Effect of lipid-lowering therapy on the progression of intracranial arterial stenosis.
OBJECTIVE
Intracranial arterial stenosis (IAS) is a severe disease with a high recurrent stroke rate even under the best medical treatment. Statins have been demonstrated to prevent stroke and to slow or halt atherosclerosis progression. This study was performed to observe the effect of atorvastatin on the progression of IAS, explore the factors associated with atherosclerosis regression and the recurrent rate of stroke.


METHODS
A hospital-base observation study enrolled 40 stroke patients with middle cerebral artery (MCA) or/and basilar artery (BA) stenosis. All participants had hyperlipidemia and were given atorvastatin 40 mg per day for at least six months. IAS was assessed by magnetic resonance angiogram (MRA) at the time of enrollment and then at least six months later. The primary outcome was the progression of IAS. All patients were also given antiplatelet agents for stroke prevention.


RESULTS
At the end of the study, 23 (58 %), 15 (38 %) and 2 (4 %) patients had regressed, stationary and progressed IAS, respectively. Females were likely to have regressed IAS. The recurrent stroke rate was 18 %. Among the 54 stenotic vessels, 29 (54 %) vessels were assessed as improvement in stenosis.


CONCLUSIONS
Compared with other studies, more regressed, stationary IAS and less progressed IAS were found in our study. Female gender was likely to have regressed IAS after statin treatment. Further clinical outcome trials are required to assess the effects of such therapy on morbidity and mortality in this particular group of patients.
Tan
Teng-Yeow
TY
Dept. of Neurology, Section of Cerebrovascular Disease, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Chang Gung University College of Medicine, 123, Ta-Pei Road, Niao-Sung Hsiang, Kaohsiung County 833, Taiwan. tengyeowtan@yahoo.com
Kuo
Yeh-Lin
YL
Lin
Wei-Che
WC
Chen
Ting-Yao
TY
D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage; D000069059:Atorvastatin; D002536:Cerebral Arteries / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D003251:Constriction, Pathologic / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D002537:Intracranial Arteriosclerosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011758:Pyrroles / Q000008:administration & dosage*; D055502:Secondary Prevention; D017678:Sex Distribution; D020521:Stroke / Q000188:drug therapy / Q000453:epidemiology / Q000517:prevention & control; D016896:Treatment Outcome; D014715:Vertebrobasilar Insufficiency / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology
D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D010975:Platelet Aggregation Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin