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Aim Atrial fibrillation (AF) commonly co-exists with heart failure (HF). The risk factors for and prognostic implications of incident HF development in patients with first-diagnosed AF and structurally normal hearts are poorly defined. In a cohort of patients with first-diagnosed AF and structurally normal hearts on baseline echocardiography, we investigated baseline risk factors for the development of incident HF and tested the hypothesis that incident HF was an independent predictor of adverse outcomes during a mean 10-year follow-up period. Methods and results This was a registry-based, observational cohort study of 842 patients initially diagnosed between 1992 and 2007 (mean age 51.6 ± 12.4 years), whereby 83 (9.9%) developed HF. The linearized rate of incident HF was 0.97% [95% confidence interval (CI) 0.78–1.19%] per 100 patient-years. Baseline history of hypertension, diabetes mellitus, dilated left atrium, and low-normal LVEF (50–54%) were multivariable predictors of subsequent HF (all P < 0.05). HF development was significantly associated with increased number of hospitalizations, AF progression, any stroke/peripheral thrombo-embolism, ischaemic stroke, cardiovascular death, and all-cause mortality (all P < 0.001). Kaplan–Meier 10-year estimates of survival free of the composite endpoint of AF progression, thrombo-embolism, and mortality were significantly worse for AF patients with incident HF compared with those without HF (68.8%; 95% CI 64.7–72.9 vs. 25.9% 95% CI 15.7–36.1, P < 0.001). Conclusion Underlying co-morbidities or subtle alterations such as mild left atrial dilatation or low-normal LVEF in the absence of overt underlying heart disease are baseline independent risk factors for incident HF during a long-term follow-up. Incident HF was an independent predictor of adverse outcomes in patients initially diagnosed with first-diagnosed AF and structurally normal hearts. These findings could facilitate the identification of AF patients at increased risk for adverse outcomes within the cohort perceived as being at ‘low risk’ given a structurally normal heart on echocardiography. [ABSTRACT FROM PUBLISHER]

Type 2 diabetes mellitus (T2DM) is common in patients with heart failure (HF) and associated with considerable morbidity and mortality. Significant advances have recently occurred in the treatment of T2DM, with evidence of several new glucose-lowering medications showing either neutral or beneficial cardiovascular effects. However, some of these agents have safety characteristics with strong practical implications in HF [i.e. dipeptidyl peptidase-4 (DPP-4) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1 RA), and sodium-glucose co-transporter type 2 (SGLT-2) inhibitors]. Regarding safety of DPP-4 inhibitors, saxagliptin is not recommended in HF because of a greater risk of HF hospitalisation. There is no compelling evidence of excess HF risk with the other DPP-4 inhibitors. GLP-1 RAs have an overall neutral effect on HF outcomes. However, a signal of harm suggested in two small trials of liraglutide in patients with reduced ejection fraction indicates that their role remains to be defined in established HF. SGLT-2 inhibitors (empagliflozin, canagliflozin and dapagliflozin) have shown a consistent reduction in the risk of HF hospitalisation regardless of baseline cardiovascular risk or history of HF. Accordingly, SGLT-2 inhibitors could be recommended to prevent HF hospitalisation in patients with T2DM and established cardiovascular disease or with multiple risk factors. The recently completed trial with dapagliflozin has shown a significant reduction in cardiovascular mortality and HF events in patients with HF and reduced ejection fraction, with or without T2DM. Several ongoing trials will assess whether the results observed with dapagliflozin could be extended to other SGLT-2 inhibitors in the treatment of HF, with either preserved or reduced ejection fraction, regardless of the presence of T2DM. This position paper aims to summarise relevant clinical trial evidence concerning the role and safety of new glucose-lowering therapies in patients with HF. [ABSTRACT FROM AUTHOR]