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Increased arterial stiffness in systemic lupus erythematosus (SLE) patients at low risk for cardiovascular disease: a
Karim Sacre1, Brigitte Escoubet2, Blandine Pasquet3
1Département de Médecine Interne, Hôpital Bichat, Université Paris Diderot, PRES Sorbonne Paris Cité, Assistance Publique Hôpitaux de Paris, Paris, France; INSERM U1149, Paris, France; Département Hospitalo-Universitaire FIRE (Fibrosis, Inflammation and Remodelling in Renal and Respiratory Diseases), Paris, France.
Insights
Systemic lupus erythematosus (SLE) patients show increased arterial stiffness, a marker of atherosclerosis, even with low cardiovascular disease (CVD) risk. This stiffness is linked to higher systolic blood pressure and glucocorticoid use in SLE.
Area of Science:
- Cardiology
- Rheumatology
- Vascular Biology
Background:
- Cardiovascular disease (CVD) is a leading cause of mortality in patients with systemic lupus erythematosus (SLE).
- Traditional CVD risk stratification may underestimate risk in SLE due to early atherosclerosis development.
- Arterial stiffness serves as an early surrogate marker for atherosclerosis.
Purpose of the Study:
- To investigate arterial stiffness in SLE patients with low predicted CVD risk.
- To identify traditional and non-traditional risk factors associated with arterial stiffness in SLE.
Main Methods:
- Prospective assessment of carotid-femoral pulse wave velocity (PWV) in 41 SLE patients and 35 controls.
- Logistic regression for age/Framingham score adjustment.
- Pearson's correlation and multiple linear regression for risk factor analysis.
Main Results:
- SLE patients exhibited higher PWV than controls, despite similar low 10-year CVD risk (Framingham score).
- PWV correlated with internal carotid wall thickness in SLE patients.
- Systolic blood pressure and cumulative glucocorticoid dose were independently associated with PWV in SLE.
Conclusions:
- Arterial stiffness is elevated in SLE patients, irrespective of low Framingham CVD risk scores.
- Systolic blood pressure and glucocorticoid therapy are key determinants of arterial stiffness in SLE.
- Early detection and management of arterial stiffness are crucial in SLE patients.
Abstract:
Cardiovascular disease (CVD) is a major cause of death in systemic lupus erythematosus (SLE) patients. Although the risk for cardiovascular events in patients with SLE is significant, the absolute number of events per year in any given cohort remains small. Thus, CVD risks stratification in patients with SLE focuses on surrogate markers for atherosclerosis at an early stage, such as reduced elasticity of arteries. Our study was designed to determine whether arterial stiffness is increased in SLE patients at low risk for CVD and analyze the role for traditional and non-traditional CVD risk factors on arterial stiffness in SLE. Carotid-femoral pulse wave velocity (PWV) was prospectively assessed as a measure of arterial stiffness in 41 SLE patients and 35 controls (CTL). Adjustment on age or Framingham score was performed using a logistic regression model. Factors associated with PWV were identified separately in SLE patients and in controls using Pearson's correlation coefficient for univariate analysis and multiple linear regression for multivariate analysis. SLE patients and controls displayed a low 10-year risk for CVD according to Framingham score (1.8±3.6% in SLE vs 1.6±2.8% in CTL, p = 0.46). Pulse wave velocity was, however, higher in SLE patients (7.1±1.6 m/s) as compared to controls (6.3±0.8 m/s; p = 0.01, after Framingham score adjustment) and correlated with internal carotid wall thickness (p = 0.0017). In multivariable analysis, only systolic blood pressure (p = 0.0005) and cumulative dose of glucocorticoids (p = 0.01) were associated with PWV in SLE patients. Interestingly, the link between systolic blood pressure (SBP) and arterial stiffness was also confirmed in SLE patients with normal systolic blood pressure. In conclusion, arterial stiffness is increased in SLE patients despite a low risk for CVD according to Framingham score and is associated with systolic blood pressure and glucocorticoid therapy.
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