This Article Full Text Full Text (PDF) All Versions of this Article: 37/10/2446    most recent 01.STR.0000239656.59618.d4v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Carod-Artal, F. J. Search for Related Content PubMed PubMed Citation Articles by Carod-Artal, F. J. Related Collections Clinical Studies Doppler ultrasound, Transcranial Doppler etc. Endothelium/vascular type/nitric oxide Related Article

(Stroke. 2006;37:2446.)
© 2006 American Heart Association, Inc.

Editorials

Statins and Cerebral Vasomotor Reactivity

Implications for a New Therapy?

Francisco Javier Carod-Artal, MD, PhD

From the Department of Neurology, The Sarah Network of Rehabilitation Hospitals, Sarah Hospital, Brasilia DF, Brazil.

Correspondence to Prof Francisco Javier Carod-Artal, MD, PhD, Neurology Department, Sarah Hospital, SMHS quadra 501 conjunto A. CEP 7330-150. Brasilia DF. Brazil. E-mail javier@bsb.sarah.br or fjavier4644@terra.com.br

Key Words: cerebral blood flow • cerebral hemodynamics • clinical trials • neursonology • nitric oxide • statins • TCD • transcranial Doppler

An extract of the first 250 words of the full text is provided, because this article has no abstract.

See related article, pages 2540-2545.

Animal models have shown that cholesterol-lowering therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (commonly called statins) may augment absolute cerebral blood flow (CBF) by enhancing nitric oxide synthase (eNOS).¹ Statins upregulate type III endothelial eNOS in thrombocytes, decrease platelet activation, and protect from cerebral ischemia in normocholesterolemic mice.² Statins may also provide additional beneficial effects by upregulating endogenous tissue plasminogen activator and enhancing clot lysis in a mouse model of embolic focal ischemia.³ Statins given 24 hours after experimental ischemia can enhance CBF, angiogenesis, neurogenesis and sinaptogenesis.⁴ How can these findings be applied in the clinical setting? A meta-analysis of published clinical trials showed that low-density lipoprotein–lowering with statins may decrease the risk of stroke in diabetic or hypertensive patients with normal low-density lipoprotein cholesterol at baseline, and in patients with coronary artery disease, with respectively 48%, 27% and 25% reduction in stroke incidence.⁵

Does any relationship exist among statins and cerebral vasomotor reactivity? Functional transcranial Doppler (TCD) ultrasonography permits the assessment of cognitively induced CBF velocity changes⁶ and the evaluation of cerebral vasomotor reactivity.⁷ TCD can be used to reliably evaluate age-related changes in the physiological response of the human cerebral circulation. A diminished nitric oxide–mediated cerebral vasomotor response may exist in aging subjects and in patients with vascular risk factors.⁸ Because there are no reliable markers for the functional status of the cerebral small vessels in elderly patients at risk of stroke, TCD studies may be useful. Although some parameters like von . . . [Full Text of this Article]

Related Article:

Influence of Atorvastatin Treatment on L-Arginine Cerebrovascular Reactivity and Flow-Mediated Dilatation in Patients With Lacunar Infarctions

Janja Pretnar-Oblak, Miso Sabovic, Miran Sebestjen, Tomaz Pogacnik, and Marjan Zaletel
Stroke 2006 37: 2540-2545. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				A. Niruban, P. K. Myint, and J. F. Potter Placebo-Controlled Trial of High-Dose Atorvastatin in Patients With Severe Cerebral Small Vessel Disease Stroke, September 1, 2009; 40(9): e542 - e542. [Full Text] [PDF]