Catheterization and Cardiovascular Interventions 00:00–00 (2015)
Case Report Intra-Arterial Thrombolysis of Central Retinal Artery Occlusion Following Percutaneous Atrial Septal Defect Closure Jin Pyeong Jeon,1 MD, Young Dae Cho,2* MD, and Moon Hee Han,2 MD Use of percutaneous devices for atrial septal defect (ASD) closure is growing, given the minimally invasive nature and the long-term durability of this approach. The reported rate of thrombus formation after catheter closure is 1.2%. Thrombotic risk varies according to closure device and Dacron-covered nitinol Amplatzer devices carry a 0-0.3% rate of thrombus formation; but central retinal artery occlusion (CRAO) is rarely implicated as an adverse event. Herein, we report the first successful intraarterial thrombolytic treatment of CRAO developing after ASD closure via Amplatzer device. VC 2015 Wiley Periodicals, Inc. Key words: central retinal artery occlusion; thrombolysis; atrial septal defect
INTRODUCTION
CASE
A consensus by authorities on optimal treatment of central retinal artery occlusion (CRAO) has yet to evolve. The European Assessment Group for Lysis in the Eye (EAGLE) [1] trial failed to demonstrate that intraarterial thrombolysis (IAT) is superior to conservative treatment in managing CRAO. Heterogeneity in degree of ischemic damage sustained and time intervals from onset of symptoms to treatment (mean, 11.89 5.67 hr) have hampered outcome assessments. However, ischemia of the penumbra zone may be alleviated through reperfusion therapy [2], thus indicating that early restoration of retinal blood flow has merit in this setting. Percutaneous device usage is increasingly elected for atrial septal defect (ASD) closure due to the minimally invasive nature and the long-term durability of this approach [3]. Related complications generally include cardiac perforation, aorta-to-right arterial fistula, device malposition or embolization, and thrombus formation [3,4]. Although the reported rate of thrombus development after catheter closure of ASD is 1.2% [4], CRAO is rarely implicated as an adverse event. Herein, we describe an instance where CRAO following transcatheter ASD closure by Amplatzer device was successfully resolved through IAT.
A 21-year-old woman was admitted for closure of a moderate-grade ASD. Maximal ASD diameter by transesophageal echocardiography (TEE) was 14.3 mm. A 17-mm Amplatzer septal occluder (AGA medical Corp, Golden Valley, MN) was deployed as usual for transcatheter occlusion. Aspirin (200mg daily oral dose) and heparin (750 units/hr as intravenous infusion) were administered after the procedure. No visible thrombus was evident in proximity to the device by
C 2015 Wiley Periodicals, Inc. V
1
Department of Neurosurgery, Hallym University College of Medicine, Chuncheon, Korea 2 Department of Radiology, Seoul National University College of Medicine, Seoul, Korea Conflict of interest: Nothing to report. *Correspondence to: Young Dae Cho, M.D., Department of Radiology, Seoul National University College of Medicine, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea. Email: [email protected] Received 10 March 2015; Revision accepted 14 June 2015 DOI: 10.1002/ccd.26100 Published online 00 Month 2015 in Wiley Online Library (wileyonlinelibrary.com)
2
Jeon et al.
