ABSTRACT
INTRODUCTION: NT-proBNP, a well-established diagnostic and prognostic marker in clinical practice, is significantly elevated in individuals with atrial fibrillation (AF), even in absence of heart failure or major structural heart disease. OBJECTIVES: The aim of this study was to determine the cut-off value of NT-proBNP for diagnosis of heart failure in individuals with atrial fibrillation. METHODS: We compared 44 patients (25 male/19 female) with AF and concomitant overt heart failure [age 76 (62-82) years; median (interquartile range - IQR)] versus 29 patients (16 male/13 female) with AF with no signs of heart failure [age 59 (50-67) years; median (IQR)]. We considered the underlying causes of heart failure and its severity, comorbidities, echocardiographic and selected laboratory parameters, the body mass index as well as the treatment at discharge. We determined the cut-off value for heart failure and major structural heart disease using ROC curve analysis. RESULTS: Median NT-proBNP in the group of patients with AF and concomitant heart failure was 3 218 ng/l (IQR 1 758-7 480 ng/l) vs 981 ng/l (IQR 431-1 685 ng/l) in the group of patients with AF with no signs of heart failure; this difference was statistically significant (p < 0.001). The level of NT-proBNP higher than 1 524 ng/l in patients with AF was diagnostic of major structural heart disease and pointed towards a possible heart failure (sensitivity 80%, specificity of 76%, accuracy 78%, positive predictive value 83%, negative predictive value 71%). The NT-proBNP levels significantly correlated with age (p < 0.001), left atrial diameter (p < 0.01) and furosemide dose at discharge (p < 0.05). The NT-proBNP levels significantly negatively correlated with left ventricular ejection fraction (p < 0.001) and body mass index (p < 0.05). CONCLUSION: We found out that NT-proBNP is significantly elevated in patients with AF with preserved left ventricular function and in absence of heart failure and significantly correlates with age, left ventricular ejection fraction, left atrial diameter, body mass index and the furosemide dose necessary to achieve cardiac compensation. Furthermore, we determined the NT-proBNP cut-offvalue predictive of a possible heart failure in patients with AF.
Subject(s)
Atrial Fibrillation/blood , Heart Failure/complications , Natriuretic Peptide, Brain/blood , Peptide Fragments/blood , Aged , Aged, 80 and over , Atrial Fibrillation/etiology , Atrial Fibrillation/physiopathology , Biomarkers/blood , Female , Heart Failure/diagnosis , Heart Failure/physiopathology , Humans , Male , Middle Aged , Stroke Volume , Ventricular Function, LeftABSTRACT
Albuminuria is a dominant biochemical feature of developing diabetic nephropathy. A disturbed metabolism of heparan sulphate characterized by an increased loss of anionic charges in the basement membrane has been considered as one of the main factors causing an increased albumin output into urine. All therapeutic approaches inducing a reduction of the albumin excretion rate (AER) have a protective effect on renal function. The effect of glycosaminoglycan sulodexide on albuminuria was studied in a group of 53 diabetic patients (26 Type 1 and 27 Type 2) with micro and macroalbuminuria. Sulodexide (Vessel Due F) was administered intramuscularly in one daily dose (600 lipasemic units) for 3 weeks followed by a 6 week wash-out period. A significant decrease of AER was found in a total cohort of patients following just 1 week of sulodexide treatment (mean 162 micrograms/min, range 10-2708 micrograms/min vs mean 248 micrograms/min, range 20-3160 micrograms/min, P < 0.001). This effect lasted 3-6 weeks after drug withdrawal. Similar results were obtained if Type 1 and Type 2 diabetic patients were evaluated separately but a delay of the AER reduction was observed in the latter group. In all patients the mean AER was reduced to 60-65% of the initial values. A greater effect of sulodexide on albuminuria was observed in patients with AER above 200 micrograms/min than in those with microalbuminuria (a reduction to 47 vs 65% of the initial output). Sulodexide did not significantly reduce albuminuria in 28% of diabetic patients ('non-responders'). In conclusion, glycosaminoglycan sulodexide may reduce AER in patients with micro or macroalbuminuria and it could slow down development of diabetic nephropathy.