Hyperkalaemia in Acute Heart Failure: Patient Profiles, Predictors and Outcomes in an Asian Population

Background

Acute decompensated heart failure (ADHF) is the sudden or gradual worsening of heart failure (HF) symptoms that require immediate treatment.¹ It includes three scenarios: onset of new HF, worsening chronic HF, and advanced HF, all demanding hospitalisation.² Typically, patients hospitalised with ADHF are older and exhibit severe symptoms alongside comorbidities, such as diabetes, hypertension, chronic kidney disease (CKD) and coronary heart disease.^1,3,4

Hyperkalaemia (HK) presents a significant challenge when managing patients with HF, primarily due to the medications commonly used in HF treatment, dietary potassium (K⁺) supplementation, metabolic shifts and concurrent CKD.⁵ The definition of HK varies and is commonly classified as mild (>5.0 to <5.5 mmol/l), moderate (5.5–6.0 mmol/l) or severe (>6.0 mmol/l). HK can lead to critical electrical issues arising from abnormalities in the conduction system, potentially resulting in life-threatening arrhythmias or sudden death. However, the severity of HK manifestation varies among patients; for instance, individuals with CKD may remain asymptomatic even with K⁺ levels that exceed 6.0 mmol/l.⁶

Guideline-directed medical therapies (GDMTs) for managing HF include renin–angiotensin-aldosterone system inhibitors (RAASi), which comprise angiotensin-converting enzyme inhibitors (ACEi), angiotensin II receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors (ARNI) and mineralocorticoid receptor antagonists (MRAs) and β-blockers.^7,8 RAASi have demonstrated efficacy in reducing hospitalisations and enhancing survival rates in HF. However, ACEi/ARBs and MRAs are the primary contributors to HK among patients with HF, while ARNI appear to not increase HK rates.⁹

ACEi and ARBs function by diminishing aldosterone production in the adrenal gland, while MRAs obstruct the receptor. Reports suggest that RAASi medications may cause HK in 5.2–11.8% of patients and severe HK in up to 2.5%.⁵ ACEi have the strongest association with HK, affecting approximately 10.0–38.0% of patients.^10–12 RAASi clinical trials might underestimate the prevalence of HK, potentially leading to elevated mortality and increased hospital admissions among HF patients.^13–15 This often results in discontinuation of medication or its limited use.^16–18

The 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America and the European Society of Cardiology (ESC) guidelines for managing HF recommend exercising caution when using RAASi for patients with K⁺ levels >5.0 mmol/l and suggest discontinuing MRAs if K⁺ levels cannot be maintained below <5.5 mmol/l.^7,8 However, the withdrawal of RAASi therapy has shown an increase in mortality.^19,20 Moreover, risk-scoring systems for HF typically do not include K⁺ levels or the presence of HK.²¹ This omission may complicate the clinical decision-making process concerning the continuation or withdrawal of GDMTs and affect patient outcomes. Nevertheless, the emergence of newer K⁺ binders that demonstrate long-term efficacy and tolerability hold considerable promise for patients with HF.^22–24

To better understand the clinical impact of HK in ADHF, this current study compares and characterises patients with and without HK by evaluating their clinical profiles, acute in-hospital management and outcomes. While the long-term effects of HK in HF have been extensively studied, predictors of in-hospital mortality remain insufficiently defined. Hence, this study was also designed to identify independent predictors of in-hospital all-cause mortality within the HK cohort. We also evaluated differences in RAASi use on admission and discharge in both cohorts to identify potential treatment gaps. Finally, we examined whether inadequate HK management affects long-term survival and HF readmissions.

Methods

Study Design

This study was conducted at the Institut Jantung Negara (IJN), a tertiary centre with one of the highest volumes of cardiac patients in Malaysia. IJN specialises in comprehensive cardiac care services and is the only centre in Malaysia that provides advanced HF therapy, including left ventricular assist devices (LVAD) and heart transplantation.

All medical records of patients with a primary diagnosis of ADHF who were admitted to IJN between January 2012 and December 2019 were retrospectively analysed after being retrieved from the IJN ADHF registry and the hospital health information system (TrakCare). Each inpatient admission for ADHF was counted as a separate case, including readmissions by the same patient. Outpatient visits for chronic HF management were also treated as distinct visits, corresponding to the same patients from the ADHF cases.

