Correspondence *Loyola University Chicago, Stritch School of Medicine, Department of Neurology and Neurological Surgery, 2160 South First Avenue, 2700 McGuire, Maywood, IL 60153, USA

Email rdafer@lumc.edu

Original article

Metso TM et al. (2007) Prognosis and safety of anticoagulation in intracranial artery dissections in adults. Stroke 38: 1837–1842   PubMed

Synopsis

Background

Extracranial cervicocephalic artery dissections (CCADs) are one of the most common causes of stroke in young patients and are commonly treated with anticoagulants. By contrast, intracranial artery dissections (IADs) are rarer and are considered a contraindication to anticoagulation, because they are thought to be associated with a high risk of subarachnoid hemorrhage (SAH) and poor outcome.

Objectives

To characterize different forms of IADs and to test the hypothesis that anticoagulants are contraindicated in patients with IAD and SAH.

Design and intervention

This was a retrospective review of data on 256 consecutive patients with CCADs who were treated at a Finnish hospital during the period 1994–2004. IADs, including those localized within the cranial cavity and those starting extracranially but extending intracranially, were observed in 103 patients, 81 of whom had no clinical or imaging evidence of SAH (group 1) and 22 of whom had an SAH (group 2). All patients in group 1 received anticoagulation with intravenous full-dose heparin sulfate or subcutaneous low molecular weight heparin, followed by warfarin (target International Normalized Ratio 2.0–3.0) for at least 3 months. By contrast, patients in group 2 did not receive anticoagulation.

Outcome measures

Outcome measures included the NIH Stroke Scale, Glasgow Coma Scale, Barthel Index, and modified Rankin Scale (mRS), recorded at 3 months' follow-up.

Results

In group 1, no aneurysm was detected in the acute stage. By comparison, nearly all patients in group 2 (n = 21, 95%) had a ruptured fusiform dissecting aneurysm leading to the SAH; the aneurysms were mainly located in the vertebrobasilar artery (n = 11). The condition of the patients in group 2—as assessed by the Glasgow Coma Scale—on admission was significantly worse (P <0.0001) than that of the patients in group 1, and their outcome according to the mRS was significantly poorer (P <0.0001). One patient in group 1 died of brain infarction in the acute stage, but there were no deaths, stroke recurrences or new infarctions and only one case of aneurysm during follow-up, and no intracranial bleeding was observed during anticoagulation. At 3 months, the majority (n = 63, 77.8%) of patients in group 1 had no disability (Barthel Index 100), and 64 (79.1%) had a favorable functional outcome (mRS score 0–2); only 5 (6.2%) patients were still hospitalized. By contrast, 3 patients in group 2 died soon after hospital arrival and 4 died later, resulting in a 3-month mortality rate of 31.8%. The 3-month median mRS score in this group was 4 (range 0–6), but only 7 (31.8%) patients had a favorable outcome at the end of follow-up.

Conclusion

IADs accounted for nearly a third of all CCAD cases, with an increased risk of fusiform aneurysm especially in patients with vertebrobasilar arterial dissections. Patients with IAD had a good prognosis if they had no SAH, and anticoagulation in this IAD population seems to be safe.

Commentary

CCADs are a common cause of ischemic stroke particularly in young adults, with an incidence rate of 2.6–5.0 cases of CCAD per 100,000 individuals in the general population.¹ The extracranial segments of the carotid and vertebral arteries are more commonly involved, and intracranial extensions are considered rare. Despite the absence of clear evidence-based data, anticoagulation is widely prescribed in patients with extracranial CCADs to prevent symptom recurrence, thrombus formation and cerebral ischemia. When IAD is suspected, however, anticoagulation is usually avoided because of the potential increased risk of SAH.

In their recent article in Stroke, Metso et al. present provocative and intriguing data on the potential efficacy and safety of anticoagulation in IAD. The authors describe a series of patients with IAD who were treated at the Departments of Neurology and Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland. Patients were divided into two groups: those with cerebral ischemia in the absence of cerebral aneurysm or SAH, who were treated with anticoagulation; and those with SAH or aneurysm, who did not receive anticoagulation. The authors observed a favorable outcome in the first group, in contrast to the poor outcome in the second group, and concluded that anticoagulation might be safe in patients with IAD who do not have SAH. IAD was more common than previously described, accounting for a third of all CCAD cases.

This study presents the largest series on IAD in the literature and provides important data on the safety of anticoagulation in symptomatic patients with IAD who do not have SAH. In statistical terms, however, the sample size was small, and the results should, therefore, be interpreted with caution.

Randomized studies of anticoagulation in acute arterial ischemic stroke continue to show no proven benefits in the reduction of early stroke recurrence, mortality and morbidity, and there is an increased risk of bleeding complications.² In the absence of randomized controlled trials of anticoagulation in CCAD, the use of anticoagulation in this setting is particularly controversial. In two small series of patients with CCAD, anticoagulation was associated with a favorable outcome.^{3, 4} Conversely, another small cohort study showed no benefit of heparin over aspirin in patients with CCAD.¹ In addition, the collaborating members of the Canadian Stroke Consortium reported prospective data on patients with angiographically proven acute CCAD followed for 1 year. The event rate among patients treated with anticoagulants was not significantly different from that among patients treated with aspirin.⁵ Likewise, a Cochrane review of data from nonrandomized trials did not show a significant difference in event rate between these two treatment modalities.²

Metso et al. report important data on the prevalence of IAD and address the potential safety of anticoagulation when SAH is excluded. Given the risks associated with anticoagulation in bleeding-prone patients and the absence of good clinical evidence to support its use in CCAD, however, the risks associated with anticoagulation in IAD outweigh the benefits. The usefulness of anticoagulation in patients with IAD should, therefore, be carefully revisited. We anticipate that the study by Metso et al. is unlikely to change current patterns of anticoagulant use in IAD. Data from the International Study on Cervical and Intracranial Arterial Dissection, an ongoing prospective observational trial, might shed some light on this topic in the future.

Acknowledgments

The synopsis was written by Rima M Dafer and José Biller.

References

1. Biller J et al. (1986) Cervicocephalic arterial dissections. A ten-year experience. Arch Neurol 43: 1234–1238 | PubMed | ChemPort |
2. Lyrer P and Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database of Systematic Reviews 2003, Issue 3. Art. No.: CD000255
3. Gonzalez-Portillo F et al. (2002) Outcome of extracranial cervicocephalic arterial dissections: a follow-up study. Neurol Res 24: 395–398 | Article | PubMed |
4. Fabian TC et al. (1996) Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg 223: 513–522 | Article | PubMed | ChemPort |
5. Beletsky V et al. (2003) Cervical arterial dissection: time for a therapeutic trial. Stroke 34: 2856–2860 | Article | PubMed |

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Subject areas under which this article appears: Stroke