Soluble suppression of tumorigenicity-2 for risk stratification in outpatients with heart failure.

To the Editor,

I have read the article by Gül et al. (1) entitled “Prognostic role of soluble suppression of tumorigenicity-2 on cardiovascular mortality in outpatients with heart failure,” which was published in Anatol J Cardiol 2017; 18: 200-5, with great interest. In their study, the authors reported that baseline levels of soluble suppression of tumorigenicity-2 (sST2) are an independent predictor of mortality in outpatients with heart failure (HF) with a high sensitivity of 87%. They concluded that patients who died during follow-up had higher sST2 levels than patients who survived (1). I would like to emphasize some important points about this well-written study.

It has been demonstrated that sST2 is associated with inflammatory and immune process in several diseases including cardiovascular disorders. sST2 is released into the circulation in HF patients as a response to cardiac stress as well as inflammation (2). Therefore, the authors should state if there was any difference between the two groups in terms of inflammatory states. Measuring inflammatory marker levels could provide insights into the cardiovascular role of sST2 in HF patients, as non-myocardial sources of sST2 are well-known (3).

A strong association between NYHA functional class, heart rate, body mass index, and outcomes in patients with systolic HF has been demonstrated in previous studies. Also, it has been shown that there is a correlation between NYHA functional class and sST2 levels (4, 5). So, I was wondering if there was any difference between the two groups in terms of these parameters? I think that the abovementioned factors should be taken into consideration to verify the prognostic value of sST2 on cardiovascular mortality in outpatients with HF.