This study was performed according to the principles of the Declaration of Helsinki, Good Clinical Practice (GCP) and the laws and regulations of Malaysia. The study was approved by the IJN Research and Ethics Committee (IJNREC/585/2023) in accordance with the Malaysian Guidelines for GCP and the International Council for Harmonization of Technical Requirements for Pharmaceuticals for Human Use (ICH) Guideline for GCP.

Patients

Adult Malaysians (≥18 years old) hospitalised at IJN with at least one episode of de novo ADHF or those with a history of ADHF hospitalisation with recorded K⁺ levels were included (Figure 1).

Patient and Public Involvement

This study did not have any direct involvement of patients or the public as the data was collected retrospectively from the existing IJN ADHF registry.

Data

The acute HF data extracted included the patients’ demographics, comorbidities, clinical presentations, blood investigations, cardiac interventions and clinical outcomes. A total of 8,160 ADHF admissions were identified for this study. Patient follow-ups were considered until death or final follow-up. Mortality data were matched with TrakCare and the National Registration Department. Medications and K⁺ measurements at IJN outpatient follow-ups were also recorded when available. Measures were implemented to ensure patient confidentiality and privacy by anonymising medical records.

The data were categorised into two groups – the HK cohort included all records with K⁺ levels >5.0 mmol/l, and the non-HK cohort comprised all records with K⁺ levels ≤5.0 mmol/l. For each ADHF admission record, admission serum K⁺ was based on the measurement on initial presentation while serum K⁺ on discharge was the last measurement taken before the patient was discharged. For the post-discharge outpatient records, the serum K⁺ measurement for each patient visit was taken as a separate record.

Statistical Analysis

Continuous variables were reported as mean and standard deviation if normally distributed, and as median and interquartile range (Q1, Q3) if skewed. Categorical variables were presented as frequencies and percentages.

Comparative statistical analyses were conducted using independent t-test or Mann-Whitney U-test for continuous variables and chi-square or Fisher’s exact test for categorical variables, as appropriate. Patient profiles, acute in-hospital management and in-hospital clinical outcomes between patients with and without HK were evaluated. Since in-hospital all-cause mortality was the primary outcome, multivariate analysis with confounder adjustment would not be performed if no significant difference was observed between the HK and non-HK cohorts.

Univariate and multivariate logistic regression analyses were performed to identify predictors of in-hospital all-cause mortality. Variables with p<0.05 (two-tailed) in univariate analysis were included in the multivariate model using a forward stepwise selection method. Results were reported as OR with 95% CI.

Prescribed medications and the incidence of HK were observed during outpatient visits following discharge from admissions for ADHF. Follow-up all-cause mortality and HF readmission were analysed at 30 days, 6 months and 12 months for HK and non-HK cohorts.

The Kaplan-Meier method was used to estimate survival probabilities up to 36 months follow-up for all-cause mortality and HF readmissions post-discharge, with survival curves compared between the HK and non-HK cohorts using the log-rank test.

A p-value <0.05 (two-tailed) was considered statistically significant. All statistical analyses were performed using IBM SPSS Statistics Version 28.

Results

A total of 8,160 ADHF admissions were included in this study population where the majority were ethnic Malay, followed by Indian and Chinese people (Table 1). Of these patients, 20.3% (n=1,660) had HK, defined by a K⁺ level >5.0 mmol/l (Figure 1). Patients with HK were older, with a median age of 65.6 (57.4, 73.4, p<0.001) years, along with a significantly higher prevalence of coexisting coronary artery disease (CAD), renal insufficiency, diabetes and hypertension. Sex, ethnicity, history of HF admissions, MI and coronary artery interventions did not show significant differences compared to non-HK patients (Table 1).

The clinical presentation of the patients on admission (systolic blood pressure [SBP], BMI, dyspnoea, ascites, lung crepitations and hepatomegaly) was similar between the non-HK and HK cohorts. However, a greater proportion of patients with HK presented with peripheral oedema (72.9% versus 69.7%; p=0.010) and elevated jugular venous pressure (JVP) (48.4% versus 44.8%, p=0.008). Additionally, during admission for ADHF, patients with HK had significantly higher cardiac enzyme levels and worse renal function (median estimated glomerular filtration rate [eGFR] 40.3 versus 54.7 ml/min/1.73 m²; p<0.001). At discharge, the non-HK and HK cohorts showed similar improvements in SBP, heart rate and BMI. However, the non-HK cohort experienced a decline in renal function compared to admission, while the HK cohort showed improvement. Despite this, the HK cohort still had significantly worse renal function overall at discharge (Supplementary Table 1).

