Background and Aim: The increasing prevalence and high hospitalization rates make atrial fibrillation (AF) a significant healthcare strain. However, there are limited data regarding the length of hospital stay (LOS) of AF patients. Our purpose was to determine the main drivers of extended LOS of AF patients. Methods: All AF patients, hospitalized consecutively in a tertiary cardiology center, from January 2018 to February 2020 were included in this retrospective cohort study. Readmissions were excluded. Prolonged LOS was defined as more than seven days (the upper limit of the third quartile). Results: Our study included 949 AF patients, 52.9% females. The mean age was 72.5 ± 10.3 years. The median LOS was 4 days. A total of 28.7% had an extended LOS. Further, 82.9% patients had heart failure (HF). In multivariable analysis, the independent predictors of extended LOS were: acute coronary syndromes (ACS) (HR 4.60, 95% CI 1.66–12.69), infections (HR 2.61, 95% CI 1.44–3.23), NT-proBNP > 1986 ng/mL (HR 1.96, 95% CI 1.37–2.82), acute decompensated HF (ADHF) (HR 1.76, 95% CI 1.23–2.51), HF with reduced ejection fraction (HFrEF) (HR 1.69, 95% CI 1.15–2.47) and the HAS-BLED score (HR 1.42, 95% CI 1.14–1.78). Conclusion: ACS, ADHF, HFrEF, increased NT-proBNP levels, infections and elevated HAS-BLED were independent predictors of extended LOS, while specific clinical or therapeutical AF characteristics were not.

Heart failure with preserved ejection fraction (HFpEF) represents a complex clinical syndrome, often very difficult to diagnose using the available tools. As the global burden of this disease is constantly growing, surpassing the prevalence of heart failure with reduced ejection fraction, during the last few years, efforts have focused on optimizing the diagnostic and prognostic pathways using an immense panel of circulating biomarkers. After the paradigm of HFpEF development emerged more than 10 years ago, suggesting the impact of multiple comorbidities on myocardial structure and function, several phenotypes of HFpEF have been characterized, with an attempt to find an ideal biomarker for each distinct pathophysiological pathway. Acknowledging the limitations of natriuretic peptides, hundreds of potential biomarkers have been evaluated, some of them demonstrating encouraging results. Among these, soluble suppression of tumorigenesis-2 reflecting myocardial remodeling, growth differentiation factor 15 as a marker of inflammation and albuminuria as a result of kidney dysfunction or, more recently, several circulating microRNAs have proved their incremental value. As the number of emerging biomarkers in HFpEF is rapidly expanding, in this review, we aim to explore the most promising available biomarkers linked to key pathophysiological mechanisms in HFpEF, outlining their utility for diagnosis, risk stratification and population screening, as well as their limitations.

Background/Objectives: The coexistence of heart failure (HF) and chronic kidney disease (CKD) complicates management and worsens prognosis. NT-proBNP is a recognized biomarker for HF diagnosis and prognosis, yet its interpretation in CKD can be challenging due to confounding factors increasing its levels. This study aimed to evaluate the predictive value of NT-proBNP for all-cause long-term mortality in HF patients across various stages of renal dysfunction. Methods: Hospitalized HF patients were included in this observational, retrospective analysis. NT-proBNP levels and serum creatinine were measured on admission. The primary outcome was all-cause mortality. Patients were divided into three groups according to renal function estimated using the CKD-EPI formula: eGFR1 (>60 mL/min/1.73 m²), eGFR2 (30–60 mL/min/1.73 m²) and eGFR3 (<30 mL/min/1.73 m²). Results: The study included 716 HF patients with a mean age of 71 ± 10 years, 49% males. All-cause long-term mortality was 35% after a median follow-up of 59 months. The mortality rate increased from 29% in eGFR1 patients, to 43% in eGFR2, to 68% in eGFR3. Median NT-proBNP increased from 997 pg/mL in eGFR1 patients to 1586 pg/mL in eGFR2 to 4928 pg/mL in eGFR3. Cut-off values for predicting all-cause long-term mortality were NT-proBNP >1837 pg/mL in eGFR1 patients, >1413 pg/mL in eGFR2 and >6415 pg/mL in eGFR3. In multivariable Cox analysis, NT-proBNP was an independent predictor of all-cause long-term mortality in all eGFR groups. Conclusions: NT-proBNP on admission was an independent predictor of long-term all-cause mortality in hospitalized HF patients across all eGFR subgroups, with increasing cut-off levels in patients with renal dysfunction.

Background and Aim: Atrial fibrillation (AF) is an epidemic disease with a significant global health impact. Atrial functional tricuspid regurgitation (AF-TR) is a more recently acknowledged complication of AF. The main purpose of this study was to determine the prognostic value of severe AF-TR in patients with AF, and its determinants. Methods: In this retrospective, observational study, we included AF patients admitted consecutively to a tertiary clinical hospital between January 2018 and February 2020, irrespective of cause of hospitalization. Patients with organic TR, significant pulmonary hypertension, left ventricular ejection fraction < 50%, those with implanted cardiac devices and those with in-hospital mortality were excluded. Severe TR was defined according to current guidelines. Median follow-up time was 34 (28–39) months. Primary endpoint was all-cause mortality. Results: We included 246 AF patients, with a mean age of 71.5 ± 9.4 years. 86.2% had AF-TR, while 8.1% had severe AF-TR. Mortality rate was 8.5%. Right atrial diameter (p = 0.005), systolic pulmonary artery pressure (sPAP) (p = 0.015) and NT-proBNP (p = 0.026) were independent predictors for the presence of severe valvular dysfunction. In multivariable survival analysis, severe AF-TR, was an independent predictor of all-cause mortality (HR 5.4, 95% CI 1.1–26.2, p = 0.035). Conclusion: Severe AF-TR was an independent predictor of mortality in AF patients, while mild/moderate AF-TR apparently had no impact on prognosis.