Response to Letter by Yousaf et al
2008; Lippincott Williams & Wilkins; Volume: 39; Issue: 8 Linguagem: Inglês
10.1161/strokeaha.107.524439
ISSN1524-4628
AutoresCaspar Brekenfeld, Gerhard Schroth, Marwan El‐Koussy, Krassen Nedeltchev, Michael Reinert, Johannes Slotboom, Jan Gralla,
Tópico(s)Intracerebral and Subarachnoid Hemorrhage Research
ResumoHomeStrokeVol. 39, No. 8Response to Letter by Yousaf et al Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Letter by Yousaf et al Caspar Brekenfeld, MD, Gerhard Schroth, MD and Marwan El-Koussy, MD Krassen Nedeltchev, MD Michael Reinert, MD Johannes Slotboom, PhD and Jan Gralla, MD Caspar BrekenfeldCaspar Brekenfeld Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland , Gerhard SchrothGerhard Schroth Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland and Marwan El-KoussyMarwan El-Koussy Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland Krassen NedeltchevKrassen Nedeltchev Department of Neurology, University of Bern, Bern, Switzerland Michael ReinertMichael Reinert Department of Neurosurgery, University of Bern, Bern, Switzerland Johannes SlotboomJohannes Slotboom Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland and Jan GrallaJan Gralla Institute of Interventional and Diagnostic Neuroradiology, University of Bern, Bern, Switzerland Originally published26 Jun 2008https://doi.org/10.1161/STROKEAHA.107.524439Stroke. 2008;39:e128Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 26, 2008: Previous Version 1 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.DisclosuresNone.1 Inagawa T. Cerebral vasospasm in elderly patients with ruptured intracranial aneurysms. Surg Neurol. 1991; 36: 91–98.CrossrefMedlineGoogle Scholar2 Rabb CH, Tang G, Chin LS, Giannotta SL. A statistical analysis of factors related to symptomatic cerebral vasospasm. Acta Neurochir. 1994; 127: 27–31.CrossrefMedlineGoogle Scholar3 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.LinkGoogle Scholar4 Caplan LR. Brain embolism, revisited. Neurology. 1993; 43: 1281–1287.CrossrefMedlineGoogle Scholar5 Takemae T, Branson PJ, Alksne JF. Intimal proliferation of cerebral arteries after subarachnoid blood injection in pigs. J Neurosurg. 1984; 61: 494–500.CrossrefMedlineGoogle Scholar6 Massoud TF, Vinters HV, Chao KH, Viñuela F, Jahan R. Histopathologic characteristics of a chronic arteriovenous malformation in a swine model: preliminary study. AJNR Am J Neuroradiol. 2000; 21: 1268–1276.MedlineGoogle Scholar7 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.LinkGoogle Scholar8 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.CrossrefMedlineGoogle Scholar9 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.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails August 2008Vol 39, Issue 8 Advertisement Article InformationMetrics https://doi.org/10.1161/STROKEAHA.107.524439 Originally publishedJune 26, 2008 PDF download Advertisement
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