Association Between Serum Homocysteine Concentration, Aneurysm Wall Inflammation, and Aneurysm Symptoms in Intracranial Fusiform Aneurysm.

ABSTRACT

RATIONALE AND OBJECTIVES: The pathophysiology of fusiform intracranial aneurysm (FIA) involves inflammatory processes, and homocysteine plays a role in the inflammatory processes in the vessel wall. Moreover, aneurysm wall enhancement (AWE) has emerged as a new imaging biomarker of aneurysm wall inflammatory pathologies. To investigate the pathophysiological mechanisms of aneurysm wall inflammation and FIA instability, we aimed to determine the associations between the homocysteine concentration, AWE, and FIAs' related symptoms. MATERIALS AND METHODS: We retrospectively reviewed the data of 53 patients with FIA who underwent both high-resolution magnetic resonance imaging and serum homocysteine concentration measurement. FIAs' related symptoms were defined as ischemic stroke or transient ischemic attack, cranial nerve compression, brainstem compression, and acute headache. The contrast ratio of the signal intensity of the aneurysm wall to the pituitary stalk (CRstalk) was used to indicate AWE. Multivariate logistic regression and receiver operating characteristic (ROC) curve analyses were performed to determine how well the independent factors could predict FIAs' related symptoms. Predictors of CRstalk were also investigated. Spearman's correlation coefficient was used to identify the potential associations between these predictors. RESULTS: Fifty-three patients were included, of whom 23 (43.4%) presented with FIAs' related symptoms. After adjusting for baseline differences in the multivariate logistic regression analysis, the CRstalk (odds ratio [OR]=3.207, P = .023) and homocysteine concentration (OR=1.344, P = .015) independently predicted FIAs' related symptoms. The CRstalk was able to differentiate between FIAs with and without symptoms (area under the ROC curve [AUC]=0.805), with an optimal cutoff value of 0.76. The homocysteine concentration could also differentiate between FIAs with and without symptoms (AUC=0.788), with an optimal cutoff value of 13.13. The combination of the CRstalk and homocysteine concentration had a better ability to identify symptomatic FIAs (AUC=0.857). Male sex (OR=0.536, P = .018), FIAs' related symptoms (OR=1.292, P = .038), and homocysteine concentration (OR=1.254, P = .045) independently predicted the CRstalk. CONCLUSION: A higher serum homocysteine concentration and greater AWE indicate FIA instability. Serum homocysteine concentration may be a useful biomarker of FIA instability; however, this needs to be verified in future studies.