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Abstract 2458: Atorvastatin Reduces Sympathetic Activity in Hypertensive Patients
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Background
In hypertension, a state of increased (central) sympathetic activity exists. This high sympathetic activity is associated with worse prognosis and refractoriness to pharmacological interventions. Animal experimental data suggest that HMG CoA reductase inhibitors (statins) can reduce sympathetic activity at a central level. We hypothesized that atorvastatin 80 mg/day could reduce sympathetic activity in human patients with hypertension.
Methods
Using a prospective, randomized, placebo-controlled, double-blind, cross-over design, patients were randomly assigned to atorvastatin 80 mg/day or placebo, for 3 weeks. Sympathetic nervous system activity was measured at the end of each treatment period, in 13 patients with mild to moderate hypertension by microneurography for direct muscle sympathetic nerve recording (MSNA) and plasma norepinephrine concentrations. Effects on blood pressure were assessed by 24 hour ambulatory blood pressure measurement.
Results
Atorvastatin significantly reduced MSNA (atorvastatin: 58.5±2.0 vs. placebo: 64.7±3.0 bursts/100 beats, P=0.02). Although MSNA values and plasma cholesterol levels were correlated, reduction in MSNA was independent of the degree of reduction in plasma cholesterol. Atorvastatin had no effect on plasma norepinephrine levels nor on daytime and night time blood pressure.
Conclusion:
In patients with mild to moderate hypertension, atorvastatin treatment reduces central sympathetic nervous outflow. This finding supports the concept that HMG CoA reductase regulates sympathetic nervous system activity at the central level and indicates a sympathoinhibitory role for atorvastatin in human hypertensive patients.
Ovid Technologies (Wolters Kluwer Health)
Title: Abstract 2458: Atorvastatin Reduces Sympathetic Activity in Hypertensive Patients
Description:
Background
In hypertension, a state of increased (central) sympathetic activity exists.
This high sympathetic activity is associated with worse prognosis and refractoriness to pharmacological interventions.
Animal experimental data suggest that HMG CoA reductase inhibitors (statins) can reduce sympathetic activity at a central level.
We hypothesized that atorvastatin 80 mg/day could reduce sympathetic activity in human patients with hypertension.
Methods
Using a prospective, randomized, placebo-controlled, double-blind, cross-over design, patients were randomly assigned to atorvastatin 80 mg/day or placebo, for 3 weeks.
Sympathetic nervous system activity was measured at the end of each treatment period, in 13 patients with mild to moderate hypertension by microneurography for direct muscle sympathetic nerve recording (MSNA) and plasma norepinephrine concentrations.
Effects on blood pressure were assessed by 24 hour ambulatory blood pressure measurement.
Results
Atorvastatin significantly reduced MSNA (atorvastatin: 58.
5±2.
0 vs.
placebo: 64.
7±3.
0 bursts/100 beats, P=0.
02).
Although MSNA values and plasma cholesterol levels were correlated, reduction in MSNA was independent of the degree of reduction in plasma cholesterol.
Atorvastatin had no effect on plasma norepinephrine levels nor on daytime and night time blood pressure.
Conclusion:
In patients with mild to moderate hypertension, atorvastatin treatment reduces central sympathetic nervous outflow.
This finding supports the concept that HMG CoA reductase regulates sympathetic nervous system activity at the central level and indicates a sympathoinhibitory role for atorvastatin in human hypertensive patients.
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