Upon admission, the HK cohort was in a more precarious state of health than those with normal K⁺ levels. Significantly more patients with HK presented with a left ventricular ejection fraction (LVEF) <40% (75.2% versus 72.2%; p=0.031) and required immediate life-saving interventions such as dialysis (7.1% versus 3.4%; p<0.001), mechanical ventilation (8.0% versus 5.9%; p=0.002), cardiac catheterisation (0.5% versus 1.0%; p=0.036), defibrillation (2.3% versus 1.5%; p=0.015) and cardiopulmonary resuscitation (CPR) (3.8% versus 2.8%; p=0.044).

Despite both groups having a similar median length of stay of 6 days, the distribution of hospital stays differed significantly (p<0.001; Supplementary Table 2). Our data showed a non-significant but observable trend of higher in-hospital mortality in the HK cohort compared to the non-HK cohort following ADHF admissions (5.6% versus 4.5%; p=0.057; Table 1). As the result was not significant, multivariate analysis was not performed, as such adjustments are typically made when a trend toward significance suggests the potential for meaningful insights.

A decreasing trend was observed in the use of RAASi between admission and upon discharge, with significant differences in the HK and non-HK cohorts (74.8% versus 78.8%; p<0.001; 70.7% versus 79.7%; p<0.001, respectively). Interestingly, among HK patients receiving RAASi, ARNI demonstrated an increase in prescription rates upon discharge compared with admission (4.3% versus 5.5%), whereas prescriptions for ACEi/ARB and MRA decreased (47.8% versus 41.0%; 56.1% versus 54.8%, respectively). Other medications, such as calcium channel blockers (CCBs), showed a significantly higher proportion of usage by the HK cohort on admission and upon discharge compared to the non-HK cohort (22.5% versus 18.7%; p<0.001; 21.0% versus 17.4%; p<0.001, respectively). Conversely, while the use of loop diuretics was similar between both cohorts during admission, it increased for both at discharge, with a significantly greater rise in the non-HK group compared to the HK group. Although prescription rates for β-blockers decreased at discharge in both cohorts, more than two-thirds of patients in both groups were on β-blockers during admission and discharge, whereas only one-third were on thiazides (Table 2).

On univariate analysis, the HK cohort demonstrated significantly higher in-hospital mortality if any of the following features were present: a history of MI (41.9% versus 27.7%, p=0.015), renal insufficiency (64.5% versus 44.5%; p<0.001), symptoms of ascites (41.9% versus 17.9%; p<0.001), lung crepitations (89.2% versus 79.8%; p=0.026), elevated JVP (64.5% versus 47.5%; p=0.001), hepatomegaly (6.5% versus 2.2%; p=0.024) and hypotension upon presentation (7.5% versus 0.8%; p<0.001). Additionally, higher mortality was also clinically associated with a positive troponin test (84.8% versus 69.3%; p=0.003), increased NT-proBNP levels (median 16,498.0 versus 8,914.5 pg/ml; p<0.001), lower albumin levels (median 36.0 versus 39.0 g/l; p<0.001), increased urea levels (15.6 versus 10.7 mmol/l; p<0.001), decreased renal function (median eGFR 35.9 versus 40.5 ml/min/1.73 m²; p=0.004), LVEF <40% (91.7% versus 74.2%; p<0.001), requiring defibrillation (31.2% versus 0.6%; p<0.001) or requiring a longer stay in hospital (median 10.0 versus 6.0 days; p<0.001).

Interestingly, older patients (median age 65.8 versus 61.4 years; p=0.004), those with a history of previous coronary artery bypass grafting (38.9% versus 25.8%; p=0.038), diabetes (72.0% versus 62.4%; p=0.046), hypertension (79.5% versus 60.2%; p<0.001), higher blood pressure at presentation (median SBP 127.0 versus 110.0, p<0.001), increased sodium levels (median 137.0 versus 134.0 mmol/l; p<0.001), as well as more prescriptions of HF medications such as ACEi/ARB (48.6% versus 34.4%; p=0.008), β-blockers (76.5% versus 58.1%; p<0.001), or CCBs (23.2% versus 10.8%; p=0.005) were found to have better survival in ADHF admissions with incident HK (Supplementary Table 3).

