Supplementary Table 1. Biomarker Assays, Proposed Pathophysiology, and Expected Median Levels in Chronic Heart Failure
Patients
Biomarker
Assay
Proposed Pathophysiology in Heart Failure
Median Levels
References
in Chronic HF
NT-proBNP,
Biomedica, Vienna,
- Released from cardiomyocytes in response to myocardial stress
848–1438
pg/mL
Austria
- The biological activity of natriuretic peptides includes stimulation of natriuresis and
pg/mL
(14, 34)
vasorelaxation; inhibition of renin, aldosterone, and sympathetic nervous activity;
inhibition of fibrosis; and improvement in myocardial relaxation.
Galectin-3,
BG Medicine,
β-galactoside-binding lectin produced by several tissues
14.0–19.0
(14, 34,
ng/mL
Waltham, MA, USA
Promotes cardiac fibroblast proliferation and collagen synthesis (maladaptive
ng/mL
35)
(35, 36)
remodeling)
ST2, ng/mL
Critical Diagnostics,
Member of the IL-1 receptor family that is secreted from myocytes during
23.7–38.2
New York, NY, USA
biomechanical strain
ng/mL
Possible mediator of myocardial hypertrophy and fibrosis by compromising the
favorable effects of IL-33/ST2 signaling
Copeptin,
USCN Life Science
- Stable plasma surrogate for vasopressin, which is released from the hypothalamus in
18.9–24.4
pmol/L
Inc., Wuhan, China
response to changes in plasma osmolarity and reduced cardiac output
pmol/L
(37, 38)
- Elevated levels of vasopressin contribute to development of hyponatremia,
vasoconstriction, and adverse cardiac remodeling
GDF-15, ng/L
Quantikine, R&D
- Member of the TGF-β cytokine family
Systems, Inc., MN,
- Expression in myocytes is triggered by ischemia, stretch, inflammation, and
USA
neurohormonal activation
1949 ng/L
(18)
85 ng/mL
(39)
3.2–3.7 mg/L
(34, 40)
- May protect myocytes against apoptosis and hypertrophy
NGAL, ng/L
BioPorto Diagnostics,
- Small glycoprotein released by multiple cell types during inflammation and injury
Denmark
-Involved in cell survival, inflammation, and matrix degradation
-Early marker of renal tubular damage and cardiorenal syndrome
CRP, mg/L
ALPCO Diagnostics,
- Product of inflammation whose synthesis by the liver is stimulated by cytokines in
Windham, NH, USA
response to an inflammatory stimulus
- Results from, and may exacerbate, left ventricular dysfunction, hepatic or renal
organ damage induced by low cardiac output, hypoperfusion, hypoxia, and venous
congestion