Abstract

An overactive sympathetic nervous system is a hallmark characteristic of heart failure (HF). Recent studies in pacing-induced HF rabbits have indicated that statin therapy reduces sympathetic nerve activity (SNA). The present study was designed to determine whether these findings in experimental HF can be translated to the clinical setting of human HF. We hypothesized that statin therapy reduces SNA in HF patients. Five statin-naĂŻve HF patients (NYHA class I and II) with a mean ejection fraction of 34±5 %, age of 54±2, and body mass index of 34±4 kg/m2 were studied before and after one month of Simvastatin (40 mg/day). Muscle SNA (microneurography), blood pressure (BP), heart rate, and cholesterol were measured. Treatment with Simvastatin significantly reduced resting muscle SNA from 77±2 to 65±6 bursts/100 heart beats (P=0.034). Importantly, although variable amongst subjects, all 5 patients exhibited a decrease in muscle SNA (range of −9 to −27 bursts/100 heart beats). Mean BP tended to be lower after Simvastatin, primarily due to a significant reduction in diastolic BP (81±7 to 72±6 mmHg). As expected, cholesterol was reduced by Simvastatin. In summary, short-term statin therapy reduces resting sympathetic outflow in HF patients. These preliminary findings suggest that in addition to lowering cholesterol, statins may also be beneficial in reducing sympathetic overactivity in HF patients. Supported by U of Missouri RB #3301

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