Search

Aims: Iron deficiency (ID) is common in heart failure (HF) and linked with poor prognosis regardless of anaemia. We assessed temporal trends in ID testing, ID prevalence, ID incidence, iron need, and outcomes associated with ID in HF across the ejection fraction (EF) spectrum. Methods and results: From the Swedish HF registry, we enrolled 15 197 patients from Region Stockholm with available EF and collected laboratory tests from routine practice. Iron screening improved since 2016 but remained <25% as of 2018. In 1486 patients with iron biomarkers at baseline, the prevalence of ID was 55% (HF with reduced EF 54%; mildly reduced EF 51%; preserved EF 61%). Iron need was ≥1500 mg in 72% of patients. ID was independently associated with higher risk for HF rehospitalizations (incidence rate ratio [IRR] 1.62, 95% confidence interval [CI] 1.13–2.31) and with cardiovascular (CV) death or repeated HF hospitalizations (IRR 1.63, 95% CI 1.15–2.30) regardless of EF (p‐interaction 0.21 and 0.26, respectively), but not with all‐cause death, CV death, or first HF hospitalization. Among 96 patients without ID at baseline and with follow‐up iron biomarkers, 21% developed ID within 6 months. Conclusions: Iron deficiency screening improved over time but is still limitedly implemented, despite being highly prevalent and incident, and independently associated with CV death or HF rehospitalizations regardless of EF. Most patients with ID had an iron need necessitating either repeated administrations of intravenous iron or a preparation permitting >1000 mg doses. These data highlight the need for improved screening for ID in HF. [ABSTRACT FROM AUTHOR]

Aim: We present the baseline characteristics of the PREFERS Stockholm epidemiological study on the natural history and course of new onset heart failure (HF) aiming to improve phenotyping focusing on HF with preserved left ventricular ejection fraction (HFpEF) pathophysiology. Methods and results: New onset HF patients diagnosed in hospital or at outpatient HF clinics were included at five Stockholm hospitals 2015–2018 and characterized by N‐terminal pro brain natriuretic peptide (NT‐proBNP), biomarkers, echocardiography, and cardiac magnetic resonance imaging (subset). HFpEF [left ventricular ejection fraction (LVEF) ≥ 50%] was compared with HF with mildly reduced LVEF (HFmrEF; LVEF 41–49%) and with HF with reduced LVEF (HFrEF; LVEF ≤ 40%). We included 547 patients whereof HFpEF (n = 137; 25%), HFmrEF (n = 61; 11%), and HFrEF (n = 349; 64%). HFpEF patients were older (76; 70–81 years; median; interquartile range) than HFrEF (67; 58–74; P < 0.001), more often women (49% vs. 30%; P < 0.001), and had significantly higher comorbidity burden. They more often had atrial fibrillation, hypertension, and renal dysfunction. NT‐proBNP was lower in HFpEF (896; 462–1645 ng/L) than in HFrEF (1160; 563–2370; P = 0.005). In HFpEF, left ventricular (LV) diameters and volumes were smaller (P < 0.001) and septal and posterior wall thickness and relative wall thickness higher (P < 0.001). E/é ≥ 14 was present in 26% of HFpEF vs. 32% of HFrEF (P = 0.017) and left atrial volume index > 34 mL/m2 in 57% vs. 61% (P = 0.040). HFmrEF patients were intermediary between HFpEF and HFrEF for LV mass, LV volumes, and RV volumes but had the highest proportion of left ventricular hypertrophy and the lowest proportion of elevated E/é. Conclusions: Phenotype data in new onset HF patients recruited in a broad clinical setting showed that 25% had HFpEF, were older, more often women, and had greater comorbidity burden. PREFERS is well suited to further explore biomarker and imaging components of HFpEF pathophysiology and may contribute to the emerging knowledge of HF epidemiology. Clinical trial registration: Clinicaltrials.gov identifier: NCT03671122. [ABSTRACT FROM AUTHOR]

