Hostname: page-component-586b7cd67f-t7fkt Total loading time: 0 Render date: 2024-11-27T13:51:38.939Z Has data issue: false hasContentIssue false
  • English
  • Français

Effect of Statin on Progression of Symptomatic Intracranial Atherosclerosis

Published online by Cambridge University Press:  02 December 2014

Hye-Jin Kim ,
Eun-Kyung Kim ,
Sun U. Kwon ,
Jong S. Kim  and
Dong-Wha Kang
Hye-Jin Kim
Affiliation:
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
Eun-Kyung Kim
Affiliation:
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
Sun U. Kwon
Affiliation:
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
Jong S. Kim
Affiliation:
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
Dong-Wha Kang*
Affiliation:
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
*
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, 88 olympic-ro 43-gil, Songpa-gu, Seoul 138-736, Republic of Korea. e-mail: [email protected]
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Symptomatic intracranial atherosclerosis (ICAS) is a dynamic disease that frequently progresses. Statins have been shown to have anti-atherosclerotic activity. We therefore investigated whether statins could prevent progression of ICAS.

Methods:

This retrospective cohort study assessed 55 patients with acute ischemic stroke and symptomatic ICAS in the middle cerebral or basilar arteries as shown on magnetic resonance angiography (MRA), with follow-up MRA performed more than 1 year after the index stroke. Change in ICAS was classified as progressive, regressive, or stable. Baseline clinical characteristics and risk factor control during follow-up were assessed, and laboratory tests were performed at the time of follow-up MRA. The statin group was defined as patients regularly treated with statins for more than 75% of the follow-up period; the remaining patients were defined as the non-statin group.

Results:

At a median follow-up time of 21.8 months (range, 11.8-66.1 months), the statin group consisted of 26 (47.3%) patients and the non-statin group of 29 (52.7%). During follow-up, 6 (10.9%) patients progressed, 14 (25.5%) regressed, and 35 (63.6%) remained stable. Statin treatment was significantly associated with non-progression of ICAS (p=0.024). Two patients in the non-statin group had recurrent strokes. Border-zone infarcts were associated with progression of ICAS (3/6, 50%; p=0.007), whereas risk factors and inflammatory biomarkers were not related to progression.

Conclusions:

Treatment with statins may prevent progression of symptomatic ICAS. Prospective randomized controlled trials are required to confirm that statins protect against such progression.

Résumé

RÉSUMÉ Contexte:

L'athérosclérose intracrânienne (ASIC) symptomatique est une maladie dynamique souvent progressive. Il a été démontré que les statines ont une activité antiathéroscléreuse. Nous avons donc analysé si les statines pouvaient prévenir la progression de l'ASIC.

Méthode:

Il s'agit d'une étude rétrospective de cohorte de 55 patients atteints d'un accident vasculaire cérébral aigu (AVCA) et d'ASIC symptomatique de l'artère cérébrale moyenne ou du tronc basilaire démontrée par angiographie par résonance magnétique (ARM) avec reprise de l'ARM au moins 1 an après l'AVCA. Le changement au niveau de l'ASIC était classifié comme une ASIC ayant progressé, régressé ou qui était stable. Les caractéristiques cliniques initiales de base et la réduction des facteurs de risque au cours du suivi ont été évaluées. Des épreuves de laboratoire ont été effectuées au moment de l'ARM de contrôle. Les patients qui avaient pris une statine régulièrement pendant plus de 75% de la période de suivi étaient inclus dans le groupe statine. Les autres patients étaient inclus dans le groupe sans statine.

Résultats:

Le temps médian écoulé entre l'AVCA et l'examen de suivi était de 21,8 mois (écart 11,8 à 66,1 mois). Le groupe statine incluait 26 patients (47,3%) et le groupe sans statine 29 patients (52,7%). Au cours du suivi, une progression a été observée chez 6 patients (10,9%), une régression chez 14 patients (25,5%) et 35 patients (63,6%) sont demeurés stables. Le traitement par une statine était associé de façon significative à l'absence de progression de l'ASIC (p = 0,024). Deux patients du groupe sans statine ont subi d'autres AVC. Des infarctus dans la zone limite de l'AVC antérieur étaient associés à la progression de l'ASIC (3/6, 50%; p = 0,007) alors que les facteurs de risque et les biomarqueurs de l'inflammation n'étaient par reliés à la progression.

