Abstract 425: Is Adventitial Thickening a Pathogenic Factor in Aortic Atherosclerosis?: A Controlled Transesophageal Echocardiographic Study

Background: Aortic (Ao) atherosclerosis is common in systemic lupus erythematosus (SLE), is best assessed by transesophageal echocardiography (TEE), and is characterized by increased intima-media thickness (IMT) and plaques. Although TEE may also allow characterization of Ao adventitial thickness (AT), there is limited data on the pathogenic role of adventitial thickening in Ao atherosclerosis. Methods: 68 SLE patients (62 women, age 36 ± 12 years) and 25 age-and-gender matched healthy controls (22 women, age 34 ± 11 years) underwent multiplane TEE. At a depth of 3-4 cm using narrow sector scan, 2-dimensional guided M-mode images were obtained to assess the presence of plaques, IMT outside of plaques, AT outside of plaques, and AT in plaques at three different levels of the thoracic Ao (proximal, mid, distal). At each aortic level, 3 IMT and 3 AT measurements were taken during end diastole using electronic calipers. These measurements were then averaged. Unaware of subjects’ clinical data, one observer assessed for IMT and plaques while a second observer assessed AT. For purpose of analysis, intima-media thickening was defined as >1 mm which is >2SD above the corresponding overall mean IMT in controls (0.66 ± 0.17 mm), and adventitial thickening as >1.07 mm which is >2SD above the corresponding overall mean AT in controls (0.81 ± 0.13 mm). Plaques were defined as focal-protruding IMT >50% of the surrounding vessel wall at any aortic level. Results: As shown in Table 1A, intima-media thickening and plaques were greater in patients than in controls. Similarly, adventitial thickening was more common in patients than in controls. In addition, AT was greater in patients with intima media thickening, plaques, and intima-media thickening or plaques ( Table 1B) . Furthermore, AT was greater in plaques than AT outside of plaques ( Table 1C ). Conclusion: Adventitial thickening is a pathogenic factor of Ao atherosclerosis in SLE.