February 2020 at a glance: acute heart failure and cardio‐oncology

Abstract

Hospitalizations for acute heart failure (AHF) are associated with poor outcomes.1 Sulo et al.2 examined trends in heart failure (HF) hospitalization rates in Norway. Age-adjusted HF hospitalization, but not total hospitalizations, declined in the years 2000–2014. In-hospital mortality decreased with a concomitant increase in post-discharge HF and cardiovascular readmission rates in men. Biomarker measurements have a landmark role in patients with AHF.3 Wettersten et al.4 evaluated the prognostic significance of serum and urine neutrophil gelatinase-associated lipocalin (NGAL) in 927 AHF patients. Serum NGAL outperformed urine NGAL but neither was superior to admission or peak serum creatinine for predicting adverse events. Möckel et al.5 conducted a randomized multicentre clinical trial assessing the role of serum procalcitonin (PCT) measurements in 742 patients admitted for AHF. The strategy of PCT-guided initiation of antibiotic therapy was not more effective than the standard care strategy in improving clinical outcomes. Circulating dipeptidyl peptidase 3 (cDPP3), a protease involved in angiotensin II and enkephalin degradation, was measured in patients with cardiogenic shock.6, 7 High baseline cDPP3 was associated with increased short-term mortality and more severe organ dysfunction and its rapid decrease within 24 h predicted a favourable outcome.6, 7 DPP3 administration in a mouse model induced myocardial depression and renal impairment and DPP3 inhibition by a specific antibody normalized cardiac and kidney function with reduction in oxidative stress and inflammation.7 Optimization of treatment before discharge is a major determinant of better post-discharge outcomes in patients hospitalized for AHF.3, 8, 9 Sacubitril/valsartan improves outcomes of patients with HF and reduced ejection fraction (HFrEF)10 and can be safely initiated after haemodynamic stabilization during hospitalization.11 Senni et al.12 compared the initiation of sacubitril/valsartan in patients with new-onset vs. prior HFrEF included in the multicentre, randomized, open-label, parallel group TRANSITION study. Patients with new-onset HF received a higher target dose and had fewer adverse events and a faster and larger decrease in biomarkers compared with those with prior HFrEF.12 In a meta-analysis of six randomized controlled studies, including 11 359 patients treated with intravenous serelaxin or placebo within the first 16 h of AHF admission, serelaxin administration was associated with a reduction in 5-day worsening HF, markers of renal dysfunction and all-cause mortality.13 Outcomes of patients with takotsubo syndrome differ according to their clinical presentation and treatment.14 Although indicated after an acute coronary event, aspirin had no impact on clinical events in these patients in a propensity score-based analysis.15 Cancer therapies may cause HF.16 Jacobse et al.17 evaluated the association between anthracycline use and HF in young breast cancer survivors. Patients treated with anthracyclines had lower left ventricular ejection fraction and higher global longitudinal strain and N-terminal pro-B-type natriuretic peptide compared to the others. Boekel et al.18 demonstrated a dose-dependent increase in HF risk after anthracycline therapy. Radiotherapy increased HF risk only in those on concomitant anthracycline treatment. HF occurred >10 years after diagnosis of breast cancer in 21/33 women who had received anthracyclines without trastuzumab while all cases of HF occurred ≤4 years after cancer diagnosis in those who received trastuzumab. Finally, a meta-analysis including 61 studies and 5691 patients on cancer therapy showed that troponin, but not natriuretic peptide levels, predicts cancer therapy-related left ventricular dysfunction and that HF therapies decrease troponin levels.19