title: Predictors of symptomatic and asymptomatic intracranial atherosclerosis: what is different and why?
abstract: OBJECTIVE
  The prognoses of symptomatic and asymptomatic intracranial atherosclerotic stenosis(ICAS) differ. Understanding the underlying pathomechanisms and predictors of progression or regression may help to clarify the differences. We herein attempted to compare the course and predictors of symptomatic ICAS to those of coexisting asymptomatic ICAS.
  
  
  METHODS
  This was a post-hoc analysis of the 'Trials of Cilostazol in Symptomatic intracranial arterial stenosis-2(TOSS-2)' study, which recruited patients with acute symptomatic ICAS receiving intensive medical treatment. Changes in the status of ICAS were classified as being indicative of regression, progression or no changes. Univariate and multivariate ordinal regression analyses were performed to identify predictors of symptomatic and asymptomatic ICAS based on clinical, laboratory and radiologic data.
  
  
  RESULTS
  Of the 409 patients, symptomatic ICAS demonstrated regression in 110(27%) cases and progression in 52(13%) cases. Among these patients, 250(61.1%) had asymptomatic ICAS, which regressed in 38(15%) cases and progressed in 16(6%) cases. Severe baseline stenosis, a high high-density lipoprotein(HDL) cholesterol level and the use of cilostazol were found to be independently associated with a favorable course of symptomatic ICAS(p＜0.001, p=0.005 and p=0.038, respectively). Regarding asymptomatic ICAS, severe stenosis, the use of angiotensin receptor antagonists and a low fasting glucose level were associated with a favorable course(p＜0.001, p=0.011 and p=0.007, respectively).
  
  
  CONCLUSIONS
  Changes in atherosclerosis are more dynamic in patients with symptomatic ICAS, and the predictors of symptomatic and asymptomatic ICAS differ. In this study, changes in the status of symptomatic ICAS were associated with the level of HDL cholesterol, which is known to affect the regression of atherosclerosis and vascular remodeling.
authors.affiliation: Department of Neurology, Asan Medical Center, University of Ulsan.
authors.forename: Bum Joon
authors.initials: BJ
authors.lastname: Kim
authors.forename: Keun-Sik
authors.initials: KS
authors.lastname: Hong
authors.forename: Yong-Jin
authors.initials: YJ
authors.lastname: Cho
authors.forename: Ju-Hun
authors.initials: JH
authors.lastname: Lee
authors.forename: Ja-seong
authors.initials: JS
authors.lastname: Koo
authors.forename: Jong-Moo
authors.initials: JM
authors.lastname: Park
authors.forename: Dong-Wha
authors.initials: DW
authors.lastname: Kang
authors.forename: Jong S
authors.initials: JS
authors.lastname: Kim
authors.forename: Seung-Hoon
authors.initials: SH
authors.lastname: Lee
authors.forename: Sun U
authors.initials: SU
authors.lastname: Kwon
mesh_terms: D000368:Aged; D001158:Arteries / Q000473:pathology*; D050197:Atherosclerosis; D008076:Cholesterol, HDL; D000077407:Cilostazol; D003251:Constriction, Pathologic / Q000473:pathology; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000175:diagnosis* / Q000188:drug therapy*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012044:Regression Analysis; D012307:Risk Factors; D013777:Tetrazoles / Q000627:therapeutic use; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D008076:Cholesterol, HDL; D013777:Tetrazoles; D014665:Vasodilator Agents; D000077407:Cilostazol