San Diego Veterans Affairs Medical Center and University of California, Division of Cardiology.
When we began using sST2 in the hospital and the heart failure clinic nearly two years ago, I would often be asked: Why should we use sST2 when our present way of managing heart failure is sufficient? The answer is both simple and complex. Take the example of patients presenting with acute heart failure. Most are treated exactly the same-meaning intravenous followed by oral diuretics followed by discharge. Some patients do fine; some are readmitted within 30 days; other die. The discouraging fact here that it is difficult up front to tell which patient will suffer which fate. High BNP levels (above the dry BNP) correlates with volume overload, which is often obvious to the physician. However, our experience thus far suggests that sST2 levels give us insight into the state of heart failure far beyond the state of intravascular volume or physical exam findings. While it is certainly additive to what NPs bring to the table, we believe that sST2 might potentially be looked at as the HbA1c of heart failure (figure one); in other words, the sST2 value has inputs from wall stress, inflammation, macrophage activation (fibrosis) and a number of still-to-be determined stimuli. Just as better glucose control drops HbA1c levels into a better prognostic range, better control of heart failure appears to lower sST2 levels.