Should we consider serum potassium level as a mortality predictor in ST-elevation myocardial infarction?

To the Editor,

I read the article by Uluganyan et al. (1) entitled “Admission serum potassium level is associated with in-hospital and long-term mortality in ST-elevation myocardial infarction” with great interest, which was published online in your Anatol J Cardiol 2015 Febr 11. In their study, the authors reported that the admission serum potassium (sK) level of >4.5 mmol/L was associated with increased long-term mortality in patients with ST-elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (pPCI). I would like to emphasize some confounding factors that can affect the results of the present study.

First, Uluganyan et al. (1) reported that patients were treated with drugs according to the European Society of Cardiology guidelines on myocardial revascularization. However, there are no data about the type of dual antiplatelet therapy (DAPT). It has been demonstrated that DAPT with ticagrelor reduced mortality than DAPT with clopidogrel in patients with STEMI who underwent pPCI (2). Additionally, in patients with STEMI undergoing pPCI, prasugrel is more effective than clopidogrel for the prevention of cardiovascular death and ischemic events (3). Hence, the higher incidence of treatment with ticagrelor and prasugrel in patients with sK levels of <4.5 may be a reason for lower mortality rates for these patients. Authors should state the incidence of DAPT with prasugrel, ticagrelor, and clopidogrel for each group, respectively.

Second, the authors did not report any data about the usage of aldosterone antagonists. The study by Uluganyan et al. (1) includes patients with impaired left ventricular systolic function. Aldosterone antagonists significantly reduce mortality in post-STEMI patients with left ventricular systolic dysfunction (ejection fraction<40%) (4). Hence, less treatment with aldosterone antagonists may be a reason for higher mortality rates for patients with sK levels of >4.5 mmol/L.

Finally, in the present study by Uluganyan et al. (1), there are no data about time to reperfusion and door-to-balloon time. It is known that delay in reperfusion and longer door-to-balloon time cause higher mortality rates (5, 6). Delay in time to reperfusion and longer door-to-balloon time may be another reason for higher mortality rates in patients with sK levels of >4.5 mmol/L when compared with patients with sK levels of <4.5 mmol/L. Therefore, the authors should state the time to reperfusion and door-to-balloon time for each group, respectively.

In conclusion, sK levels of >4.5 mmol/L may indicate worse outcomes in patients with STEMI undergoing pPCI. However, medical treatments, time to reperfusion, and door-to-balloon time may still affect the results of the study by Uluganyan et al. (1). To define the sK level of >4.5 mmol/L as a predictor of mortality, all factors associated with mortality should be considered.