Rheolytic Thrombectomy for Thromboembolic Occlusion of the Internal Carotid Artery Complicating Coronary Intervention

Stroke is a relatively rare but catastrophic complication of percutaneous coronary intervention (PCI), and is the cause of substantial morbidity and mortality rates. The incidence of stroke after PCI is reported to be 0.3 to 0.5%, which has not changed dramatically over the last decade despite advancement of techniques and devices.^1-3 PCI-related stroke is almost always embolic in origin. Intra-arterial thrombolysis has been used with limited success, but there are no widely accepted strategies for acute ischemic stroke occurring during PCI. We present a case of thromboembolic occlusion of an internal carotid artery (ICA) during right coronary artery intervention in which the AngioJet® rheolytic thrombectomy device (Possis Medical, Inc., Minneapolis, Minnesota) was used in an attempt to re-establish cerebral circulation. Case Report. A 55-year-old diabetic man was admitted for recent myocardial infarction. Several days prior to the admission, the patient experienced chest pressure and jaw pain lasting over 2 hours while playing golf. He had been feeling weak and had lightheadedness on the morning of the admission. Physical examination was unremarkable, but an ECG showed abnormal Q-waves in inferior leads, with persistent, mild ST-segment elevations. Creatine kinase and troponin I were 197 IU/l, and 13.2 ng/ml, respectively. Oral aspirin, beta-blocker and systemic heparin were started. Coronary angiography showed total occlusion of the proximal right coronary artery (RCA), and left ventriculography revealed severe hypokinesis of the inferior wall, with an ejection fraction of 40% (Figure 1). Based on the history of recent myocardial infarction and angiographic findings, PCI was undertaken. A total of 6,000 Units of heparin was administered and a double bolus of eptifibatide with continuous infusion was commenced. The RCA was engaged with a 6 Fr JR4 guiding catheter, and the occluded segment was crossed with a 0.014 inch Choice PT Graphix wire (Boston Scientific Corporation, Natick, Massachusetts), which was exchanged for a 0.014 inch Forte wire (Boston Scientific Corporation, Natick Massachusetts). Rheolytic thrombectomy using the AngioJet device was attempted because of the thrombus-rich appearance of the lesion, but the AngioJet catheter could not pass through the total occlusion. The lesion was dilated several times with a 3.0 × 15 mm balloon. After the balloon was removed from the guiding catheter, the pressure waveform from the distal tip of the catheter became muted. The catheter was appropriately engaged in the RCA, and kinking of the catheter was not noted. The entire system was pulled out for fear of possible thrombotic occlusion of the catheter. Inspection of the catheter revealed a large clot coming out of the catheter. When a new guiding catheter was advanced, the patient was found to be unresponsive. This state rapidly evolved to a global aphasia with right hemiplegia. Considering the severity of the neurological status, emergent carotid angiography was performed, and showed total occlusion of the left internal carotid artery (ICA), 4 to 5 cm above the bifurcation (Figure 2). A 6 Fr Arrow sheath (Arrow International, Inc., Reading, Pennsylvania) was engaged in the left common carotid artery and a 0.014 inch coronary guidewire was advanced into the distal ICA. Within 10 minutes from the onset, the AngioJet catheter was passed through the sheath into the ICA over the wire. Thrombectomy was performed several times, but the next angiography showed embolization of the clot to the distal ICA (Figure 3). Angioplasty with a 3.0 mm balloon was not effective and intra-arterial thrombolysis with recombinant tissue plasminogen activator (rtPA) was attempted in the distal ICA. Totals of 30 mg of rtPA and 10 mg of abciximab were injected into the clotted segment over a 20-minute period. Final angiography revealed patent, antegrade filling of the left anterior cerebral artery (ACA), with remaining occlusion of the proximal portion of the left middle cerebral artery (MCA) (Figure 4). Contralateral carotid angiography revealed poor collateral supply. A computed tomography (CT) scan of the brain showed a large, hypodense area without hemorrhage suggestive of subtotal left middle cerebral artery infarction. Unfortunately, the neurological status gradually declined, and the patient expired as a result of cerebral edema 6 days later. Discussion. This report illustrates the case of a patient with an acute stroke caused by thromboembolization from the native coronary artery during percutaneous coronary intervention, in whom AngioJet rheolytic thrombectomy was used in an attempt to re-establish patency of an occluded internal carotid artery. The incidence of stroke occurring during PCI has been 0.3–0.5%.