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Atorvastatin therapy improves endothelial-dependent vasodilation in patients with systemic lupus erythematosus: an 8
G A Ferreira1, T P Navarro, R W Telles
1Rheumatology Division, Universidade Federal de São Paulo-Escola Paulista de Medicina, São Paulo, Brazil.
Insights
Atorvastatin significantly improved blood vessel function in systemic lupus erythematosus (SLE) patients, enhancing vasodilation regardless of traditional coronary heart disease risk factors. This study highlights atorvastatin
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Pharmacology
Background:
- Systemic lupus erythematosus (SLE) is associated with impaired endothelium-dependent vasodilation.
- Statins may improve endothelial function independent of their lipid-lowering effects.
Purpose of the Study:
- To assess atorvastatin's efficacy in enhancing vasodilation in SLE patients.
- To determine if atorvastatin's effects differ based on the presence of conventional coronary heart disease (CHD) risk factors.
Main Methods:
- Sixty-four SLE women received atorvastatin (20 mg/day) for 8 weeks.
- Patients were stratified by the presence (n=33) or absence (n=31) of CHD risk factors.
- Brachial artery diameter was measured using high-resolution ultrasound at baseline and 8 weeks, assessing resting, reactive hyperemia, and nitroglycerin-mediated dilation.
Main Results:
- Atorvastatin significantly increased flow-mediated dilation (FMD) from 3.8% to 6.9% (P < 0.001).
- This improvement in FMD was observed in both patients with and without conventional CHD risk factors.
- Resting brachial artery diameter also increased significantly in the atorvastatin group, unlike in the control group.
Conclusions:
- Atorvastatin (20 mg/day) effectively improved endothelium-dependent vasodilation in SLE patients over 8 weeks.
- The beneficial effects on vasodilation were independent of conventional atherosclerotic disease risk factors.
Introduction:
Patients with systemic lupus erythematosus (SLE) have recognized reduction in endothelium-dependent vasodilation. Evidence demonstrates that statins are able to improve endothelial function independently on their hypolipemic action.
Objectives:
To evaluate the efficacy of atorvastatin in improving vasodilation in SLE patients with and without conventional risk factors for coronary heart disease (CHD).
Patients And Methods:
Sixty-four SLE women, mean age 31 +/- 8 yrs, received atorvastatin 20 mg/day during 8 weeks. Thirty-one patients in this intervention group did not have conventional risk factors for CHD, while 33 others had hypertension, dyslipidaemia and/or obesity. Twenty-four SLE control patients, mean age 34 +/- 7.5 yrs, not receiving atorvastatin were followed during the same time period. High-resolution ultrasound was used to measure brachial artery diameter in resting conditions, during reactive hyperaemia and after sub-lingual glyceryl trinitrate (GTN). Measurements were performed at baseline and at the end of the study (8 weeks).
Results:
Atorvastatin was associated with a significant increase in flow-mediated dilation (FMD) [3.8 (2.8-7.9%) vs 6.9 (4.2-10.7%), P < 0.001] while GTN-mediated dilation (GTND) was unaffected [20.9 (16.6-26.1%) vs 20.1(16.6-25.4%), P = 0.514]. FMD increase was observed in patients with conventional risk factors [4.1 (3.1-8.7%) vs 6.5 (4-10%), P = 0.046] and also for those without conventional risk factors for CHD [3.6 (2.6-7.3%) vs 7.1 (4.5-10.9%), P = 0.001]. Resting brachial artery diameter also increased significantly in patients receiving atorvastatin (2.79 +/- 0.30 mm vs 2.92 +/- 0.40 mm, P < 0.001). No significant difference in artery diameter and FMD was seen in control patients at the end of the study. When compared to the control patients, atorvastatin treatment was associated with significant increase in resting diameter (+0.13 +/- 0.1 mm vs -0.02 +/- 0.07 mm, P < 0.001) and FMD (+1.9 +/- 3.9% vs -0.3 +/- 1.8%, P = 0.009).
Conclusion:
Our results demonstrate that an 8-week 20 mg/day atorvastatin series improved endothelium-dependent vasodilation in SLE patients independently on the presence of conventional risk factors for atherosclerotic disease.
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