In the HK cohort, several factors were found to have increased the risk of in-hospital mortality (Figure 2). A prior HF hospitalisation was a significant predictor, with previously admitted patients having >18 times the risk of in-hospital mortality during the current ADHF admission. This highlights the heightened vulnerability of these patients compared to those with de novo HF. Higher bilirubin and uric acid levels also contributed to in-hospital all-cause mortality risk suggesting that even modest increases in these markers for liver and kidney function significantly affect outcomes due to the added strain on these organs. Other important factors included the need for dialysis, mechanical ventilation and CPR. Patients who needed these interventions were >70 times more likely to die during hospitalisation, underscoring the severity of their illness and the impact of intensive interventions. Last, the absence of loop diuretic therapy during hospitalisation was significantly associated with in-hospital mortality, suggesting that the lack of this essential treatment for fluid overload management in patients with HF contributes to a higher risk of poor survival outcomes.

A total of 15,897 follow-up visits were analysed, of which 77.7% (n=12,355) patients had normal K⁺ levels and 22.3% (n=3,542) had incident HK (Supplementary Table 4). More than 50% of patients on RAASi and β-blockers had incident HK (75.7% and 79.2%, respectively). Among the RAASi group, 54.2% of patients on MRAs had HK, compared to 42.4% and 16.7% of patients on ACEi/ARB and ARNI, respectively.

Post-discharge mortality at 30 days, 6 months and 12 months was significantly higher in the HK cohort than the non-HK cohort (6.5% versus 4.3%, p<0.001; 27.2 versus 21.3%, p<0.001; 40.5 versus 33.2%, p<0.001, respectively). Additionally, HF readmissions consistently increased over the same time periods (Supplementary Table 5). This was further supported by Kaplan-Meier estimates (Supplementary Figures 1 and 2), which showed significant differences in freedom from all-cause mortality (log rank p<0.001) and HF readmission events (log rank p=0.007) between cohorts.

Discussion

Malaysia has a multi-ethnic population, consisting of Malays (61.8%), Chinese (21.4%), Indians (6.4%), and other ethnic communities (10.4%), and offers a representative Asian context for studying HK.²⁵ Global estimates using varying definitions and thresholds suggest an HK prevalence of approximately 6.3%, with Asia ranking among the top three continents with 10.4%. This may be partly attributable to the region’s potassium-rich diet. In contrast, HK prevalence in Europe (5.9%) and North America (5.0%) is about half that of Asia.^26,27 In the ADHF patients in this study, we defined HK as K⁺ levels >5.0 mmol/l and this had a prevalence of 20.3%. The Asian sudden cardiac death in Heart Failure (Asian-HF) registry, which uses a similar HK definition, reported a HK prevalence of 5–10% in Malaysia, China, Japan and South Korea for both acute and chronic HF patients. The higher prevalence of HK in our study may reflect our hospital’s role as a specialised cardiovascular (CV) tertiary centre, the HF-targeted patient cohort and Asian dietary patterns.^28–30

In a large, real-world HF population (n=52,253), traditional CV risk factors, renal insufficiency and a prior diagnosis of CV conditions were all significantly associated with HK (p<0.001 for all).³⁰ In our ADHF patient group, the HK cohort had more elderly patients and those with hypertension, diabetes, a history of CAD and worse renal function than in the non-HK cohort. Similar to European and American studies, our HK cohort demonstrated comparable baseline characteristics but a higher proportion of HK at ADHF presentation.^28–30

HK is a common electrolyte disturbance in ADHF patients and may potentially be life-threatening in the short- and long-term.^5,13,14 Our findings are reinforced by analyses conducted using data from the PROTECT and COACH trials that found K⁺ levels and their fluctuations during admission can serve as a surrogate marker of concurrent clinical characteristics (such as renal impairment) that are potential predictors of mortality.²⁹ A large study revealed that the predicted risk of all-cause mortality increases for every 0.5 mmol/l rise in K⁺ level above 4.5 mmol/l.³¹ Even though our observed overall in-hospital all-cause mortality rate is comparable to the 6.7% reported in a study of a Chinese population, it is approximately half the rate observed in a Spanish study (12.3%).^32,33 Additionally, the aggregate in-hospital all-cause mortality rates between our HK and non-HK cohorts were not significantly different, unlike both studies that reported significant differences in outcomes.

