INTRODUCTION Acute kidney injury (AKI) during hospitalization is associated with increased mortality in patients with acute heart failure (AHF). In 2016, the European Society of Cardiology introduced the category of heart failure (HF) with mid-range ventricular ejection fraction (HFmrEF) as a distinct category from HF with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF). OBJECTIVES The aim of this study was to evaluate in-hospital mortality risk associated with AKI in patients with AHF, with a focus on the HFmrEF group. PATIENTS AND METHODS A total of 365 health records of patients with a primary diagnosis of acute decompensated heart failure (ADHF) were reviewed. AKI was defined according to Acute Kidney Injury Network criteria. HF was diagnosed based on Framingham criteria. Patients with ADHF were evaluated as 3 separate groups, based on ventricular ejection fraction: HFpEF (≥50%), HFmrEF (40%-49%), and HFrEF (<40%). Risk and survival analyses were conducted on de-identified data. RESULTS The AKI-associated in-hospital mortality odds ratios for HFmrEF and HFrEF groups were 4.55 (95% CI, 1.46-14.18) and 2.59 (95% CI, 1.05-6.41), respectively, with a highly significant difference between the groups (P = 0.002; Mantel-Haenszel test). The hazard ratios in the Cox proportional hazards model were 4.79 (95% CI, 1.54-14.96) and 2.94 (95% CI, 1.27-6.80) for HFmrEF and HFrEF groups, respectively. CONCLUSIONS AKI was associated with a higher risk of mortality in patients with HFmrEF when compared with those with HFrEF, suggesting a stronger prognostic impact of AKI in patients with HFmrEF.

Heart failure is a disease affecting millions of patients each year, and is responsible for burdening the world with high mortality rates. More concerns come from its numerous hospital readmissions (with an estimated number of 2.6 million per year which makes it one of the leading diseases responsible for national healthcare expenditures). Despite drastic improvement of therapies in recent years, heart failure remains a progressive disease. Thus, more attention has been given to finding potential biomarkers involved in the pathological mechanisms of this disease that would potentially lead to faster diagnosis and improved prognosis. One of the emerging biomarkers that has just recently come into the spotlight is galectin-3. It was associated in recent clinical trials with both the progression and severity of heart failure. Ventricular remodelling and myocardial fibrosis are essential for heart failure development and are linked to poor outcomes. An ever-growing body of evidence places galectin-3 as an important link between inflammation and fibrosis, which play a prominent role in cardiac remodelling.This review sums up the most relevant experimental and clinical studies about galectin-3 and its potential prognostic value in heart failure. The article also provides a better understanding of this molecule's involvement in heart failure pathology by modulating cardiac fibrosis. It also weighs whether the available data on galectin-3 are consistent enough to reduce readmissions and mortality while improving diagnosis and future therapies for heart failure, versus the possibility that it is simply"another brick in the wall?"

BackgroundHeart failure is accompanied by abnormalities in ventricular-vascular interaction due to increased myocardial and arterial stiffness. Galectin-3 is a recently discovered biomarker that plays an important role in myocardial and vascular fibrosis and heart failure progression.ObjectivesThe aim of this study was to determine whether galectin-3 is correlated with arterial stiffening markers and impaired ventricular-arterial coupling in decompensated heart failure patients.MethodsA total of 79 inpatients with acute decompensated heart failure were evaluated. Serum galectin-3 was determined at baseline, and during admission, transthoracic echocardiography and measurements of vascular indices by Doppler ultrasonography were performed.ResultsElevated pulse wave velocity and low arterial carotid distensibility are associated with heart failure in patients with preserved ejection fraction (p = 0.04, p = 0.009). Pulse wave velocity, carotid distensibility and Young’s modulus did not correlate with serum galectin-3 levels. Conversely, raised galectin-3 levels correlated with an increased ventricular-arterial coupling ratio (Ea/Elv) p = 0.047, OR = 1.9, 95% CI (1.0‑3.6). Increased galectin-3 levels were associated with lower rates of left ventricular pressure rise in early systole (dp/dt) (p=0.018) and raised pulmonary artery pressure (p = 0.046). High galectin-3 levels (p = 0.038, HR = 3.07) and arterial pulmonary pressure (p = 0.007, HR = 1.06) were found to be independent risk factors for all-cause mortality and readmissions.ConclusionsThis study showed no significant correlation between serum galectin-3 levels and arterial stiffening markers. Instead, high galectin-3 levels predicted impaired ventricular-arterial coupling. Galectin-3 may be predictive of raised pulmonary artery pressures. Elevated galectin-3 levels correlate with severe systolic dysfunction and together with pulmonary hypertension are independent markers of outcome.

Galectin-3 can predict long-term mortality in patients with AHF. The results of our study suggest a possible relation between left ventricular remodeling and increasing galectin-3 levels.

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