Vascular Complications of Cocaine Use
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 neurovascular complications of cocaine use. Early use of platelet-inhibiting agents such as aspirin and smoking cessation must be considered in suspected cases.
- ↵Conway JE, Tamargo RJ. Cocaine use is an independent risk factor for cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke. 2001; 32: 2338–2343.
- ↵Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001; 5: 351–358.
- ↵Heesch CM, Wilhelm CR, Ristich J, Adnane J, Bontempo FA, Wagner WR. Cocaine activates platelets and increases the formation of circulating platelet containing microaggregates in humans. Heart. 2000; 83: 688–695.
- ↵Chiou HY, Huang WI, Su CL, Chang SF, Hsu YH, Chen CJ. Dose-response relationship between prevalence of cerebrovascular disease and ingested inorganic arsenic. Stroke. 1997; 28: 1717–1723.
- ↵Smith KR, Klei LR, Barchowsky A. Arsenite stimulates plasma membrane NADPH oxidase in vascular endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2001; 280: 442–449.
We have read with interest the letter by Dr Bernard Noël. In his letter, Dr Noël discusses thromboangiitis obliterans and its possible relationship to cocaine exposure. He then suggests that the cerebral vasospasm experienced by patients after aneurysmal subarachnoid hemorrhage (aSAH) associated with acute cocaine exposure may be due to a cerebral variant of thromboangiitis obliterans. In addition, Dr Noël notes that adulterants found in some illicit drugs may be associated with cerebrovascular complications.
In our opinion, cerebral vasospasm after aSAH associated with recent cocaine exposure is identical to that experienced after aSAH in general. Cerebral vasospasm in cocaine users has the same clinical course as vasospasm experienced by patients suffering aSAH without cocaine exposure. The onset of vasospasm; its response to hypervolemic, hypertensive therapy; and reversibility are similar in the 2 patient populations.
To our knowledge, there exist no data suggesting that vasospasm after aSAH is a cerebral variant of thromboangiitis obliterans caused by cocaine or adulterants. Vasospasm experienced after aSAH is clinically different than the vasculopathy seen with thromboangiitis obliterans. Vasospasm after aSAH has a distinct and limited time course; is often responsive to hypervolemic, hypertensive therapy; and is reversible. By contrast, thromboangiitis obliterans has a prolonged, progressive course with acute attacks and remissions; is not responsive to therapy; and is not reversible.
We and other authors have investigated the role of inflammation in the pathogenesis of cerebral vasospasm after aSAH.1–5⇓⇓⇓⇓ While we agree with Dr Noël that an inflammatory response is involved in the pathogenesis of cerebral vasospasm after aSAH, we do not feel that it is unique to those patients with acute cocaine exposure or a variant of thromboangiitis obliterans.
- ↵Thai QA, Oshiro EM, Tamargo RJ. Inhibition of experimental vasospasm in rats with the periadventitial administration of ibuprofen using controlled-release polymers. Stroke. 1999; 30: 140–147.
- ↵Oshiro EM, Hoffman PA, Dietsch GN, Watts MC, Pardoll DM, Tamargo RJ. Inhibition of experimental vasospasm with anti-intercellular adhesion molecule-1 monoclonal antibody in rats. Stroke. 1997; 28: 2031–2037.
- ↵Aihara Y, Kasuya H, Onda H, Hori T, Takeda J. Quantitative analysis of gene expressions related to inflammation in canine spastic artery after subarachnoid hemorrhage. Stroke. 2001; 32: 212–217.
- ↵Bavbek M, Polin R, Kwan AL, Arthur AS, Kassell NF, Lee KS. Monoclonal antibodies against ICAM-1 and CD18 attenuate cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits. Stroke. 1998; 29: 1930–1935.