Post-discharge, we observed that the all-cause mortality rate within 12 months in our HK cohort was lower than that reported by Maggioni et al. (87.8% versus 40.5%).²⁸ However, we found a significant difference in the probability of survival up to 36 months, consistent with the high 3-year mortality seen in a real-world study of HF patients with HK.³⁰

In our core investigation of the HK cohort, we identified key factors that were independently associated with in-hospital mortality. A history of HF hospitalisations strongly predicted the outcome, highlighting the impact of worsening CV function and increased comorbidities.^34,35 Elevated bilirubin and uric acid levels were also associated with increased mortality, emphasising the role of liver and kidney dysfunction.^36,37 The need for interventions such as dialysis, mechanical ventilation and CPR could be due to kidney damage, major respiratory issues and the development of arrhythmias. These findings underscore the progressive nature of severe ADHF, where rapid and aggressive treatment is necessary not just for managing HK, but also for addressing multi-organ dysfunction. Additionally, the inadequate use of loop diuretics during hospitalisation suggests that suboptimal fluid management may worsen patient stability.³⁸ Understanding in-hospital mortality predictors within the HK cohort is crucial for providing actionable insights into management in the acute phase, enabling timely, life-saving interventions.

Patients with HK face a higher risk of RAASi being modified, which poses a challenge to the achievement of an optimal balance in HF management. Suboptimal doses, compared to guideline-recommended levels, can lead to poorer CV-related outcomes and mortality.³⁰ Doses are often down-titrated or discontinued in a substantial number of patients who experience moderate-to-severe HK (47.0%) and those with mild HK (38.0%).¹⁷ Evidence suggests that patients receiving the highest doses of RAASi (13.7%) can benefit from lower mortality rates in HF compared to those who are down-titrated (27.7%), with the highest rates observed in patients whose medication is discontinued (30.1%).^17,18

Patients with HF often have concurrent CKD, which independently increases the risk of HK.³⁹ Our study revealed a significantly higher incidence of renal insufficiency with lower eGFR levels in the HK cohort than in the non-HK cohort. Additionally, significantly more patients with renal insufficiency and lower eGFR levels died in the HK cohort. RAASi have demonstrated benefits in CKD management, however, concern about the added risk of HK among patients with HF and CKD has limited their use. A large study among hospitalised HF patients from the Get With the Guidelines Heart Failure registry revealed a progressive decline in GDMT prescriptions upon discharge as the eGFR decreased, which was paralleled by an increase in mortality rates.⁴⁰ This is concerning, as even among HF patients with an eGFR ≥90 ml/min/1.73 m², the use of GDMT was found to be only 38.0%. This highlights the need to optimise the use of GDMTs in patients with HF and CKD, even at eGFR levels that are not contraindicated for their use.

Similar to the Chinese study, our findings revealed that the in-hospital mortality rate in the HK cohort was significantly lower among those who received GDMTs, including ACEi/ARB, than those who did not.³² In contrast, the Spanish study reported approximately 65% higher ACEi/ARB use, no ARNI use, and about 22% lower MRAs use compared to our patients, which may explain the higher in-hospital mortality rate observed in that study.³³ In our study, we noted a RAASi modification pattern from admission to discharge in both cohorts, with more changes in ACEi/ARB yet stable MRA prescriptions. However, there were significantly fewer patients on ACEi/ARBs and MRAs in the HK cohort compared to the non-HK cohort reflecting a common practice with RAASi prescriptions in these patients.¹⁶ This observation is consistent with a study analysing patients with ADHF from the Italian Network on Heart Failure cardiology registry.²⁸ The reduction in RAASi use at discharge likely reflects concerns over renal dysfunction and HK during acute instability. In contrast, the rise in RAASi use in outpatients reflects physicians’ confidence in safely reintroducing and optimising these drugs after stabilisation, reinforcing its proven benefits in HF management.⁶

While concerns regarding the potential of RAASi to cause HK in at-risk populations have limited its use and dose optimisation, maintaining or even up-titrating MRA and ACEi/ARB doses at discharge has produced lower 180-day mortality in these patients.^{9,16,18,32,41,42,43} Moreover, the 3-year mortality rate was twice as high among all HF patients with HK who were not treated with RAASi compared to those who were (62.0% versus 30.0%, p<0.001), regardless of the severity of the condition.³⁰ Although there were various risk factors for HF readmission, the OPTIMIZE-HF study demonstrated that post-discharge ACEi/ARB use was an independent prognostic factor.⁴⁴ This might explain why the rehospitalisation rates between our HK and non-HK cohorts were significantly different, with rehospitalisation being consistently higher in the HK cohort.

