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Traditional risk factor assessment does not capture the extent of cardiovascular risk in systemic lupus erythematosus
A B Lee1, T Godfrey, K G Rowley
1Department of Medicine, The University of Melbourne, St. Vincent's Hospital, Melbourne, Victoria, Australia.
Insights
Systemic lupus erythematosus (SLE) patients show impaired endothelial function and higher cardiovascular risk factors, indicating increased atherosclerosis vulnerability. Traditional risk factor assessments may be insufficient for SLE patients.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Vascular Biology
Background:
- Systemic lupus erythematosus (SLE) is linked to accelerated atherosclerosis.
- Endothelial dysfunction and its relation to cardiovascular risk factors in SLE require further investigation.
Purpose of the Study:
- To assess endothelial function in SLE patients.
- To examine the relationship between traditional and novel cardiovascular risk factors and endothelial dysfunction in SLE.
Main Methods:
- A case-control study involving 35 SLE patients and 35 matched controls.
- Measurements included arterial elasticity, lipid profiles, homocysteine, inflammation, and oxidative stress markers.
Main Results:
- SLE patients exhibited significantly lower small artery elasticity (SAE) and higher plasma homocysteine.
- Elevated levels of sVCAM-1, oxidized LDL, and CD40 ligand were observed in SLE patients.
- Oxidized LDL, age at diagnosis, and disease damage scores correlated inversely with SAE.
Conclusions:
- Clinically stable SLE is characterized by impaired endothelial function (decreased SAE) and adverse cardiovascular risk factor profiles.
- SLE patients are vulnerable to atherosclerosis, necessitating assessments beyond traditional risk factors.
Background:
Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerosis. However, the degree of endothelial dysfunction and its relationship to traditional and novel cardiovascular risk factors have not been examined in SLE.
Methods:
In a case-control design, 35 patients with clinically stable SLE and 35 control subjects matched for age, sex, body mass index and smoking status were studied. Arterial elasticity, lipid profile, homocysteine, measures of inflammation and oxidative stress were determined.
Results:
Among traditional vascular risk factors, there was a nonsignificant trend towards lower blood pressure in the control subjects, whereas low-density lipoprotein (LDL) cholesterol levels were significantly lower in the SLE group (2.5 vs 3.3 mmol/L, P < 0.001). Patients with SLE had significantly lower small artery elasticity (SAE; 4.9 vs 7.0 ml/mmHg x 100, P < 0.001) and higher plasma homocysteine (11.4 vs 8.3 mmol/L, P = 0.002) than control subjects. Levels of serum sVCAM-1 (614 vs 494 ng/mL, P = 0.002), oxidized LDL (144 vs 97, P < 0.001) and CD40 ligand (4385 vs 1373 pg/ml, P = 0.001) were significantly higher in SLE. Oxidized LDL levels, older age at SLE diagnosis and higher disease damage scores correlated inversely with SAE but not traditional risk factors.
Conclusion:
Impaired endothelial function as shown by decreased SAE, and an adverse profile of novel proatherogenic and prothrombotic vascular disease risk factors were prevalent in clinically quiescent SLE. These findings show the vulnerability of patients with SLE for atherosclerosis, and emphasize that assessments based on traditional risk factors alone may be inadequate.
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