As a baseline value added to traditional clinical and biochemical characteristics including NT-proBNP, ST2 added independent information in predicting total cardiovascular events, but, more importantly, as a serial biomarker measured every three months during the treatment period of the study, only ST2 provided incremental prognostic information. Specifically, patients with persistently elevated ST2 levels were at more than three-and-a-half times the risk of experiencing a cardiovascular event, such as an unplanned hospitalization, than patients who had low ST2 levels.
"Beyond the baseline measurement, only sST2 appeared to provide incremental prognostic information and reflect changes in myocardial remodeling over time," note the authors. "A novel biomarker's dynamic ability to reflect the underlying HF [heart failure] biology makes it an ideal candidate for potentially monitoring and guiding HF management. In the present analysis, sST2 [soluble ST2) appeared to add prognostic information above the natriuretic peptides across multiple time points of measurement, and indicate significant dynamic change of the biomarker in parallel with risk for adverse events and myocardial remodeling."
Furthermore, this study also shows there was a direct relationship between the percent of time spent with ST2 below its
Note the authors: "More time spent in sST2 response predicted decreasing LVEDi [left ventricle end diastolic volume index] after adjusting for relevant baseline characteristics."
"Concentrations of sST2 are increasingly accepted to reflect important prognostic information not already revealed by natriuretic peptides," remark the authors, "In the present analysis, sST2 appeared to add prognostic information above the natriuretic peptides across multiple time points of measurement, and indicate significant dynamic change of the biomarker in parallel with risk for adverse events and myocardial remodeling."
Moreover, study further shows change in beta blocker dose in heart failure patients was directly associated with a change in subsequent levels of ST2. The findings reiterate those of another paper from this study just published that show that patients above 35 ng/mL who were taking low doses of beta blocker were almost seven times as likely to experience a cardiovascular event, such as an unplanned hospitalization, than patients who had low ST2 levels and were on high-doses of beta blocker.
"Notably, we found a significant relationship between b blocker [beta blocker] changes and sST2," state the authors. "As b blockers have been shown to reverse myocardial remodeling, we are currently examining the potential link between this class of agents and sST2 in more depth . . . the link between b blockers dose changes and sST2 changes may be leveraged in identifying patients who may particularly benefit from aggressive b blocker titration."
ST2 was recently included in the 2013 ACC/AHA Guideline For The Management of Heart Failure, recognizing ST2 as "not only predictive of hospitalization and death in patients with HF but also additive to natriuretic peptide levels in [its] prognostic value." The guideline gives ST2 its highest classification ("A") for the body of evidence supporting its recommendation.
Findings from the
Patients who didn't show at least a 20 percent drop in their ST2 levels within 48 hours of admission had an alarming better-than-even (50/50) chance of dying within one year, whereas patients whose ST2 level decreased by at least 42% had only about a one in seven chance of dying within one year. Powerfully, it was also shown that if these high-risk patients received more intensive outpatient therapy their risk of adverse events was reduced to be comparable to that of the low risk group.
The investigators in the
The authors further state: "[W]e were not able to show that HF [heart failure] medications with symptom-related or mortality benefits had effects on galectin-3 levels . . . There have thus far been no studies in humans demonstrating that medications can lower galectin-3 levels, and one study reported that initiation of CRT [Cardiac Resynchronization Therapy, a type of pacemaker to treat symptoms associated with congestive heart failure] had no effect on galectin-3 concentrations." Consequently, "in this study, HF therapies had no clear effects on galectin-3 levels."
"Interestingly, in our study," continue the authors, "drugs with beneficial effects on remodeling had no appreciable effects on galectin-3 levels. This finding suggests that, despite the role of galectin-3 in the development of fibrosis, currently applied HF therapies may not lower galectin-3 concentrations and galectin-3 effects may not be easily reversible."
This is the fourth paper published in the last few months that permits direct comparisons between the biomarkers ST2 and galectin-3. An
"In this analysis of the HF-ACTION study, ST2 was significantly associated with long-term outcome even after an adjustment for clinical covariates," stated the study authors. "To our knowledge, this is the most robust test of this novel biomarker [ST2] to date with regard to covariate adjustment in a large, multicenter cohort of ambulatory heart failure patients."
In contrast, as the authors made note of in a separate paper published on the use of galectin-3 evaluating the same cohort of patients: "In a final model adjusting for all predictors of the primary endpoint in the HF-ACTION dataset as a whole . . . as well as NTproBNP, there was no evidence for an independent association between galectin-3 and outcomes . . . Given the unique nature of the randomized intervention in the HF-ACTION study (exercise training), we examined the interaction between baseline galectin-3 levels and treatment assignment. There was no significant interaction between galectin-3 levels and exercise training for any of the 3 study endpoints [all-cause death or hospitalization, cardiovascular death or cardiovascular hospitalization, and for cardiovascular death or heart failure hospitalization.]"
Keywords for this news article include: Pharmaceuticals, Therapy, Hospital, Proteins, Treatment, Cardiology, Amino Acids, Heart Attack, Patient Care, Heart Disease, Peptide Hormones,
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