Lanzino, Giuseppe

Introduction: Uric acid (UA) level within carotid plaque specimens and its association with cerebrovascular events has not been detected or quantified. Systemically, serum uric acid (SUA) is a marker of inflammation and risk factor for atherosclerosis. However, its association with carotid plaque instability and subsequent cerebrovascular events remains unclear. Hypothesis: We hypothesized that UA may play a role in carotid artery atherosclerosis and stroke pathogenesis. In patients undergoing carotid endarterectomy (CEA), we aimed to determine whether UA is present differentially in carotid plaques of symptomatic versus asymptomatic patients and whether SUA is associated with cerebrovascular symptoms before surgery and major adverse cardiovascular events (MACE) in the follow-up to CEA. Methods: We prospectively collected 32 carotid plaques during CEA. We qualitatively assessed the presence of UA by using Gomori methenamine silver (GMS) staining and immunohistochemistry with anti-UA antibodies. We extracted and measured the quantity of UA in carotid plaques by using an enzymatic colorimetric assay. A retrospective analysis of a clinical database of 534 consecutive patients who underwent CEA was performed. We defined as symptomatic those patients with history of stroke, TIA and amaurosis fugax. Results: UA positive staining was detected in higher number of carotid plaques from symptomatic compared to asymptomatic patients on both staining, GMS [20 (86.9%) vs 2 (22.2%); p=0.001] and immunohistochemistry anti-UA [16 (69.5%) vs 1 (11.1%); p=0.004]. Moreover, we found a significantly higher concentration of UA in carotid plaque from symptomatic compared to asymptomatic patients [25.1 (9.5) μg/g vs 17.9 (3.8) μg/g; p=0.021]. SUA level in patients prior to CEA was significantly higher in the symptomatic compared to the asymptomatic group [6.0 (4.8-7.1) mg/dL vs 5.2 (4.4-6.3) mg/dL; p<0.001] and it was significantly higher in patients who developed MACE after CEA versus those that did not [6.0 (4.8-7.1) mg/dL vs 5.4 (4.5-6.6) mg/dL; p=0.021]. Conclusions: UA may provide a mechanistic explanation as systemic biomarker and potential tissue contributor for carotid plaque instability and subsequent cerebrovascular and cardiovascular symptoms.

Introduction: High-resolution vessel wall imaging (HR-VWI) of the intracranial vasculature may aid in the diagnosis and management of Moyamoya Disease (MMD). The patterns of HR-VWI findings of the cerebral vasculature of MMD patients remains uncertain, however. We sought to describe HR-VWI findings in a single-center cohort of MMD patients. Methods: Consecutive patients who were evaluated at a Midwest American medical center with a HR-VWI exam were included. Fourteen anterior circulation arterial segments in each patient were analyzed: proximal and distal supraclinoid Internal Carotid Artery, proximal M1 segment of the Middle Cerebral Artery, mid-portion of the M1, distal M1, proximal A1 segment of the Anterior Cerebral Artery and distal A1. Imaging variables that were collected from each segment included the presence of wall thickening (concentric vs eccentric), degree and pattern (concentric or eccentric) of contrast enhancement, and presence of positive or negative vessel remodeling. The total number and percentage of vessel segments demonstrating these characteristics were calculated. The number and percentage of patients with at least one segment demonstrating these characteristics were calculated. Results: Thirty-six patients (32 females, 88.9%) with a diagnosis of MMD were included. Overall, 221 of 504 segments (43.8%) demonstrated negative remodeling in 29 (75%) patients. Ninety-eight segments (19.4%) demonstrated wall enhancement (71 concentric, 27 eccentric; 22 high grade, 76 low grade) in 32 (88.9%) patients. Eighty-seven segments (17.3%) demonstrated wall thickening (52 concentric, 35 eccentric) in 32 patients (88.9%). Conclusions: Negative remodeling was the most-commonly observed vessel wall abnormality in all segments analyzed. However, a high percentage of patients had at least one segment demonstrating wall enhancement, wall thickening and negative remodeling. Continued study is necessary to further elucidate the HR-VWI patterns of the cerebral arterial system in MMD patients.