Larry H Bernstein, MD, FCAP, Curator
Leaders in Pharmaceutical Intelligence
Predictive value of plasma galectin-3 levels in heart failure with
reduced and preserved ejection fraction
RA. de Boer, DJ.A. Lok, T Jaarsma1, P van der Meer, AA. Voors, HL. Hillege
& DJ. van Veldhuisen
Annals of Medicine 2011; 43: 60–68.
http://dx.doi.org:/10.3109/07853890.2010.538080
We studied 592 HFpatients who had been hospitalized for HFand were followed
for 18 months. The primary end-point was a composite of all-cause mortality and
HF hospitalization. A doubling of galectin-3 levels was associated with a hazard
ratio (HR) of 1.97 (1.62–2.42) for the primary outcome (P = 0.001). After
correction for age, gender, BNP, eGFR, and diabetes the HR was 1.38 (1.07–
1.78; P = 0.015). Galectin-3 levels were correlated with higher IL-6 and CRP
levels (P = 0.002). Changes of galectin-3 levels after 6 months did not add
prognostic information to the base-line value (n = 291); however, combining
plasma galectin-3 and BNP levels increased prognostic value over either
biomarker alone (ROC analysis, P = 0.05). The predictive value of galectin-3
was stronger in patients with preserved LVEF (n = 114) compared to
patients with reduced LVEF (P = 0.001).
Galectin-3 in Ambulatory Patients with Heart Failure: Results
from the HF-ACTION Study
GM Felker, M Fiuzat, LK. Shaw, R Clare, ,DJ. Whellan, et al.
Circ Heart Fail. 2012 Jan; 5(1): 72–78.
http://dx.doi.org:/10.1161/CIRCHEARTFAILURE.111.963637
Galectin-3 is a soluble ß-galactoside-binding lectin released by activated
cardiac macrophages. Elevated levels of galectin-3 have been found to
be associated with adverse outcomes in patients with heart failure. We
evaluated the association between galectin-3 and long-term clinical
outcomes in ambulatory heart failure patients enrolled in the HF-ACTION
study.
Galectin-3 is elevated in ambulatory heart failure patients and is
associated with poor functional capacity and other known measures of
heart failure severity. In univariate analysis, galectin-3 was significantly
predictive of long-term outcomes, but this association did not
persist after adjustment for other predictors, especially NTproBNP.
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This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.
A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.