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Published on: February 20, 2017
Systemic lupus erythematosus predicts increased left ventricular mass
Janice Pieretti1, Mary J Roman, Richard B Devereux
1Division of Cardiology, Weill Medical College of Cornell University and the Hospital for Special Surgery, New York, NY 10021, USA.
Insights
Systemic lupus erythematosus (SLE) is linked to increased left ventricular (LV) mass and hypertrophy, even without other heart conditions. This suggests inflammation-related arterial stiffening may impact cardiac health in SLE patients.
Area of Science:
- Cardiology
- Rheumatology
- Vascular Biology
Background:
- Systemic lupus erythematosus (SLE) is known to accelerate atherosclerosis and vascular stiffening.
- The impact of SLE on left ventricular (LV) structure and function, independent of valvular or coronary artery disease, remains unclear.
Purpose of the Study:
- To investigate whether SLE alters LV structure and function in patients without overt cardiovascular disease.
- To explore the relationship between SLE, arterial stiffness, and LV remodeling.
Main Methods:
- Age and gender-matched comparison of SLE patients (n=173) and a reference group (n=173).
- Echocardiography for LV structure and function assessment.
- Carotid ultrasonography for atherosclerosis detection and radial applanation tonometry for arterial stiffness measurement.
Main Results:
- SLE patients exhibited significantly higher LV mass (P<0.001) and a greater prevalence of LV hypertrophy (17.9% vs. 6.4%, P<0.001) compared to controls.
- LV mass in SLE patients was independently associated with SLE itself (P<0.001) and arterial stiffness (P<0.001).
- Hypertension exacerbated LV mass increase in SLE patients.
Conclusions:
- Systemic lupus erythematosus is a predictor of increased LV mass, potentially mediated by inflammation-induced arterial stiffening.
- Elevated LV hypertrophy in SLE may contribute to the observed increase in cardiac morbidity and mortality.
Background:
Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis and vascular stiffening. Whether SLE alters left ventricular (LV) structure and function in the absence of valvular and clinical coronary artery disease is unknown.
Methods And Results:
SLE patients without clinical or echocardiographic evidence of valvular or coronary disease were age and gender matched to a reference group (n=173 in both groups). Subjects underwent echocardiography to quantify LV structure and function and carotid ultrasonography to detect atherosclerosis. Disease characteristics and radial applanation tonometry to measure arterial stiffness were evaluated in SLE patients. The 2 groups were similar in subjects' body size, hypertension and diabetes status, smoking status, and cholesterol levels. LV mass (38.3 versus 32.8 g/m(2.7)), ejection fraction (71% versus 67%), and prevalence of LV hypertrophy (17.9% versus 6.4%) were higher in SLE patients than in referent subjects (all P<0.001). The combination of SLE and hypertension further increased LV mass. In multivariable analysis, LV mass was associated with SLE (P<0.001) in addition to body mass index, diabetes mellitus, and hypertension. Among SLE patients, LV mass was associated with arterial stiffness (P<0.001). Carotid atherosclerosis, SLE duration, damage index, serum creatinine, and homocysteine were significantly related to LV mass in univariate but not multivariable analyses.
Conclusions:
SLE predicts increased LV mass, possibly because of inflammation-related arterial stiffening. Excess LV hypertrophy may contribute to the increased cardiac morbidity and mortality observed in SLE patients.
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