Published online before print June 12, 2003, doi: 10.1161/01.STR.0000078561.40741.B4
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(Stroke. 2003;34:1728.)
© 2003 American Heart Association, Inc.
Editorial Comment |
Editorial Comment—Thromboembolic Events During Neuroendovascular Procedures
Cerebrovascular Program, Department of Neurology and Neurosciences, University of Medicine and Dentistry of New Jersey, Newark, New Jersey
Thromboembolic and ischemic complications occur frequently during and after endovascular procedures because of associated arterial injury and the thrombogenic characteristics of arterial catheters, contrast agents, and implanted devices such as coils and stents.1,2 With the growing use of endovascular procedures in neurosurgical practice, adequate knowledge of the basic pathophysiological and pharmacological principles that are involved is important.
When blood first contacts a foreign surface, the sequence of events initiated often ends in blood coagulation and thrombus formation.3 Initially, a thin layer of platelets and fibrinogen covers the surface of the foreign material. The magnitude of the initial reaction depends on the surface charge, chemical properties, and topographic features of the vascular device and the pattern of blood flow in the vicinity.1,3 The basic equipment used during endovascular procedures includes angiographic catheters, guidewires, and microcatheters. Several investigators have suggested that vascular catheters used for diagnostic and therapeutic purposes are not biologically inert but may serve as nidi for thrombosis.1,4 Anderson et al5 observed that guidewires (both stainless steel and Teflon-coated) also exhibited surface irregularities that promote platelet aggregation and fibrin deposition. Even contrast agents may promote clotting in catheters and syringes, placing patients at risk of thromboembolism.1,6 Gasperetti et al6 observed that the use of nonionic contrast material during coronary angioplasty was associated with a higher risk of intravascular thrombosis.
Both coils and stents are intravascularly implanted devices that invoke thrombogenic responses when placed in vessels. The coils most commonly used in endovascular procedures are platinum Guglielmi detachable coils.7 The purpose of the coils is to induce thrombosis at the site of deployment, via electrothrombosis. Platinum is 3 to 4 times more thrombogenic than stainless steel. Although the initial thrombotic reaction after coil placement is important for aneurysm obliteration, fresh thrombus in the aneurysmal sac can embolize to distal distributions. In vivo studies have demonstrated that platelets accumulate rapidly on the stent surface after placement.8 Platelet accumulation is most pronounced when stents are placed within a mechanically injured arterial surface. Other factors that contribute to stent thrombogenicity are plaque around the stent and the surface area of the stent.1
Vessel occlusion can occur during or shortly after endovascular procedures as a result of local thrombosis or distal embolization. Intra-arterial thrombolysis is an attractive treatment for such occlusions because expedient local delivery of thrombolytics is possible as a result of existing arterial access. Cronqvist et al9 reviewed 19 cases of thromboembolic events that occurred during endovascular treatment of aneurysms. Embolisms associated with the procedure were observed in the middle cerebral artery for 14 patients, the anterior cerebral artery for 3, and the basilar trunk for 2. Complete recanalization was observed for 10 of the 19 patients after intra-arterial administration of urokinase (mean dose, 975 000 IU; range, 450 000 to 1 300 000 IU; infusion rate, 20 000 IU/min). Partial recanalization was observed for 9 patients. The authors observed that recanalization was best achieved when mechanical fragmentation of the thrombus and superselective drug infusion were possible. Nine of 10 patients who underwent complete recanalization experienced good recovery, whereas only 5 of 9 patients who underwent partial recanalization experienced good recovery. Intracerebral hemorrhage (ICH) occurred in 1 patient, and aneurysm rupture with subarachnoid hemorrhage occurred in 2 patients. In the accompanying article, Hähnel et al10 describe 9 patients who suffered thromboembolic complications during neuroendovascular procedures. These patients were treated by intra-arterial thrombolysis with the use of rtPA (maximum dose of 0.9 mg/kg). Successful recanalization was achieved in 4 of 9 patients. All 9 patients suffered cerebral ischemic infarctions, and none of the patients sustained ICH. The ischemic stroke was fatal in 2 patients, 4 patients remained moderately disabled, and 3 patients were severely disabled 3 months after thrombolysis.
Despite rapid delivery of intra-arterial thrombolytics, the recanalization rates and clinical outcome in these patients are suboptimal. Further research is required to determine whether the composition of thrombus formed during endovascular procedures is different from that of spontaneously formed thrombus. Platelet activation and aggregation are important components of processes occurring at the surface of endovascular devices and site of intimal injury within the arteries.1 It is possible that thrombus formation related to endovascular procedures may be platelet-rich and therefore more resistant to thrombolytic therapy. Nonetheless, strategies for effective prevention and treatment of thromboemboli during neuroendovascular procedures must be developed to improve the overall efficacy of these procedures.
References
1. Qureshi AI, Luft AR, Sharma M, Guterman LR, Hopkins LN. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures, part I: pathophysiological and pharmacological features. Neurosurgery. 2000; 46: 1344–1359.[CrossRef][Medline] [Order article via Infotrieve]
2. Qureshi AI, Luft AR, Sharma M, Guterman LR, Hopkins LN. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures, part II: clinical aspects and recommendations. Neurosurgery. 2000; 46: 1360–1375.[CrossRef][Medline] [Order article via Infotrieve]
3. Baier RE, Dutton RC. Initial events in interactions of blood with a foreign surface. J Biomed Mater Res. 1969; 3: 191–206.[CrossRef][Medline] [Order article via Infotrieve]
4. Jacobsson B, Schlossman D. Angiographic investigation of formation of thrombi on vascular catheters. Radiology. 1969; 93: 355–359.[Medline] [Order article via Infotrieve]
5. Anderson JH, Gianturco C, Wallace S, Dodd GD. A scanning electron microscopic study of angiographic catheters and guide wires. Radiology. 1974; 111: 567–571.[Medline] [Order article via Infotrieve]
6. Gasperetti CM, Feldman MD, Burwell LR, Angello DA, Haugh KH, Owen RM, Powers ER. Influence of contrast media on thrombus formation during coronary angioplasty. J Am Coll Cardiol. 1991; 18: 443–450.[Abstract]
7. Guglielmi G, Viñuela F, Sepetka I, Macellari V. Electrothrombosis of saccular aneurysms via endovascular approach, part 1: electrochemical basis, technique, and experimental results. J Neurosurg. 1991; 75: 1–7.[Medline] [Order article via Infotrieve]
8. Krupski WC, Bass A, Kelly AB, Marzec UM, Hanson SR, Harker LA. Heparin-resistant thrombus formation by endovascular stents in baboons: Interruption by a synthetic antithrombin. Circulation. 1990; 82: 570–577.
9. Cronqvist M, Pierot L, Boulin A, Cognard C, Castaings L, Moret J. Local intraarterial fibrinolysis of thromboemboli occurring during endovascular treatment of intracerebral aneurysm: a comparison of anatomic results and clinical outcome. AJNR Am J Neuroradiol. 1998; 19: 157–165.[Abstract]
10. Hähnel S, Schellinger PD, Gutschalk A, Geletneky K, Hartmann M, Knauth M, Sartor K. Local intra-arterial fibrinolysis of thromboemboli occurring during neuroendovascular procedures with recombinant tissue plasminogen activator. Stroke. 2003; 34: 1723–1729.
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