Abstract 2404: Sympathetic Cardiorenal Interaction Becomes Exaggerated When Cardiac and Renal Functions Are Both Deteriorated
The pathophysiology of the cardiorenal interaction remains poorly understood. We tested the hypothesis that renal insufficiency (RI) and cardiac dysfunction would contribute to the elevated sympathetic activity in patients with heart failure. In 79 patients with heart failure (ejection fraction (EF) < 0.45), the resting muscle nerve sympathetic activity (MSNA), plasma norepinephrine (NE), brain natriuretic peptide (BNP) were determined. Estimated glomerular filtration rates (eGFR) less than 60ml/min/1.73m2 measured by simplified Modification of Diet in Renal Disease equation for Japanese was used to identify RI. Although NE and BNP were comparable between RI group (n = 30, eGFR 45 ± 10) and no RI group (n = 49, eGFR 76 ± 10), MSNA was higher in RI group (burst rate, 54 ± 14 versus 46 ± 14 bursts/minute, p < 0.05; burst incidence, 77 ± 19 versus 68 ± 18 bursts/100beats, p < 0.05). For patients with preserved EF (≥ 0.30), MSNA was similar between those with and without RI, while for patients with low EF (< 0.30), MSNA was significantly higher in those with RI than in those without RI (burst rate, 62 ± 10 versus 49 ± 15 bursts/minute, p < 0.01; burst incidence, 88 ± 12 versus 68 ± 18 bursts/ 100beats, p < 0.01). The difference of MSNA between patients with low EF and with preserved EF was significantly greater in RI group than in no RI group (interaction, p < 0.05). These findings suggest that sympathetic cardiorenal interaction might become exaggerated when cardiac and renal functions are both deteriorated.