Renin-angiotensin-aldosterone system (RAAS) inhibitor therapy has been shown to be beneficial in patients with reduced left ventricular systolic function after an acute myocardial infarction, chronic systolic heart failure, and resistant hypertension. Although RAAS inhibitors are widely regarded as life-saving drugs, their use is often associated with changes in renal function, reducing elimination of potassium from the body. This can result in elevated concentrations of serum potassium, known as hyperkalaemia, which can in turn lead to potentially life-threatening conduction abnormalities and cardiac arrhythmias, and is associated with increased risk of death.
RAAS inhibitors are intrinsically linked to hyperkalaemia, with renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and mineral corticoid receptor antagonists all increasing serum potassium levels. The consequences of this side effect are treatment discontinuation or underdosing in patients with heart failure, which may contribute to a higher rate of heart failure-related hospitalisations and deaths. However, since the benefits of RAAS inhibitors outweigh the risks of hyperkalaemia, there remains the need to overcome these challenges rather than withdraw treatment.
Treatment options currently available for reducing potassium concentrations have many limitations, including uncertain efficacy, potential safety issues, as well as the fact that many therapies are temporising, only reducing serum potassium levels for a short amount of time, rather than eliminating excess potassium from the body. The clinical need to improve hyperkalaemia treatment options has led to the emergence of two novel agents: patiromer, which has been approved in the USA, and sodium zirconium cyclosilicate (SZC) which is currently in the clinical development stage. Studies have shown that these two new agents are efficacious in terms of achieving and maintaining normal potassium levels for up to 1 year and are well tolerated.
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