Aims: Whether to continue or stop mineralocorticoid receptor antagonists (MRA) after an episode of hyperkalaemia is a challenge in clinical practice. While stopping MRA may prevent recurrent hyperkalaemias, it deprives patients of their cardioprotection. We here assessed the association between stopping vs. continuing MRA therapy after hyperkalaemia and the subsequent risks of adverse health events. Methods and results: Observational study from the Stockholm CREAtinine Measurements (SCREAM) project 2006–2018. We identified patients initiating MRA and surviving a first‐detected episode of hyperkalaemia (plasma potassium >5.0 mmol/L). Using target trial emulation methods, we assessed the association between stopping vs. continuing MRA within 6 months after hyperkalaemia and subsequent outcomes. The primary outcome was the composite of hospital admission with heart failure, stroke, myocardial infarction, or death. The secondary outcome was occurrence of another hyperkalaemia event. Among 39 518 patients initiating MRA, we identified 7366 who developed hyperkalaemia. Median age was 76 years, 45% were women and 69% had a history of heart failure. Following hyperkalaemia, 2222 (30%) discontinued treatment. Compared with continuing MRA, stopping therapy was associated with a lower 2‐year risk of recurrent hyperkalaemia [hazard ratio (HR) 0.75, 95% confidence interval (CI) 0.72–0.79], but a higher risk of the primary outcome (HR 1.10, 95% CI 1.06–1.14). Similar results were observed in patients with heart failure, after censoring when treatment decision was changed, and across pre‐specified subgroups. Conclusions: Stopping MRA after an episode of hyperkalaemia was associated with reduced risk for recurrent hyperkalaemia, but higher risk of death or cardiovascular events. Recurrent hyperkalaemia was common in either strategy. [ABSTRACT FROM AUTHOR]

Aims: The cardiorenal syndrome refers to a bidirectional relationship between the kidney and the heart. However, epidemiological evidence of cardiovascular disease (CVD) as a risk factor for chronic kidney disease (CKD) progression is actually scarce. Methods and results: We examined the slopes of estimated glomerular filtration rate (eGFR) decline in the 2 years before vs. after an incident hospitalization with heart failure (HF) (n = 20 420), coronary heart disease (CHD) (n = 18 152), or stroke (n = 1808) using data from a complete laboratory data collection in Stockholm, Sweden between 2006 and 2011. eGFR slopes were estimated using mixed‐effect models with unstructured residual correlation. Overall, incident hospitalization with HF and CHD, but not stroke, was significantly associated with a subsequent accelerated decline in eGFR, with a faster eGFR decline and greater slope change after HF than CHD. The pre‐event vs. post‐event eGFR slopes (mL/min/1.73 m2 per year) were −1.67 (−1.77 to −1.57) vs. −2.76 (−2.82 to −2.71), with a Δslope of −1.09 (−1.16 to −1.02) for HF; −1.09 (−1.20 to −0.98) vs. −1.87 (−1.92 to −1.81), with a Δslope of −0.78 (−0.85 to −0.70) for CHD; and −1.00 (−1.37 to −0.63) vs. −0.99 (−1.19 to −0.78), with a Δslope of 0.02 (−0.24 to 0.27) for stroke. The accelerated declines in eGFR after HF and CHD were consistent across the spectrum of eGFR, although pre‐event eGFR slopes were steeper in lower eGFR (e.g. pre‐event eGFR slope for HF −0.64 (−0.76 to −0.53) for eGFR ≥60 mL/min/1.73 m2, −1.43 (−1.57 to −1.30) for eGFR 30–59 mL/min/1.73 m2, and −2.42 (−2.71 to −2.12) for eGFR <30 mL/min/1.73 m2). Conclusions: Incident hospitalization with cardiac diseases (i.e. HF and CHD) was significantly associated with a subsequent acceleration of eGFR decline. [ABSTRACT FROM AUTHOR]

Background Small-scale studies suggest that hyperkalaemia is a less threatening condition in chronic kidney disease (CKD), arguing adaptation/tolerance to potassium (K+) retention. This study formally evaluates this hypothesis by estimating the distribution of plasma K+ and its association with mortality across CKD stages. Methods This observational study included all patients undergoing plasma K+ testing in Stockholm during 2006–11. We randomly selected one K+ measurement per patient and constructed a cross-sectional cohort with mortality follow-up. Covariates included demographics, comorbidities, medications and estimated glomerular filtration rate (eGFR). We estimated K+ distribution and defined K+ ranges associated with 90-, 180- and 365-day mortality. Results Included were 831 760 participants, of which 70 403 (8.5%) had CKD G3 (eGFR <60–30 mL/min) and 8594 (1.1%) had CKD G4–G5 (eGFR <30 mL/min). About 66 317 deaths occurred within a year. Adjusted plasma K+ increased across worse CKD stages: from median 3.98 (95% confidence interval 3.49–4.59) for eGFR >90 to 4.43 (3.22–5.65) mmol/L for eGFR ≤15 mL/min/1.73 m2. The association between K+ and mortality was U-shaped, but it flattened at lower eGFR strata and shifted upwards. For instance, the range where the 90-day mortality risk increased by no more than 100% was 3.45–4.94 mmol/L in eGFR >60 mL/min, but was 3.36–5.18  in G3 and 3.26–5.53 mmol/L in G4–G5. In conclusion, CKD stage modifies K+ distribution and the ranges that predict mortality in the community. Conclusion Although this study supports the view that hyperkalaemia is better tolerated with worse CKD, it challenges the current use of a single optimal K+ range for all patients. [ABSTRACT FROM AUTHOR]