Cardiorenal syndrome in acute decompensated systolic heart failure

Abstract

Acute decompensated heart failure (ADHF) is a growing health problem worldwide. In Hong Kong, ADHF is one of the major causes of hospitalization with a dramatic surge of incidence after the age of 65.Inthe recent decades, the phenomenon of cardiorenal syndrome (CRS), the acute deterioration in renal function in the context of ADHF has been increasingly recognised. Epidemiological studies revealed that one-fourth to one-third of systolic heart failure patients developed CRS and that CRS was a significant predictor of morbidity and mortality in ADHF. The pathophysiology of CRS is multifactorial, with a complex interaction between haemodynamics, neuro-hormonal activation, inflammatory changes and use of pharmacological agents. However, data regarding the acute changes of haemodynamics and volume status in ADHF patients is limited. Little is known about ways to predict and prevent the worsening of kidney function. Hence, the goals of this study are to elucidate the serial changes of haemodynamics, fluid distribution, biomarkers including B-type natriuretic peptide (BNP) and neutrophil gelatinase-associated lipocalin (NGAL), to investigate the relationship between these variables and renal function, and to identify associated predictors of the development of CRS. In this study, 51 patients admitted for ADHF were recruited. They were assessed for three consecutive days and prospectively followed up for 60days. Data pertaining to baseline demographics, medications, fluid intake and output were acquired from clinical records. Our study had shown a high incidence of CRS (35.3%) in ADHF. Moreover, we demonstrated that more significant basal hypervolemia and venous congestion were protective from worsening renal function. Patients without CRS had a higher ratio of early transmitral inflow velocity to early diastolic mitral annular velocity (E:E’), lower inferior vena cava collapsibility index (IVCCI)and higher BNP level at baseline. We observed significant difference in ratio of extracellular water to total body water (ECW:TBW) but not in baseline body weight and TBW in patients who developed CRS comparing to those who did not. In addition, more marked reduction in blood pressure and sodium concentration was associated with creatinine rise. Of note, baseline serum creatinine and NGAL did not correlate with creatinine change. Furthermore, we found that non-prescription of mineralocorticoid blocker, higher IVCCI, lower E:E’, lower BNP and lower ECW:TBW predicted occurrence of CRS. BNP and E:E’ remained independent predictors of CRS in the multivariable analysis. Among these predictors, ECW:TBW had the best performance with the greatest area under receiver operating characteristic curve. The optimal cut-off value for ECW:TBW to predict CRS was ≤0.404 (sensitivity = 66.7% and specificity =75.0%). No significant difference in clinical outcomes was observed. In summary, CRS is prevalent in acute decompensated systolic heart failure. This study highlights the importance of fluid assessment and blood pressure control in the management of ADHF patients.