Sympathoinhibitory effect of statins in chronic heart failure

Increased (central) sympathetic activity is a key feature of heart failure and associated with worse prognosis. Animal studies suggest that statin therapy can reduce central sympathetic outflow. This study assessed statin effects on (central) sympathetic activity in human chronic heart failure (CHF) patients. Sympathetic activity was measured in eight patients with CHF patients during 8 weeks after discontinuation and 4 weeks after restart of statin therapy by microneurography for direct muscle sympathetic nerve recording (MSNA) and measurement of arterial plasma norepinephrine concentrations. During discontinuation of statin therapy, MSNA was significantly increased (73 +/- A 4 vs. 56 +/- A 5 and 52 +/- A 6 bursts/100 beats, p = 0.01). Burst frequency was significantly higher after statin discontinuation (42 +/- A 3 burst/min without statin vs. 32 +/- A 3 and 28 +/- A 3 burst/min during statin therapy, p = 0.004). Mean normalized burst amplitude and total normalized MSNA were significantly higher after statin discontinuation (mean normalized burst amplitude 0.36 +/- A 0.04 without statin vs. 0.29 +/- A 0.04 and 0.22 +/- A 0.04 during statin, p < 0.05; total normalized MSNA 15.70 +/- A 2.78 without statin, vs. 9.28 +/- A 1.41 and 6.56 +/- A 1.83 during statin, p = 0.009). Arterial plasma norepinephrine levels and blood pressure were unaffected. Statin therapy inhibits central sympathetic outflow in CHF patients, as measured by MSNA.