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(Stroke. 2003;34:e108.)
© 2003 American Heart Association, Inc.

Letters to the Editor

Vascular Smooth Muscle Proliferation as a Target for Therapeutic Intervention

Departments of Neurosurgery, Physiology, and Pathology, University of Maryland School of Medicine, Baltimore, Maryland

Thomas A. Kent, MD

Departments of Neurology and Pharmacology, The Program in Neurosciences, University of Texas Medical Branch, Galveston, Texas

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

To the Editor:

We read with great interest the recent article by Borel et al,¹ as well as the accompanying editorial comment by Dr Bhardwaj.² The hypothesis that vascular cell proliferation may play an important role in the pathogenesis of cerebral vasospasm has been prominently discussed for more than 15 years, and has been supported by a variety of data that have been presented over those years. We were pleased to see the addition of further support for this concept, in the form of new data showing increased levels of platelet-derived growth factor in the cerebrospinal fluid of patients with subarachnoid hemorrhage.

We would like to call attention to a misrepresentation in the article. The hypothesis that a beneficial effect of dihydropyridine calcium channel blockers in vasospasm might be attributed to block of a proliferative response and subsequent phenotypic change in vascular smooth muscle was first put forth and tested by us.³ We presented this hypothesis as an extension of previous work on the pathogenesis of atherosclerosis. In our report, which was specifically aimed at elucidating mechanisms of vasospasm, we documented the presence of L-type calcium channels in cultured smooth muscle cells and showed that proliferation (in response to serotonin) was inhibited by blocking these channels.

As noted by Dr Bhardwaj, tremendous progress has been made in advancing our understanding of cerebral vasospasm. Yet, equally tremendous gaps remain in our knowledge, including our ignorance of the molecular pathogenesis of this disorder. Only by building on prior knowledge can we hope . . . [Full Text of this Article]

Cecil O. Borel, MD

Departments of Anesthesiology and Surgery, Duke University Medical Center, Durham, North Carolina

Laura Niklason, MD, PhD

Departments of Anesthesiology and Biomedical Engineering, Duke University Medical Center, Durham, North Carolina