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(Stroke. 2002;33:1747.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Vascular Complications of Cocaine Use

Bernard Noël, MD

Department of Dermatology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

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

To the Editor:

In their article on the neurovascular complications of cocaine use, Conway and Tamargo concluded that vessels narrowing and delayed clinical deficit after aneurysmal subarachnoid hemorrhage were due to cocaine-induced vasospasm.¹ However, cerebral thromboangiitis obliterans (TAO), which is often unrecognized, may have the same clinical and angiographic presentation.

Many cases of peripheral arteritis very similar to TAO have recently been reported with cocaine use.^2–4 The same type of vascular lesions can be observed in cerebral and coronary arteries of patients exposed to cocaine.^5,6 Platelet activation and microaggregate formation have also been reported, explaining the beneficial effects of antithrombogenic agents such as aspirin on cerebral blood flow in chronic cocaine users.^7,8 Cerebral TAO is therefore probably more frequent than supposed and must be considered in the differential diagnosis of the cerebrovascular complications of cocaine use.

The vascular effects of impurities and adulterants found in cocaine are probably also underestimated. They are sometimes more dangerous than the psychoactive substance. Arsenic, for example, which is a frequent contaminant of recreational drugs, is suspected to be an important trigger of TAO.⁹ Interestingly, a dose-response relationship between the prevalence of cerebrovascular disorders and arsenic ingestion has also been found among populations at risk of arsenic poisoning.¹⁰ The mechanism of arsenic toxicity on endothelial cells seems to involve the activation of plasma membrane NADPH.¹¹ Platelet aggregation and reduction of cAMP level have also been observed.¹²

In conclusion, additional studies are warranted to determine more precisely which substances and what kind of vascular lesions are responsible for the . . . [Full Text of this Article]

James E. Conway, MD, PhD Rafael J. Tamargo, MD

Division of Vascular Neurosurgery, Department of Neurosurgery, The Johns Hopkins Hospital, Baltimore, Maryland