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Invited Commentary
January 2017

Hyperkalemia, Sacubitril/Valsartan, and Mineralocorticoid Antagonists in Patients With Heart Failure

Author Affiliations
  • 1Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
  • 2Canadian VIGOUR Centre, University of Alberta, Edmonton, Alberta, Canada
JAMA Cardiol. 2017;2(1):86-87. doi:10.1001/jamacardio.2016.4731

There are many risks in medicine, especially for patients with heart failure (HF). Some of the risks that patients with heart failure and clinicians alike fear are those of potassium excess (hyperkalemia) and potassium depletion (hypokalemia) and the resultant cellular and electrical instability that ensues. Death can occur with small shifts in the homeostasis of the environment despite the best of intentions.

The element potassium, the 19th element of the periodic table, is a core electrolyte when treating a patient with HF. A clinician must decide whether to add or subtract potassium supplements, or whether to reduce, hold, or increase the doses of lifesaving medications—those medications interfering with the renin-angiotensin-aldosterone system. Those caring for patients with HF often have to limit the up-titration to target doses owing to hyperkalemia, counsel patients on the food sources high in potassium that would otherwise be endorsed (eg, nuts, bananas, and spinach), or introduce binding agents to lower the plasma potassium level. Finally, the addition of other medications—such as mineralocorticoid antagonists (MRAs)—for appropriate patients is further limited, depriving a patient of a 24% to 30% relative risk reduction in all-cause mortality.1,2

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