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Sympathoinhibitory effect of statins in chronic heart failure
Marc E Gomes1, Jacques W M Lenders, Louise Bellersen
1Department of Cardiology, University Medical Center Nijmegen, Nijmegen, The Netherlands. mergomes@hotmail.com
Insights
Statin therapy significantly reduces central sympathetic outflow in patients with chronic heart failure (CHF). This reduction in muscle sympathetic nerve activity (MSNA) suggests a beneficial effect of statins in managing CHF.
Area of Science:
- Cardiology
- Neuroscience
- Pharmacology
Background:
- Increased central sympathetic activity is a hallmark of chronic heart failure (CHF), correlating with poorer patient prognosis.
- Preclinical studies indicate that statin therapy may attenuate central sympathetic outflow.
Purpose of the Study:
- To investigate the direct effects of statin therapy on central sympathetic activity in human patients with chronic heart failure (CHF).
Main Methods:
- Muscle sympathetic nerve activity (MSNA) was directly measured using microneurography in eight CHF patients.
- Measurements were taken during periods of statin discontinuation and after statin therapy restart over 8 and 4 weeks, respectively.
- Arterial plasma norepinephrine concentrations were also assessed.
Main Results:
- Statin discontinuation led to a significant increase in MSNA burst frequency and amplitude.
- Total normalized MSNA was markedly higher after statin withdrawal compared to during statin therapy.
- No significant changes were observed in arterial plasma norepinephrine levels or blood pressure.
Conclusions:
- Statin therapy effectively inhibits central sympathetic outflow in patients suffering from chronic heart failure (CHF).
- The findings demonstrate a direct sympatholytic effect of statins in this patient population, measured via MSNA.
Objectives:
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.
Methods:
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.
Results:
During discontinuation of statin therapy, MSNA was significantly increased (73 +/- 4 vs. 56 +/- 5 and 52 +/- 6 bursts/100 beats, p = 0.01). Burst frequency was significantly higher after statin discontinuation (42 +/- 3 burst/min without statin vs. 32 +/- 3 and 28 +/- 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 +/- 0.04 without statin vs. 0.29 +/- 0.04 and 0.22 +/- 0.04 during statin, p < 0.05; total normalized MSNA 15.70 +/- 2.78 without statin, vs. 9.28 +/- 1.41 and 6.56 +/- 1.83 during statin, p = 0.009). Arterial plasma norepinephrine levels and blood pressure were unaffected.
Interpretation:
Statin therapy inhibits central sympathetic outflow in CHF patients, as measured by MSNA.
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