For the first time, systemic arterial stiffening has been linked with left ventricular hypertrophy and dysfunction in patients with pediatric-onset lupus, according to Dr. Pak-Cheong Chow and colleagues from the department of paediatrics and adolescent medicine of the University of Hong Kong.
An increase in carotid arterial stiffness was previously observed among patients with adult-onset systemic lupus erythematosus (SLE), but these older patients typically also have premature atherosclerosis, hypertension, dyslipidemia, and other potentially confounding factors.
Systemic arterial stiffness has been documented in children with other vasculitic diseases, such as polyarteritis nodosa, but arterial function in young SLE patients has not been studied, the investigators said.
In order to investigate this aspect of pediatric-onset lupus, they studied 32 patients and 15 controls, performing pulsed-wave Doppler and standard M-mode echocardiography, tissue Doppler imaging, and imaging of the right and left common carotid arteries.
Mean age at diagnosis was 11.7 years, mean disease duration was 6.3 years, and mean systemic lupus erythematosus disease activity index (SLEDAI) was 4. A total of 21 patients had nephritis, 11 had antiphospholipid antibodies, and two had antiphospholipid syndrome. At the time of the study, 28 patients were receiving prednisone, with a mean daily dose of 5.4 mg.
Echocardiographic findings among the lupus group included thicker interventricular septum, thicker left ventricular (LV) posterior wall, greater indexed LV mass, and lower LV fractional shortening and ejection fraction compared with controls.
They also showed reductions in LV free wall systolic strain and strain rate, as well as a lower mitral annular systolic velocity, findings that are indicative of LV systolic dysfunction. Patients also had significantly lower E wave velocity, E deceleration time, E/A ratio, and diastolic strain rates, suggesting LV diastolic dysfunction relating to impaired relaxation.
In addition, the average carotid arterial stiffness index was significantly greater among the lupus patients, and on univariate analysis, this index correlated significantly with SLEDAI, albeit not with age, body mass, diastolic blood pressure, damage index, daily prednisone dosage, or duration of disease. On multiple linear regression analysis, SLEDAI and systolic blood pressure remained significantly correlated with carotid stiffness index after adjustment for these variables.
With regard to the relation between arterial stiffness and LV structure and function, the average carotid arterial stiffness index correlated positively with LV posterior wall thickness, interventricular septal thickness, indexed LV mass, and myocardial performance index. Negative correlations were seen with E wave velocity, em velocity, or strain rates.
Multiple regression analysis determined carotid arterial stiffness was a significant determinant of indexed LV mass, em velocity, and left ventricular strain rate after adjustment for age, sex, body mass index, and blood pressure.
“Our study provides the first evidence that systemic arterial stiffening is associated with LV hypertrophy and dysfunction in a young cohort of patients with pediatric-onset SLE,” wrote the authors (J. Rheumatol. 2007;34 [Epub ahead of print]).
The study also found that arterial stiffness correlated with the disease activity score and was an independent determinant of LV mass and function.
The authors noted arterial stiffening in SLE likely links to immune complex-induced complement activation and inflammatory cell infiltration in the arterial wall. Longitudinal studies are needed to see if reducing stiffness and improving ventricular function reduce the risk of early cardiovascular disease in these patients.