A recent randomized trial in people with implanted cardioverter-defibrillators (ICDs) found that deliberately keeping serum potassium in the high-normal range produced better cardiovascular outcomes over roughly three years. The study enrolled about 1,200 high-risk patients and tracked a composite of clinically important events — sustained ventricular tachycardia, lifesaving ICD therapy, unplanned hospital stays >24 hours for arrhythmia or heart failure, and death. The key finding: patients whose potassium was raised to a target window of 4.5–5.0 mmol/L experienced fewer of these events than those whose potassium was not actively treated.
What the trial did and what it found
Participants began with an average baseline potassium around 4.01 mmol/L. Those randomized to the active strategy received one or more measures to increase their serum potassium: mineralocorticoid receptor antagonists (MRAs) and/or oral potassium supplements, tailored dietary advice to boost potassium intake, and stepwise reduction or discontinuation of potassium-wasting diuretics. The intervention aimed to reach the 4.5–5.0 mmol/L range within about 85 days, with close biochemical follow-up (blood tests every other week).
After an average follow-up of 3.3 years, the composite event rate was 22.7% in the high-normal-potassium arm versus 29.2% in the control arm. More detailed outcomes included a reduction in ventricular tachycardia events or required ICD therapy (15.3% vs 20.3%) and fewer hospitalizations for arrhythmia (6.7% vs 10.7%) in the treated group. Importantly, there were no statistically significant increases in hospitalizations for either dangerously high (hyperkalemia) or low (hypokalemia) potassium levels between the groups.
Why potassium matters for the heart
Potassium is central to cardiac electrical stability. The heart’s action potentials and repolarization depend on tightly regulated potassium gradients between the inside and outside of cardiomyocytes. If potassium drifts too low or too high, the risk of unstable rhythms rises. Severely low levels (below 2.5 mmol/L) are especially dangerous; moderately low levels (2.5–2.9 mmol/L) also carry substantial risk. On the other hand, excessively high potassium can provoke malignant arrhythmias such as ventricular fibrillation or even asystole, and cause muscle weakness including diaphragmatic impairment.
Beyond arrhythmia, potassium influences blood pressure regulation, vascular tone, and kidney function. Diets naturally higher in potassium — such as those rich in fruits, vegetables, and legumes — have long been associated with lower hypertension risk. The trial suggests that carefully controlled potassium elevation may offer a therapeutic extension of this principle, specifically tailored to those most vulnerable to electrical instability.
Interpreting the results — promise and practical limits
The trial suggests there may be a narrow therapeutic sweet spot where slightly higher potassium improves electrical stability without tipping into harm. For high-risk patients with ICDs, modest potassium elevation reduced arrhythmia burden and hospitalizations in this controlled setting.
However, translating the protocol into routine practice raises several caveats:
- Monitoring intensity. The trial relied on frequent lab checks (every two weeks) to safely titrate potassium — a level of monitoring that can be hard to replicate outside a trial.
- Narrow window and risks. The benefit depends on keeping potassium inside a tight range; overshooting can cause life-threatening hyperkalemia. Some clinicians observed more electrolyte-related hospitalizations in real-world follow-up, underscoring the narrow therapeutic window.
- Delayed mortality signal. Any mortality benefit appeared late; benefits were more evident only after several years, so short trials may miss long-term outcomes.
- Potential confounders. Differences in baseline characteristics (for example, duration since prior ICD therapy) may affect outcomes, so broader confirmation is needed in diverse populations.
How this could change care — and what’s needed next
For clinicians caring for people with significant arrhythmia risk, the trial raises the possibility that targeted potassium optimization — through diet, MRAs, and selective supplementation — could become an adjunctive strategy to reduce arrhythmia burden. Practical adoption would require clear protocols: who to treat, which agents to use first, monitoring frequency, and escalation rules for hyperkalemia. Point-of-care potassium testing, telemonitoring, and care pathways that integrate nephrology and cardiology input could make safe implementation more feasible.
Crucially, broader studies are needed to confirm benefits in patients without ICDs, in different types of heart disease, and to weigh long-term mortality and safety. Comparative research could also clarify whether dietary approaches, MRAs, or supplements provide the best risk–benefit profile.
Bottom line for patients
Potassium balance matters a great deal for people with heart disease. While this trial indicates that keeping serum potassium in a high-normal range (4.5–5.0 mmol/L) may reduce arrhythmias and hospitalizations among very high-risk patients, the approach requires careful medical supervision. Do not self-prescribe potassium supplements or adjust prescription diuretics on your own. Talk with your cardiologist about whether potassium optimization is appropriate for your situation and how it could be done safely with structured monitoring.
