Tissue plasminogen activator (tPA) in acute ischaemic stroke: time for collegiate communication and consensus
Published online: 3 January 2005
Christopher R Levi (on behalf of the Australasian Stroke Unit Network, the New South Wales Greater Metropolitan Clinical Taskforce Stroke Initiative, and the Towards A Safer Culture Stroke Expert Working Group)
Director, Acute Stroke Services, John Hunter Hospital, Locked Bag No. 1, Hunter Region Mail Centre, NSW 2310. christopher.leviAThunter.health.nsw.gov.au
In reply: We thank the authors for their comments on our recent position statement.1 We fully agree and accept the view of Rogers and colleagues that emergency physicians are central to the timely and safe delivery of emergency medical care in our health system. This is especially the case for a therapy such as intravenous tPA, given the narrow therapeutic window and coordination challenges. We view the development of linkages with our colleagues in emergency medicine as crucial in implementing not only tPA but also a number of acute stroke therapies showing great promise in the advanced stages of development.2 Our position statement is a starting point for broader discussion, and we are pleased that discussions between the key groups are under way.
We agree that, when considering patient suitability for intravenous tPA, a number of uncertainties remain, and we fully support the rationale for the ongoing clinical trials of thrombolysis in acute ischaemic stroke (see www.astn.org.au/epithet/index.html and www.ist3.com/). The risk–benefit ratio will be improved in the 0–90-minute window, as indicated by Fatovich. However, it is likely that some patients at much later time points will also gain benefit. We would emphasise, however, that according to Australia’s independent arbiter of therapeutic safety and efficacy, the Therapeutic Goods Administration, intravenous tPA is an approved therapy if given within a 3-hour window, under appropriate clinical circumstances and within appropriate healthcare settings.
Regarding the comments by Fatovich on number needed to harm, it is important to recognise that the most serious adverse outcome of intravenous tPA — fatal intracerebral haemorrhage — is already accounted for in the calculations of number needed to treat (for patients to survive free from dependency). Intra-arterial thrombolytic therapy in the form of prourokinase has been found to be effective in reducing dependency in acute ischaemic stroke, shown angiographically to be caused by middle cerebral artery occlusion.3 Feasibility issues, however, presently limit the application of the intra-arterial approach, and the relative risk of intracranial haemorrhage, even with this more targeted approach, is similar to that seen with intravenous therapy.
The importance of cross-disciplinary teamwork in the effective application of current and future acute stroke therapies cannot be underestimated. Central to this is the need to develop an effective dialogue between the leaders of these teams — stroke physicians and emergency physicians. The Australasian Stroke Unit Network, the New South Wales Greater Metropolitan Clinical Taskforce Stroke Initiative, and the Towards A Safer Culture Stroke Expert Working Group are committed to the task of helping to build better links between stroke units and emergency departments.
References
- Levi CR, on behalf of the Australasian Stroke Unit Network, the New South Wales Greater Metropolitan Transition Taskforce Stroke Initiative, and the Towards A Safer Culture Stroke Expert Working Group. Tissue plasminogen activator (tPA) in acute ischaemic stroke: time for collegiate communication and consensus. Med J Aust 2004; 180: 634-636.
- Mayer SA, Brun N, Broderick J, et al. Recombinant factor VIIa for acute intracerebral haemorrhage. Presented at the 5th World Stroke Congress, 23–26 June 2004, Vancouver, Canada. Stroke 2004; 35 (6). i1085662
- Furlan A, Higashida R, Wechsler L, et al, for the PROACT investigators. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA 1999; 282: 2003-2011. CBBJHJGF
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