Background and Aims: Acute heart failure (AHF) promotes inflammatory activation, which is associated with worse outcomes. Colchicine has proven effective in other cardiovascular conditions characterized by inflammatory activation, but has never been evaluated in the setting of AHF. Methods: This multicenter, randomized, double-blind, and placebo-controlled trial included patients with AHF, requiring ≥40 mg of intravenous furosemide, regardless of their left ventricular ejection fraction (LVEF) and inpatient or outpatient setting. Patients were randomized within the first 24 h of presentation to receive either colchicine or placebo, with loading dose of 2 mg, followed by 0.5 mg every 12 h for 8 weeks. Results: A total of 278 patients [median age 75 years, LVEF 40%, baseline N-terminal pro-B-type natriuretic peptide (NT-proBNP) 4262 pg/mL] were randomized to colchicine (n = 141) or placebo (n = 137). The primary endpoint, the time-averaged reduction in NT-proBNP levels at 8 weeks, did not differ between the colchicine group [−62.2%, 95% confidence interval (CI) −68.9% to −54.2%] and the placebo group (−62.1%, 95% CI −68.6% to −54.3%) (ratio of change 1.0). The reduction in inflammatory markers was significantly greater with colchicine: ratio of change 0.60 (P < .001) for C-reactive protein and 0.72 (P = .019) for interleukin-6. No differences were found in new worsening heart failure episodes (14.9% with colchicine vs. 16.8% with placebo, P = .698); however, the need for intravenous furosemide during follow-up was lower with colchicine (P = .043). Diarrhea was slightly more common with colchicine, but it did not result in differences in medication withdrawal (8.5% vs. 8.8%). Conclusions: Colchicine was safe and effective in reducing inflammation in patients with AHF; however, colchicine and placebo exhibited comparable effects on reducing NT-proBNP and preventing new worsening heart failure events.

Aims As evidenced by scintigraphy imaging, the prevalence of transthyretin (TTR) cardiac amyloidosis in heart failure patients with preserved ejection fraction (HFpEF) and left ventricular hypertrophy (LVH) ranges between 13% and 19%. The natural evolution of cardiac amyloidosis begins with the deposition of amyloid material in the myocardium, with LVH ensuing at later stages. With current imaging modalities, it is possible to detect TTR cardiac amyloidosis before the hypertrophic stage. The aim of this study was to determine the prevalence of TTR cardiac amyloidosis in HFpEF patients without LVH. Methods and results The study prospectively enrolled patients admitted for HF with LV ejection fraction (LVEF) ≥ 50% and LV wall thickness <12 mm. TTR cardiac amyloidosis was diagnosed according to accepted criteria, which include positive cardiac 99‐Tc‐DPD scintigraphy in the absence of monoclonal protein expansion in blood. Transthyretin gene sequencing was performed in positive patients. From July 2017 to January 2020, 329 patients with HFpEF and LV thickness <12 mm were identified. After exclusions, 58 patients completed the study with cardiac scintigraphy (79 years, 54% men; median LVEF 60% and LV wall thickness 10.5 mm). Three patients (5.2%) were positive for TTR cardiac amyloidosis; genetic analysis excluded the presence of hereditary TTR amyloidosis. Positive patients baseline characteristics (84 years, 67% men, LVEF 60%, and LV wall thickness 11 mm) were similar to patients without TTR, except for troponin levels (0.05 vs. 0.02 ng/mL, P = 0.03) and glomerular filtration rate (82 vs. 60 mL/min, P = 0.032), which were higher in TTR patients. Conclusions In a cohort of patients with HFpEF without LVH, the prevalence of TTR cardiac amyloidosis was 5%. Early diagnosis of cardiac involvement in TTR amyloidosis (before manifest LVH) would seem recommendable because newly approved specific treatments can prevent additional deposition of amyloid material.

Natriuretic peptides are established biomarkers related to the prognosis of heart failure. New biomarkers have emerged in the field of cardiovascular disease. The prognostic value of these biomarkers in heart failure with reduced left ventricular ejection fraction is not well-established. We conducted a prospective, single-centre study, including (July 2019 to March 2023) 104 patients being consecutively admitted with a diagnosis of acute heart failure with reduced ejection fraction decompensation. The median follow-up was 23.5 months, during which 20 deaths (19.4%) and 21 readmissions for heart failure (20.2%) were recorded. Plasma biomarkers, such as NT-proBNP, GDF-15, sST2, suPAR, and FGF-23, were associated with an increased risk of all-cause mortality. However, a Cox regression analysis showed that the strongest predictors of mortality were an estimated glomerular filtration rate (HR 0.96 [0.93–0.98]), GDF-15 (HR 1.3 [1.16–1.45]), and sST2 (HR 1.2 [1.11–1.35]). The strongest predictive model was formed by the combination of the glomerular filtration rate and sST2 (C-index 0.758). In conclusion, in patients with acute decompensated heart failure with reduced ejection fraction, GDF-15 and sST2 showed the highest predictive power for all-cause mortality, which was superior to other established biomarkers such as natriuretic peptides. GDF-15 and sST2 may provide additional prognostic information to improve the prognostic assessment.

(1) Background: The validation of new lines of therapy for the elderly is required due to the progressive ageing of the world population and scarce evidence in elderly patients with HF with reduced ejection fraction (HFrEF). The purpose of our study is to analyze the effect of SGLT2 inhibitors (SGLT2i) in this subgroup of patients. (2) Methods: A single-center, real-world observational study was performed. We consecutively enrolled all patients aged ≥ 75 years diagnosed with HFrEF and for treatment with SGLT2i, and considered the theoretical indications. (3) Results: A total of 364 patients were recruited, with a mean age of 84.1 years. At inclusion, the mean LVEF was 29.8%. Median follow-up was 33 months, and there were 122 deaths. A total of 55 patients were under SGLT2i treatment. A multivariate Cox logistic regression test for all-cause mortality was performed, and only SGLT2i (HR 0.39 [0.19–0.82]) and glomerular filtration rate (HR 0.98 [0.98–0.99]) proved to be protective factors. In parallel, we conducted a propensity-score-matched analysis, where a significant reduction in all-cause mortality was associated with the use of SGLT2i treatment (HR 0.39, [0.16–0.97]). (4) Conclusions: Treatment with SGLT2i in elderly patients with HFrEF was associated with a lower rate of all-cause mortality. Our data show that SGLT2i therapy could improve prognosis in the elderly with HFrEF in a real-world study.