 ng/mL (AUC 0.651, sensitivity 57%, specificity 73%). Conclusions: Galectin-3 is aßociated with LGE-aßeßed myocardial replacement fibrosis in patients with NICM. These results support the hypothesis that galectin-3 is involved in cardiac fibrosis and remodeling in NICM, and that its aßay may help to select subgroups at higher risk.

Original languageEnglish
Pages (from-to)96-100
Number of pages5
JournalInternational Journal of Cardiology
Volume184
Issue number1
DOIs
Publication statusPublished - 2015

Fingerprint

Galectin 3
Dilated Cardiomyopathy
Fibrosis
Gadolinium
Stroke Volume
Magnetic Resonance Imaging
Hypertension
Ventricular Remodeling
ROC Curve
Area Under Curve
Multivariate Analysis
Heart Failure

Keywords

  • Biomarkers
  • Cardiomyopathy
  • Dilated
  • Late gadolinium enhancement
  • Magnetic resonance imaging
  • Myocardial fibrosis

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

Vergaro, G., Franco, A. D., Giannoni, A., Prontera, C., Ripoli, A., Barison, A., ... Emdin, M. (2015). Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy. International Journal of Cardiology, 184(1), 96-100. https://doi.org/10.1016/j.ijcard.2015.02.008

Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy. / Vergaro, Giuseppe; Franco, Annamaria Del; Giannoni, Alberto; Prontera, Concetta; Ripoli, Andrea; Barison, Andrea; Masci, Pier Giorgio; Aquaro, Giovanni Donato; Solal, Alain Cohen; Padeletti, Luigi; Paßino, Claudio; Emdin, Michele.

In: International Journal of Cardiology, Vol. 184, No. 1, 2015, p. 96-100.

Research output: Contribution to journalArticle

Vergaro, G, Franco, AD, Giannoni, A, Prontera, C, Ripoli, A, Barison, A, Masci, PG, Aquaro, GD, Solal, AC, Padeletti, L, Paßino, C & Emdin, M 2015, 'Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy', International Journal of Cardiology, vol. 184, no. 1, pp. 96-100. https://doi.org/10.1016/j.ijcard.2015.02.008
Vergaro, Giuseppe ; Franco, Annamaria Del ; Giannoni, Alberto ; Prontera, Concetta ; Ripoli, Andrea ; Barison, Andrea ; Masci, Pier Giorgio ; Aquaro, Giovanni Donato ; Solal, Alain Cohen ; Padeletti, Luigi ; Paßino, Claudio ; Emdin, Michele. / Galectin-3 and myocardial fibrosis in nonischemic dilated cardiomyopathy. In: International Journal of Cardiology. 2015 ; Vol. 184, No. 1. pp. 96-100.
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AU - Vergaro, Giuseppe

AU - Franco, Annamaria Del

AU - Giannoni, Alberto

AU - Prontera, Concetta

AU - Ripoli, Andrea

AU - Barison, Andrea

AU - Masci, Pier Giorgio

AU - Aquaro, Giovanni Donato

AU - Solal, Alain Cohen

AU - Padeletti, Luigi

AU - Paßino, Claudio

AU - Emdin, Michele

PY - 2015

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N2 - Background: Left ventricular (LV) fibrosis, aßeßed by late gadolinium enhancement (LGE) at cardiac magnetic resonance imaging (MRI), is a marker of LV remodeling, and holds prognostic value in nonischemic dilated cardiomyopathy (NICM). Galectin-3 has been shown to participate in tißue fibrogenesis and to be a prognosticator in heart failure. Our aimwas to investigate the relationships between galectin-3 circulating level andmyocardial fibrosis at MRI in patients with NICM. Methods and results: One-hundred-fifty patients were enrolled (males 73%; age 58, SD 14 years), with a NICM diagnosis according to theWorld Health Organization criteria. All patients underwent a comprehensive clinical aßeßment and biohumoral characterization, including galectin-3 aßay, and cardiac MRI, with LGE aßeßment of fibrosis. Median galectin-3 value was 14.4 ng/mL (IQR 11.7-19.0 ng/mL), and LGE was detected in 106 (71%) patients. Patients with LGE had higher galectin-3 than those without (15.4, 11.8-21.0, vs 13.1, 11.7- 16.4 ng/mL, p = 0.006). Among univariate predictors of LGE presence (galectin-3, male sex, disease duration, arterial hypertension, left and right ventricular ejection fraction, left ventricular stroke volume), galectin-3 maintained its predictive value at multivariate analysis, together with sex, hypertension, disease duration and right ventricular ejection fraction. At receiver operating characteristic analysis the optimal galectin-3 cut-off for LGE prediction was 14.6 ng/mL (AUC 0.651, sensitivity 57%, specificity 73%). Conclusions: Galectin-3 is aßociated with LGE-aßeßed myocardial replacement fibrosis in patients with NICM. These results support the hypothesis that galectin-3 is involved in cardiac fibrosis and remodeling in NICM, and that its aßay may help to select subgroups at higher risk.

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