Cardiac Sympathetic Responses to Acute Vasodilation

Abstract

Background Although there is indirect evidence of impaired baroreflex control of sympathetic outflow directed at heart muscle, the regulation of cardiac sympathetic activity in the setting of heart failure is largely unexplored. We used the norepinephrine spillover method to address the hypothesis that baroreflex control of cardiac sympathetic activity is reduced in heart failure. Methods and Results Twenty-three patients were studied, 17 in a group with heart failure and 6 in a group with normal ventricular function. In both groups, cardiac norepinephrine spillover was assessed in response to nitroprusside infused to steady-state conditions. Nitroprusside resulted in significant reductions in mean systemic arterial pressure (normal group, −15±3% [mean±SEM]; heart failure group, −13±1%) and mean pulmonary artery pressure (normal group, −25±10%; heart failure group, −29±4%). In response to nitroprusside, there was a 98±16% increase in cardiac norepinephrine spillover in the normal group (from 81±10 to 159±25 pmol/min, P <.05). Despite similar hemodynamic responses to nitroprusside in the heart failure group, there was only a 28±14% increase in cardiac spillover (from 211±71 to 245±59 pmol/min, P =NS), a response that was significantly smaller than that seen in the normal group. Conclusions In patients with heart failure compared with subjects with normal ventricular function, there was a significantly smaller increase in cardiac sympathetic activity in response to a steady-state infusion of nitroprusside. This result provides evidence for reduced baroreflex control of cardiac sympathetic activity in heart failure.