Conclusions:

Le traitement par les statines peut prévenir la progression de l'ASIC. Notre observation que les statines protègent contre la progression de l'ASIC devra être confirmée par des essais cliniques prospectifs randomisés et contrôlés par placebo.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 39 , Issue 6 , November 2012 , pp. 801 - 806
Copyright
Copyright © The Canadian Journal of Neurological 2012

References

1. Gorelick, PB, Han, J, Huang, Y, Wong, KS. Epidemiology. In: Jong, S. Kim, Louis, R Caplan, K. S. Lawrence Wong, editors. Intracranial Atherosclerosis. Oxford: Wiley-Blackwell; 2008. p. 33–44.Google Scholar
2. Gorelick, PB, Wong, KS, Bae, HJ, Pandey, DK. Large artery intracranial occlusive disease: a large worldwide burden but a relatively neglected frontier. Stroke. 2008;39(8):2396–9.Google Scholar
3. Kern, R, Steinke, W, Daffertshofer, M, Prager, R, Hennerici, M. Stroke recurrences in patients with symptomatic vs asymptomatic middle cerebral artery disease. Neurology. 2005;65(6):859–64.Google Scholar
4. Lovett, JK, Coull, AJ, Rothwell, PM. Early risk of recurrence by subtype of ischemic stroke in population-based incidence studies. Neurology. 2004;62(4):569–73.CrossRefGoogle ScholarPubMed
5. Mazighi, M, Tanasescu, R, Ducrocq, X, et al. Prospective study of symptomatic atherothrombotic intracranial stenoses: the GESICA study. Neurology. 2006;66(8):1187–91.Google Scholar
6. Kang, DW, Kwon, SU, Yoo, SH, et al. Early recurrent ischemic lesions on diffusion-weighted imaging in symptomatic intracranial atherosclerosis. Arch Neurol. 2007;64(1):50–4.Google Scholar
7. Akins, PT, Pilgram, TK, Cross, DT, 3rd, Moran, CJ. Natural history of stenosis from intracranial atherosclerosis by serial angiography. Stroke. 1998;29(2):433–8.Google Scholar
8. Wong, KS, Li, H, Lam, WW, Chan, YL, Kay, R. Progression of middle cerebral artery occlusive disease and its relationship with further vascular events after stroke. Stroke. 2002;33(2):532–6.Google Scholar
9. Thijs, VN, Albers, GW. Symptomatic intracranial atherosclerosis: outcome of patients who fail antithrombotic therapy. Neurology. 2000;55(4):490–7.Google Scholar
10. Arenillas, JF, Molina, CA, Montaner, J, et al. Progression and clinical recurrence of symptomatic middle cerebral artery stenosis: a long-term follow-up transcranial Doppler ultrasound study. Stroke. 2001;32(12):2898–904.Google Scholar
11. Spence, JD, Hackam, DG. Treating arteries instead of risk factors: a paradigm change in management of atherosclerosis. Stroke. 2010;41(6):1193–9.Google Scholar
12. Spence, JD, Coates, V, Li, H, et al. Effects of intensive medical therapy on microemboli and cardiovascular risk in asymptomatic carotid stenosis. Arch Neurol. 2010;67(2):180–6.CrossRefGoogle Scholar
13. Spence, JD. Carotid plaque measurement is superior to IMT. Atherosclerosis. 2012;220(1):34–5.Google Scholar
14. Nissen, SE, Nicholls, SJ, Sipahi, I, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA. 2006;295(13):1556–65.Google Scholar
15. Crouse, JR 3rd, Raichlen, JS, Riley, WA, et al. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR Trial. JAMA. 2007;297(12):1344–53.Google Scholar
16. Molina, CA, Montaner, J, Abilleira, S, et al. Timing of spontaneous recanalization and risk of hemorrhagic transformation in acute cardioembolic stroke. Stroke. 2001;32(5):1079–84.Google Scholar
