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Recent data from national registries suggest that acute heart failure (AHF) outcomes might vary in men and women, however, it is not known whether this observation is universal. The aim of this study was to evaluate the association of biological sex and 1-year all-cause mortality in patients with AHF in various regions of the world. We analysed several AHF cohorts including GREAT registry (22 523 patients, mostly from Europe and Asia) and OPTIMIZE-HF (26 376 patients from the USA). Clinical characteristics and medication use at discharge were collected. Hazard ratios (HRs) for 1-year mortality according to biological sex were calculated using a Cox proportional hazards regression model with adjustment for baseline characteristics (e.g. age, comorbidities, clinical and laboratory parameters at admission, left ventricular ejection fraction). In the GREAT registry, women had a lower risk of death in the year following AHF [HR 0.86 (0.79–0.94), P < 0.001 after adjustment]. This was mostly driven by northeast Asia [n = 9135, HR 0.76 (0.67–0.87), P < 0.001], while no significant differences were seen in other countries. In the OPTIMIZE-HF registry, women also had a lower risk of 1-year death [HR 0.93 (0.89–0.97), P < 0.001]. In the GREAT registry, women were less often prescribed with a combination of angiotensin-converting enzyme inhibitors and beta-blockers at discharge (50% vs. 57%, P = 0.001). Globally women with AHF have a lower 1-year mortality and less evidenced-based treatment than men. Differences among countries need further investigation. Our findings merit consideration when designing future global clinical trials in AHF.

The present meta-analysis aimed to evaluate effects of tolvaptan on fluid retention in patients with heart failure who were non-responsive to conventional treatment and to assess differences between effects of low (≤ 15 mg/day) and high (> 15 mg/day) tolvaptan doses.Randomized controlled trials comparing add-on tolvaptan therapy and placebo or therapy with other diuretics in patients with heart failure were identified through a database search. The primary outcomes were changes in body weight and urine volume, and the secondary outcomes were changes in serum sodium and creatinine levels.In total, 14 reports were analyzed using a random effects model. Add-on tolvaptan was associated with increased urine volume [mean difference (MD), 1.44 L; 95% confidence interval (CI), 0.96 to 1.92], decreased body weight (MD, -0.99 kg; 95% CI, -1.24 to -0.74), and increased serum sodium levels (MD, 3.66 mEq/L; 95% CI, 3.43 to 3.88) within 2 days. Serum creatinine levels on day 7 were not different between the groups (MD, -0.03 mg/dL; 95% CI, -0.09 to 0.03). The high-dose group showed greater changes in urine volume, body weight, and serum sodium levels than the low-dose group. Serum creatinine levels slightly increased in the high-dose group (MD, 0.06; 95% CI, 0.04 to 0.08) and slightly decreased in the low-dose group (MD, -0.10; 95% CI, -0.19 to -0.01).Our findings suggest that add-on tolvaptan therapy for heart failure improves fluid retention in the early therapy phase. However, this drug should be properly used to avoid the worsening of renal function, which may occur at high doses.

Agents with vasodilator properties (AVDs) are frequently used in the treatment of acute heart failure (AHF). AVDs rapidly reduce preload and afterload, improve left ventricle to aorta and right ventricle to pulmonary artery coupling, and may improve symptoms. Early biomarker changes after AVD administration have suggested potentially beneficial effects on cardiac stretch, vascular tone, and renal function. AVDs that reduce haemodynamic congestion without causing hypoperfusion might be effective in preventing worsening organ dysfunction. Existing AVDs have been associated with different results on outcomes in randomized clinical trials, and observational studies have suggested that AVDs may be associated with a clinical outcome benefit. Lessons have been learned from past AVD trials in AHF regarding preventing hypotension, selecting the optimal endpoint, refining dyspnoea measurements, and achieving early randomization and treatment initiation. These lessons have been applied to the design of ongoing pivotal clinical trials, which aim to ascertain if AVDs improve clinical outcomes. The developing body of evidence suggests that AVDs may be a clinically effective therapy to reduce symptoms, but more importantly to prevent end-organ damage and improve clinical outcomes for specific patients with AHF. The results of ongoing trials will provide more clarity on the role of AVDs in the treatment of AHF.