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(Stroke. 2008;39:e128.)
© 2008 American Heart Association, Inc.
Letters to the Editor |
Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland
Department of Neurology, University of Bern, Bern, Switzerland
Department of Neurosurgery, University of Bern, Bern, Switzerland
Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland
Response:
We deeply appreciate the interest of Dr Yousaf and his colleagues in our study and we understand their concerns. Certainly, differences in vessel characteristics exist between species and vascular territories, especially when compared to human brain vessels. Therefore, care must be taken when comparing complication rates assessed by animal models to complication rates in humans. However, we encounter a large variety of vessel conditions even in humans during our daily work: from young and straight vessels to elongated, sclerotic and dilated vessels, from vessels prone to spasm (more often found in younger patients) to less reactive arteries.1,2 These different vessel characteristics are associated with different complications during angiography (ie, vessel spasm, dissection, perforation, thromboembolization). Furthermore, different thrombus compositions are encountered in human ischemic stroke that influence thrombus stability and consecutively the success rate of mechanical thrombectomy.3,4 Hence, it is very challenging to establish an in vivo stroke model that reproduces all the above mentioned variables reliably.
In vivo models using swine have been applied to several neurovascular diseases.5–7 The small diameter of the intracranial arteries of the swine (
1.0 mm) as well as the rete mirabile impede the assessment of mechanical devices in this territory.8 On the other hand, the external carotid artery branches of the swine resemble human brain vessels to some extent: vessel diameter of 2.5 to 3.0 mm, similar distance of puncture site (catheter sheath) to the target vessel in the head, and passage of the aortic arch and carotid arteries by the endovascular devices.9 This allows for an experimental setting consistent with the procedure in humans with regard to the tested material used. As mentioned by Dr Yousaf et al, endovascular interventions are feasible in other vascular territories (eg, renal or visceral arteries) with vessel diameters similar to that of human brain arteries. However, we did not carry out assessment of neurovascular devices in those territories because of the significantly different endovascular approach.
For the first time, our model provides visualization of the radio-opaque thrombus during endovascular procedures and allows the assessment of thrombus movement, fragmentation and possible embolization. We regret that the figures presented have created uncertainty for the reader. Figures with a large field-of-view, which are necessary to illustrate the position of both the balloon catheter and the thrombus/device, have less resolution than figures with a smaller field-of-view. The latter illustrate in more detail the thrombus-device interaction. We would be pleased to provide additional illustrations to interested readers, which might improve comprehension of the figures presented in the study.
To conclude, it is clear that we need an in vivo model for the assessment of the numerous devices that have been introduced recently for acute stroke treatment. Despite various limitations, the presented model provides an anatomic and hemodynamical setting similar to humans. Furthermore, it allows for visualization of the thrombus during angiography and therefore enables assessment of the thrombus-device interaction. Though we are confident about the abilities of our swine model, we are also aware that modeling of human ischemic stroke needs further research and development.
Acknowledgments
Disclosures
None.
References
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2. Rabb CH, Tang G, Chin LS, Giannotta SL. A statistical analysis of factors related to symptomatic cerebral vasospasm. Acta Neurochir. 1994; 127: 27–31.[CrossRef][Medline] [Order article via Infotrieve]
3. Marder VJ, Chute DJ, Starkman S, Abolian AM, Kidwell C, Liebeskind D, Ovbiagele B, Vinuela F, Duckwiler G, Jahan R, Vespa PM, Selco S, Rajajee V, Kim D, Sanossian N, Saver JL. Analysis of thrombi retrieved from cerebral arteries of patients with acute ischemic stroke. Stroke. 2006; 37: 2086–2093.
4. Caplan LR. Brain embolism, revisited. Neurology. 1993; 43: 1281–1287.
5. Takemae T, Branson PJ, Alksne JF. Intimal proliferation of cerebral arteries after subarachnoid blood injection in pigs. J Neurosurg. 1984; 61: 494–500.[Medline] [Order article via Infotrieve]
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7. Culp WC, Porter TR, Lowery J, Xie F, Roberson PK, Marky L. Intracranial clot lysis with intravenous microbubbles and transcranial ultrasound in swine. Stroke. 2004; 35: 2407–2411.
8. Reinert M, Brekenfeld C, Taussky P, Andres R, Barth A, Seiler RW. Cerebral revascularization model in a swine. Acta Neurochir Suppl. 2005; 94: 153–157.[CrossRef][Medline] [Order article via Infotrieve]
9. Gralla J, Schroth G, Remonda L, Fleischmann A, Fandino J, Slotboom J, Brekenfeld C. A dedicated animal model for mechanical thrombectomy in acute stroke. AJNR Am J Neuroradiol. 2006; 27: 1357–1361.
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