^1-3 Surprisingly, the rate has not changed appreciably over the last decade despite advancement in devices and techniques. Most strokes during cardiac catheterization are embolic in origin and account for 5 to 10 % of all deaths after PCI. Fuchs et al. demonstrated that risk factors for PCI-related stroke include the emergency use of intra-aortic balloon pumps, advanced age and saphenous vein graft intervention.1 Whereas these risk factors may reflect underlying severe atherosclerosis of the aorta, clot inside the coronary artery or the vein graft can be sources of embolization. Sandoval and Laufer reported a case of middle cerebral artery embolus caused by retrograde migration of a vein graft thrombus.⁴ Although release of coronary thrombus to the systemic circulation is a relatively rare event, operators should be aware of several technical pitfalls when a thrombus-rich lesion is treated. First, the balloon should be given a generous amount of time to be deflated before it is pulled back. An incompletely deflated balloon may catch clots on its surface. Second, stable and steady engagement of the guiding catheter is essential. Third, when thrombotic occlusion of the guiding catheter is suspected, the guidewire should be first withdrawn from the coronary artery. Then, the catheter has to be retrieved with negative pressure applied to its lumen. If the wire is not covered by the catheter, the wire can pick up and release thrombus from the coronary artery. Acute ICA occlusion is a potentially catastrophic event and frequently results in bleak outcomes. Whereas intra-arterial thrombolysis can improve clinical outcomes of patients with MCA occlusions within 6 hours from the onset,⁵ the mortality rate of acute ICA occlusion approaches 50%, even with early intra-arterial thrombolysis.⁶ The time frame form onset to treatment seems to be an important predictor for favorable outcomes. Rabinstein et al. reported a case of complete neurological recovery after intracranial carotid bifurcation occlusion with intra-arterial rtPA started less than 3 hours after onset.⁷ In our case, the treatment started within 30 minutes after the onset, but the proximal ICA occlusion evolved into distal embolization to the bifurcation of the ACA and the MCA. The poor response to the intra-arterial thrombolysis and endovascular therapy may reflect the size of the clot or the inadequacy of the thrombolytics. The clot was likely to have been extremely large in our case, as it completely occluded the proximal ICA. Currently, there are no widely accepted approaches for PCI-related stroke. Sandoval and Laufer reported successful recanalization of embolic MCA occlusion occurring during vein graft intervention with 50 mg of rtPA infused at 1 mg/minute.4 In our case, a total of 30 mg of rtPA was administered over 20 minutes in combination with GP IIb/IIIa inhibitors, and several follow-up CT scans did not show any evidence of hemorrhagic transformation. A higher total dose of rtPA infused at a slower rate may have led to more favorable results. However, the optimal dose and regimen of thrombolytics and antiplatelet agents for PCI-related stroke remains unclear. To our knowledge, the use of the AngioJet for thromboembolic occlusion device of the carotid artery during native coronary artery intervention has not been previously reported. The AngioJet rheolytic thrombectomy system is an aspiration device that uses the Venturi effect whereby a low-pressure zone is created around the catheter by the high-speed saline jet inside the catheter. This results in mechanical disruption, aspiration and retrieval of the surrounding thrombus through the side holes. It has theoretical advantages over thrombolytic therapy because it can re-establish blood flow more expeditiously and reduce the dose of thrombolytics. Bellon et al. reported the use of rheolytic thrombectomy of the acute occluded ICA for 3 patients.⁸ Although rheolytic thrombectomy is a potential approach to acute occlusion of the carotid artery, it can be associated with distal embolization, as was the case with our patient. In addition, the inherent stiffness of the AngioJet catheter precludes its use in the distal carotid artery, such as petrous and cavernous portions. To prevent distal embolization, simultaneous use of a distal protection device is strongly recommended.⁹ Finally, operators addressing thrombotic proximal coronary artery lesions should take meticulous care to avoid embolization of coronary thrombus to the systemic circulation.

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