Hyperkalemia occurred in 16% of heart failure patients but did not independently predict mortality, whereas consistent RAASi use significantly improved survival (HR 0.48).
Does hyperkalemia worsen mortality or prevent the maintenance of guideline-directed medical therapy in heart failure patients?
In a specialized heart failure setting, hyperkalemia does not prevent the maintenance of guideline-directed medical therapy, and continued RAASi use remains strongly protective against mortality.
Absolute Event Rate: 0% vs 0%
Aim To assess the impact of hyperkalemia on the optimization of heart failure therapy and clinical outcomes in a specialized tertiary care center. Methods We retrospectively analyzed data from 690 heart failure patients, categorized into hyperkalemia and no-hyperkalemia groups based on the occurrence of serum potassium greater than 5 mEq/l at any time during follow-up. Baseline characteristics and long-term therapy patterns were compared. Predictors of hyperkalemia were evaluated through logistic regression analysis. Survival outcomes were assessed using Kaplan–Meier curves and Cox proportional hazards models. Four sensitivity analyses were performed, considering moderate hyperkalemia ( K ≥ 5.5 mEq/l), propensity score-matched cohorts, heart failure with reduced ejection fraction (HFrEF), and HFrEF population after the approval of sacubitril/valsartan in Italy. Results Hyperkalemia occurred in 16% of patients and was associated with chronic kidney disease and lower ejection fraction. Baseline use of renin–angiotensin–aldosterone system inhibitors (RAASi), beta-blockers, and mineralocorticoid receptor antagonists (MRAs) was similar between groups, with consistent prescription patterns during follow-up. Approximately 75% of patients in both groups maintained stable RAASi therapy, defined as continuous treatment throughout follow-up. Survival curves showed no significant difference between hyperkalemia and no-hyperkalemia patients. However, those maintaining or initiating RAASi therapy had significantly better long-term survival, regardless of hyperkalemia status. Hyperkalemia was not an independent predictor of mortality hazard ratio 1.04, 95% confidence interval (CI) 0.72–1.52, P = 0.83, while consistent RAASi use was strongly protective (hazard ratio 0.48, 95% CI 0.33–0.71, P < 0.001). Similar results were observed for secondary endpoints, as well as across all sensitivity analyses. Conclusion In a structured heart failure outpatient setting, hyperkalemia is not an insurmountable barrier to maintaining guideline-directed therapy. Continued RAASi use confers significant prognostic benefit, highlighting the importance of specialized follow-up.
Toma et al. (Thu,) reported a other. Hyperkalemia occurred in 16% of heart failure patients but did not independently predict mortality, whereas consistent RAASi use significantly improved survival (HR 0.48).
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