Clinicians must navigate the delicate balance of optimising HF treatment while avoiding the potentially life-threatening complications of HK. This requires careful patient selection, adequate serum K⁺ levels and renal function monitoring, and identification of effective and tolerable prevention strategies.⁴⁵ Serum K⁺ should be closely monitored during the initiation, titration and final dose adjustments of RAASi.⁴⁶ Regular monitoring of all patients receiving RAASi therapy is recommended thereafter. Although dietary K⁺ restriction has been practised to prevent HK, the association between K⁺ intake and serum K⁺ concentrations is weak.⁴⁷ The efficacy of K⁺-depleting diuretics may depend on the patient’s kidney function and the predictability of the response remains uncertain.⁴⁷ The traditional K⁺ binder available in Malaysia, calcium polystyrene sulfonate, is widely used for short-term management of HK. However, concerns have been raised about its use in the medium-to-long term due to serious gastrointestinal side effects.⁴⁸

The availability of novel K⁺-lowering agents, such as sodium zirconium cyclosilicate (SZC) and patiromer, presents an effective and safe short- and long-term solution for effectively controlling K⁺ levels in patients with HK.^23,24,49 SZC maintained mean serum K⁺ at 4.7 mmol/l over 3–12 months, and 88% and 99% of patients achieved serum K⁺ ≤5.1 and ≤5.5 mmol/l, respectively.²⁴ This demonstrates that RAASi could be maintained and optimised in HF patients, potentially reducing the severity and frequency of ADHF exacerbations, subsequent hospital admissions and mortality.^23,24 Further, maintaining normal K⁺ levels reduces the risk of life-threatening cardiac arrhythmias associated with HK.⁶ As the consistent use of RAASi can effectively reduce disease progression and HF-related mortality rates, the ESC added SZC as a recommended option to treat patients with CVD with chronic or recurrent HK to optimise GDMTs.⁶

It is essential to emphasise that, while K⁺-lowering agents present significant advantages in managing HK, close monitoring is necessary to prevent hypokalaemia, which can also pose risks. Therefore, a multidisciplinary approach involving healthcare providers specialising in HF management, cardiology and nephrology is essential for individualised care to optimise treatment strategies and improve outcomes in patients with HF during ADHF admissions and follow-up care.⁵⁰ This study marks our institution’s first step in exploring HK in ADHF, laying the foundation for future research on its long-term impact and implications for chronic HF management. Early identification of high-risk patients can enable timely recognition and appropriate management, ultimately improving clinical outcomes.

Limitations

Treating each ADHF admission as an independent event enabled a detailed analysis of HK’s impact on disease progression and treatment changes. While this approach reflects real-world practice, it may have overrepresented patients with frequent hospitalisations and introduced correlations compared to analyses based solely on index admissions. The lack of adjustment for clustering effects and long-term patient-level trends should be considered when interpreting our findings. Although the retrospective nature of this study is a limitation, it provides valuable insight into routine clinical practice, capturing clinician-recorded data. While this design may introduce potential biases in data completeness and patient follow-up accuracy, it offers a meaningful snapshot of everyday clinical outcomes. The study faced challenges with medication usage reporting, as some outpatient records lacked detailed information. However, this gap provided broader insights into RAASi usage, without affecting our overall analysis. All efforts were also made by the authors to verify the data. This was also a single-centre design, and a multicentre approach would have provided more robust data. While limitations exist, our findings present valuable insights with the potential to improve clinical practice and research, particularly in our region. By shedding light on the issue of HK in HF patients, this work can inspire further advancements and support more informed decision-making in the field.

Conclusion

Our research provides significant findings regarding the occurrence and implications of HK in a diverse population of patients hospitalised for ADHF. It is imperative to thoroughly examine the intricate relationship between HK and the effective management of HF. It is also crucial to acknowledge the challenges posed by first-line GDMTs, such as RAASi and the potential advantages of newer K⁺-lowering agents in enhancing the treatment of patients with HF to improve clinical outcomes. In essence, HK presents a significant barrier to optimising GDMTs in our local Asian population, which translates into higher mortality among patients with HK.

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