Abstract 632: Premature Aortic and Carotid Stiffness in Systemic Lupus Erythematosus: Which One is First or Worse?

Abstract

Background: Increased aortic and carotid stiffness are common in patients with systemic lupus erythematosus (SLE) and are associated with increased morbidity and mortality. Although the aorta and carotid arteries have different anatomy, hemodynamics, and cardiovascular disease implications, it is unknown whether stiffness affects these arterial beds in a parallel or divergent fashion. Methods: 43 SLE patients (41 women, age 36 ± 11 years) and 17 age-and-sex matched healthy volunteers (14 women, age 34 ± 12 years) underwent clinical and laboratory evaluations and multiplane transesophageal echocardiography and carotid ultrasonography for assessment of aortic and carotid stiffness, respectively. Stiffness at the proximal, mid, and distal thoracic aorta and stiffness of the right common carotid artery were assessed using a standard Pressure-Strain Elastic Modulus, defined as = k (sBP – dBP)/[(sD - dD)/dD)] where k = conversion factor from mmHg to Nm -2 (Pascal units), sBP = systolic blood pressure, dBP = diastolic blood pressure, sD = systolic diameter, and dD = diastolic diameter. Results: Aortic stiffness was significantly higher in SLE patients than in controls after adjusting for age and atherogenic risk factors (7.96 ± 4.16 versus 5.77 ± 2.32 units, p = 0.01). However, carotid stiffness was similar in patients and controls (6.39 ± 2.70 versus 5.55 ± 2.68 units, p = 0.29). In SLE patients, aortic stiffness was significantly higher than carotid stiffness (7.96 ± 4.17 versus 6.39 ± 2.70 units, p = 0.02). In relation to age at diagnosis of SLE, aortic stiffness occurred earlier and was greater than carotid stiffness (RM ANCOVA, p = 0.03). Conclusion: Aortic stiffness is higher and precedes carotid stiffness in young adult SLE patients. These findings of an accelerated and divergent pathogenesis of aortic as compared to carotid stiffness may be explained by SLE-related chronic or recurrent autoimmune-mediated inflammation and thrombogenesis superimposed on the severe anatomic curvature, higher pulse pressure, and higher reciprocating shear stresses of the aorta as compared to the nearly straight and less oscillating shear forces of the carotid arteries.