Why do some people with heart failure develop cardiac fibrosis relatively quickly, with an equally dramatic impact on heart function? Why do other patients with the same clinical status go around for decades, with slightly reduced EF (ejection fraction) and, apart from rare periods of decompensation, take it in their stride? One factor specifically in the case of heart failure that contributes to differing courses of progress for the illness is the protein galectin-3. For this biomarker there is now in existence for the first time a blood test approved by the U.S. Food and Drug Administration, which is available to U.S. doctors for everyday clinical practice.
Keen interest from the foremost in the diagnostics industry
Galectin-3 is an interesting protein. It binds in the heart to myofibroblasts and stimulates in this way collagen synthesis and cardiac remodeling. According to BG Medicine, the company that developed the below mentioned galectin-3 test, galectin-3 meaures at an increased level in about 30 percent of patients with heart failure. These patients tend to develop a progressive cardiac fibrosis. “The fact that there is now a galectin-3 test to identify these high-risk patients is another big step towards a more efficient and more targeted therapy for patients with chronic heart failure,” says Professor Bertram Pitt, a cardiologist at the University of Michigan School of Medicine and one of the movers and shakers in clinical cardiology in the United States. It isn’t only Pitt, but also large diagnostic companies who are interested in the new test. There are already several cooperation agreements, including with Abbott, Alere, LabCorp, Siemens and bioMérieux, which want to offer the ELISA-technique based assay as part of their respective platforms.
The limit of Galectin-3 BG Medicine is stated as being at a value of 17.8 ng/ml. Whoever has higher values, in comparison to the group of heart failure patients with galectin-3 levels of less than 17.8 ng/ml, runs a higher risk of outcomes such as hospital admissions and death. There exists up to a galectin-3 level of 25.9 ng/ml a grey zone, in which results are to be interpreted carefully. Galectin-3 is also non-specific to the heart. Increased galectin-3 levels also occur, aside from instances of heart failure, with some cancers and other fibrotic diseases.
Test positive. And then?
Even though by this time there exist relatively strong foundation studies suggesting the involvement of Galectin-3 in heart failure, the key question remains about what determining galectin-3 levels really brings to everyday life. Even the manufacturer admits on his website under the heading Interpreting Galectin-3 Results that the conclusions that come from the determined measures are hardly worth highlighting: a doctor may in essence tell a patient, in which galectin-3 is elevated, that he is at a higher risk of a poor outcome arising from his or her heart failure. Because galectin-3 levels over the course of the disease are fairly constant, the parameter is not suitable – unlike natriuretic peptides – for the diagnosis of heart failure. It is also independent of episodes of decompensation and independent of heart failure therapy, therefore for pharmacological monitoring applications it is out of the question.
Nevertheless, galectin-3 may play an important future role in therapy management since the measure at least allows something to be said in the matter of distinguishing patients, for whom a more intensive treatment or monitoring could be particularly useful. One option would be managed-care scenarios, not addressing patients at risk of heart falure uniformly, but applying specifically to those with increased risk. The use of telemonitoring could be stratified based on the galectin-3 levels too.
Ideally it would of course be in the future, if new therapies on the market were to bring additional benefits specifically to heart-failure patients with an increased level of galectin-3. This is not yet to be excluded, its only the case that until now there is not much to be seen.