Author + information
- Received September 6, 2018
- Accepted October 4, 2018
- Published online December 31, 2018.
- Gianluigi Savarese, MD, PhDa,∗,
- Hong Xu, MDb,∗,
- Marco Trevisan, MScb,
- Ulf Dahlström, MD, PhDc,
- Patrick Rossignol, MD, PhDd,
- Bertram Pitt, MD, PhDe,
- Lars H. Lund, MD, PhDa,†∗ ( and )
- Juan J. Carrero, PharmD, PhDb,†
- aDivision of Cardiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
- bDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
- cDepartments of Cardiology Medical and Health Sciences, Linkoping University, Linkoping, Sweden
- dUniversité de Lorraine, INSERM CIC-P 1433, Centre Hospitalier Régional Universitaire de Nancy, and INSERM U1116, FCRIN INI-Cardiovascular and Renal Clinical Trialists, Nancy, France
- eDepartment of Medicine, University of Michigan, Ann Arbor, Michigan
- ↵∗Address for correspondence:
Dr. Lars H. Lund, Department of Medicine, Karolinska Institutet, and Heart and Vascular Theme, Karolinska University Hospital, FoU Tema Hjärta Kärl, Norrbacka, S1:02, 171 76 Stockholm, Sweden.
Objectives This study investigated 1-year incidence and predictors of dyskalemia (dysK) and its outcome associations in heart failure with preserved ejection fraction (HFpEF), HF with mid-range EF (HFmrEF), and HF with reduced EF (HFrEF).
Background DysK in real-world HF is insufficiently characterized. Fear of dyskalemia may lead to underuse or underdosing of renin-angiotensin-aldosterone system inhibitors.
Methods Patients enrolled in the SwedeHF (Swedish Heart Failure) Registry from 2006 to 2011 in Stockholm, Sweden were included in the analyses. Multivariate Cox regression analysis identified independent predictors of dysK within 1 year. Time-dependent Cox models assessed outcomes associated with incident dysK (all-cause death, HF, and other cardiovascular disease [CVD] hospitalizations) within 1 year from baseline.
Results Of 5,848 patients, 24.4% experienced hyperkalemia (hyperK [K >5.0 mmol/l]) at least once, and 10.2% had moderate or severe hyperK (K >5.5 mmol/l). Adjusted risk of moderate or severe hyperK was highest in HFpEF and HFmrEF. Similarly, 20.3% of patients had at least one episode of hypokalemia (hypoK [<3.5 mmol/l]), and 3.7% had severe hypoK (<3.0 mmol/l). Adjusted risk of any hypoK was highest in HFpEF. Independent predictors of both hyperK and hypoK were sex, baseline potassium and estimated glomerular filtration rate, low hemoglobin, chronic obstructive pulmonary disease (COPD), inpatient status, and higher New York Heart Association functional class. Incident dysK was associated with increased risk of mortality. Furthermore, hypoK was associated with increased CVD hospitalizations (HF-related excluded). There was no association between dysK and HF hospitalization risk, regardless of EF.
Conclusions DysK is common in HF and is associated with increased mortality. Risk of moderate or severe hyperK was highest in HFpEF and HFmrEF, whereas risk of hypoK was highest in HFpEF. HF severity, low hemoglobin, COPD, baseline high and low potassium, and low eGFR were relevant predictors of dysK occurrence.
- heart failure
- mid-range ejection fraction
- preserved ejection fraction
- reduced ejection fraction
↵∗ Drs. Savarese and Xu contributed equally to this work and are joint first authors.
↵† Drs. Lund and Carrero contributed equally to this work and are joint senior authors.
Supported by institutional grants from Vifor Fresenius Medical Care Renal Pharma and Relypsa to Karolinska Institutet, Swedish Heart and Lung Foundation, Swedish Research Council, Stockholm County Council (including ALF projects), AstraZeneca, and Martin Rind’s and Westman’s Foundations. Dr. Lund is supported by Swedish Research Council grants 2013-23897-104604-23 and 523-2014-2336, and Swedish Heart Lung Foundation grants 20120321 and 20150557; has received grants from Relypsa, Vifor Pharma, AstraZeneca, and Novartis through his institution; and consults for Relypsa, Vifor Pharma, AstraZeneca, Novartis, and Sanofi. Dr. Rossignol is supported by French National Research Agency public grant ANR-15-RHU-0004 as part of the second Investissements d’Avenir program FIGHT-HF and by French PIA project Lorraine Université d’Excellence grant ANR-15-IDEX-04-LUE; consults for Novartis, Relypsa, AstraZeneca, Grünenthal, Stealth Peptides, Fresenius, Idorsia, Vifor Fresenius Medical Care Renal Pharma, Vifor, and CTMA; has received lecture fees from Bayer and CVRx; and is a cofounder of CardioRenal. Dr. Savarese has received research grants from Merck and Co. and Boehringer Ingelheim; and has received honoraria from Vifor and AstraZeneca. Dr. Carrero has received research support from AstraZeneca. Dr. Pitt has received fees from Bayer, Sanofi, AstraZeneca, KDP Pharmaceuticals, Relypsa/Vifor, Cpharmaceuticals, Tricida, Stealth Peptides, Sarfez Pharmaceuticals, and G3 Pharmaceuticals; and is a patent pending holder for eplerenone delivery. Dr. Dahlström has received research support from AstraZeneca through his institution; and has received honoraria from and consults for AstraZeneca and Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 6, 2018.
- Accepted October 4, 2018.
- 2019 American College of Cardiology Foundation