17. Cho, AH, Kwon, SU, Kim, JS, Kang, DW. Evaluation of early dynamic changes of intracranial arterial occlusion is useful for stroke etiology diagnosis. J Neurol Sci. 2012;312(1–2):127–30.Google Scholar
18. Kwon, SU, Cho, YJ, Koo, JS, et al. Cilostazol prevents the progression of the symptomatic intracranial arterial stenosis: the multicenter double-blind placebo-controlled trial of cilostazol in symptomatic intracranial arterial stenosis. Stroke. 2005;36(4): 782–6.Google Scholar
19. Endres, M, Laufs, U, Huang, Z, et al. Stroke protection by 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors mediated by endothelial nitric oxide synthase. Proc Natl Acad Sci USA. 1998;95(15):8880–5.CrossRefGoogle ScholarPubMed
20. Amarenco, P, Bogousslavsky, J, Callahan, A 3rd, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006;355(6):549–59.Google Scholar
21. Anand, SS. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systematic review and meta-analysis. Law MR, Wald NJ, Rudnicka AR. BMJ 2003; 326: 1407–8.Google Scholar
22. Mok, VC, Lam, WW, Chen, XY, et al. Statins for asymptomatic middle cerebral artery stenosis: the regression of cerebral artery stenosis study. Cerebrovasc Dis. 2009;28(1):18–25.Google Scholar
23. Tan, TY, Kuo, YL, Lin, WC, Chen, TY. Effect of lipid-lowering therapy on the progression of intracranial arterial stenosis. J Neurol. 2009;256(2):187–93.Google Scholar
24. Chimowitz, MI, Lynn, MJ, Howlett-Smith, H, et al. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. 2005;352(13):1305–16.Google Scholar
25. Chimowitz, MI, Lynn, MJ, Derdeyn, CP, et al. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med. 2011;365(11):993–1003.Google Scholar
26. Chaturvedi, S, Turan, TN, Lynn, MJ, et al. Risk factor status and vascular events in patients with symptomatic intracranial stenosis. Neurology. 2007;69(22):2063–8.Google Scholar
27. Arenillas, JF, Alvarez-Sabin, J, Molina, CA, et al. Progression of symptomatic intracranial large artery atherosclerosis is associated with a proinflammatory state and impaired fibrinolysis. Stroke. 2008;39(5):1456–63.Google Scholar
28. Kim, JT, Kim, HJ, Yoo, SH, et al. MRI findings may predict early neurologic deterioration in acute minor stroke or transient ischemic attack due to intracranial atherosclerosis. Eur Neurol. 2010;64(2):95–100.Google Scholar
29. Bang, OY, Lee, PH, Heo, KG, Joo, US, Yoon, SR, Kim, SY. Specific DWI lesion patterns predict prognosis after acute ischaemic stroke within the MCA territory. J Neurol Neurosurg Psychiatry. 2005;76(9):1222–8.Google Scholar
30. Choi, CG, Lee, DH, Lee, JH, et al. Detection of intracranial atherosclerotic steno-occlusive disease with 3D time-of-flight magnetic resonance angiography with sensitivity encoding at 3T. AJNR Am J Neuroradiol. 2007;28(3):439–46.Google Scholar
31. Rother, J, Schwartz, A, Rautenberg, W, Hennerici, M. Middle cerebral artery stenoses: assessment by magnetic resonance angiography and transcranial doppler ultrasound. Cerebrovasc Dis. 1994;4: 273–9.CrossRefGoogle Scholar
32. Kwon, SU, Hong, KS, Kang, DW, et al. Efficacy and safety of combination antiplatelet therapies in patients with symptomatic intracranial atherosclerotic stenosis. Stroke. 2011;42(10): 2883–90.Google Scholar