Galectin-3 and Natriuretic Peptides*
Galectin-3 and natriuretic peptides are measures of separate and distinct biological processes. Galectin-3 levels reflect the presence of an underlying disease process independent of the degree of damage or stress at a particular moment.
Natriuretic peptides are released by the heart muscle in response to increased cardiac pressure or volume. In 2001, a blood test for brain natriuretic peptide (BNP) became commercially available followed in 2003 by a blood test for amino-terminal pro brain natriuretic peptide (NT-proBNP). BNP and NT-proBNP have demonstrated clinical utility in the diagnosis and evaluation of heart failure. The key characteristics of galectin-3 and natriuretic peptides are compared below.
TABLE: Key Characteristics of Galectin-3 and Natriuretic Peptides
| Galectin-3 | Natriuretic Peptides (BNP/NT-proBNP) | |
| Biology | Mediator of cardiac fibrosis and adverse remodeling | Released in response to myocardial stretch |
| Related Approved Indications for Use | Aid in prognosis | Aid in risk stratification |
| Effect of Decompensation | Not affected | Marked response |
| Stability Over Time | Stable once elevated | Highly variable |
| Response to HF Treatments | No effect from common HF medications | Generally reduce NP levels |
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Combined use of Galectin-3 and Natriuretic Peptides in Assessing Prognosis
Natriuretic peptides are indicated as an aid in the risk stratification of patients with heart failure. Elevated levels of natriuretic peptides may occur independent of the underlying disease or cause of heart failure. Elevated levels of natriuretic peptides are associated with an increased risk of hospitalization or death.
BGM Galectin-3 is indicated for use in conjunction with clinical evaluation as an aid in assessing the prognosis of patients diagnosed with chronic heart failure (CHF). Elevated levels suggest the presence of galectin-3-mediated fibrosis and adverse remodeling, an inherently progressive condition. Galectin-3 utility and aid in assessing the prognosis of chronic heart failure is attributable to the progressive nature of galectin-3-mediated fibrogenesis.
Although galectin-3 and natriuretic peptides are biologically unrelated, the presence of galectin-3-mediated disease progression increases the likelihood of decompensation and natriuretic peptide elevation. When used in combination as an aid in the assessment of prognosis of patients with chronic heart failure each marker provides independent and complementary information on the prognosis of patients with chronic heart failure. The combined use of galectin-3 and natriuretic peptides is defined by the following categories:
TABLE: Galectin-3 and Natriuretic Peptide Categories
| Description | Risk of Adverse Outcomes | |
| Low Galectin-3 and Low Natriuretic Peptides (L/L) | Absence of galectin-3-mediated progression and absence of pressure overload/myocardial stretch | Lowest |
| Discordant (L/H or H/L) | One but not the other cause of elevated risk present | Intermediate |
| High Galectin-3 and High Natriuretic Peptides (H/H) | Presence of galectin-3-mediated progression and pressure overload/myocardial stretch | High |
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For the results of the combined use of galectin-3 and NT-proBNP from the galectin-3 HF-ACTION or COACH sub-studies see under Galectin-3 Studies.
Galectin-3 levels over 17.8 ng/mL are associated with an elevated risk of adverse outcomes. No generally accepted prognostic cut-off points exist for BNP or NT-proBNP.
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