Fig. 1. Central retinal artery occlusion. (A) Unremarkable diffusion MRI. (B) Angiography of left internal carotid artery showing patent small–caliber ophthalmic artery (OA) (arrow). (C) Ethmoidal and lacrimal branches of left ECA devoid of chorodial blush. (D) Selective microcatheter angiography of OA shows faint arterial supply to inferior orbit. (E) Selective angiography of OA after intra-arterial (IA) thrombolytic uroki-
nase infusion confirms restoration of posterior ciliary artery and muscular arteries (arrows). (F) Photography of fundus after IA thrombolysis—note ischemic, edematous retina with cherry-red spot and preservation of retina supplied by ciliary artery. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
echocardiography. Twenty-eight hours later, the patient suffered sudden loss of left eye vision. Serial neurologic and ophthalmologic examinations documented a defect of left visual filed, with minimal preservation of central vision. Visual acuity was diminished 20/50 and was restricted to light perception. Examination of the fundus showed cherry-red spots and edema of left maculae, consistent with CRAO. Acute cerebral infarction was ruled out by diffusion-weighted magnetic resonance imaging (Fig. 1A). Cerebral angiography was performed (170 min after onset of symptoms) using a GE biplane angiographic system (GE Healthcare, Milwaukee, WI). The left internal carotid artery was patent, showing no occlusion of the small-caliber (0.9 mm) ophthalmic artery (OA) (Fig. 1B); but ethmoidal and lacrimal ocular branch arteries of the external carotid artery (ECA) were devoid of choroidal blush (Fig. 1C). Selective angiography via a microcatheter (Excelsior SL-10; Boston Scientifics Corp, Natick, Massachusetts, USA) revealed faint arterial supply to inferior orbit, whereas the central retinal artery was not completely occluded
(Fig. 1D). Urokinase (500,000 units; Green Cross pharmacy, Yongin, Korea) thrombolytic therapy was slowly infused through the catheter in a 75-min period. Selective angiography thereafter indicated restoration of posterior ciliary and muscular arteries (Fig. 1E), associated with prompt recovery of central and temporal portions of left visual filed after IAT. Photography of fundus after IAT showed note ischemic, edematous retina with cherry-red spot and preservation of retina supplied by ciliary artery (Fig. 1F). Goldmann perimetry testing 3 months later demonstrated improved (20/ 30) visual acuity, with a left visual field defect at inferonasal quadrant. DISCUSSION
Thrombus formation after catheter closure of ASD is a rare complication that may result in serious embolic injury. Five patients (1.2%) reported by Krumsdorf et al. [4] developed thrombi after catheter ASD closure. Such thrombi may present acutely in the periprocedural period [5] or emerge as late developments
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Intra-Arterial Thrombolysis of CRAO
up to 3 years after implantation [6]. Paroxysmal atrial fibrillation and persistent atrial septal aneurysm may accompany thrombus formation [4]. Thrombotic risk varies according to closure device. Dacron-covered nitinol Amplatzer devices carry a 0–0.3% rate of thrombus formation in patients with ASD and foramen ovale (at 4 weeks and 6 months, respectively). Although cerebral thromboembolic events are occasionally seen with Amplatzer device closure of ASD [7], CRAO has yet to be implicated. Currently, there is controversy surrounding comparative efficacies of IAT and conservative treatment in managing CRAO. A systemic review [8] concluded that IAT produced better outcomes than conventional treatment in terms of preserving vision. However, analysis of non-randomized and retrospective studies, without attention to degree of CRAO and time intervals for intervention, may be fundamentally flawed. Differences in preservation of visual function prior to delivery of IAT likely reflect variability in extent of ischemic damage that will impact treatment outcomes. One particular study has shown that early reperfusion via IAT may preferentially benefit patients with incomplete CRAO [9], compared with those suffering subtotal and total CRAO. On the other hand, the therapeutic time window for reperfusion of CRAO remains unclear. According to the literature, IAT has been performed after a lag of up to 50 hr [8,10], although Hayreh et al. [11] saw irreversible retinal damage in rhesus monkey models after 240 minutes. Few prospective studies have investigated an optimal time interval in humans, but a window of 6–12 hr is generally considered the limit for IAT [12]. Finally, Hwang et al. [12] have suggested that instances of CRAO involving milder degrees of arterial occlusion and shorter intervention delays may in fact yield better visual outcomes. We attribute the rapid symptomatic improvement of our patient after IAT to timely reperfusion (within 3 hr after symptom onset) and salvage of the ciliary artery, preserving minimal central vision. Another important factor in these circumstances is the contribution of collateral flow in maintaining tissue viability. Kim et al. [13] determined that the extent of collateral circulation seen on baseline angiography correlated with infarct volume and National Institute of Health Stroke Scale (NIHSS) scores in patients with acute middle cerebral artery occlusion. Most studies of CRAO have not addressed regional collateral flow, which may well be a confounding factor in prior studies that skews results. In our patient, choroidal blush (from ECA) was lacking (Fig. 1C). Hence, timely reperfusion via OA is especially urgent in situations where collateral circulation is poor. The major safety concerns of IAT are cerebral infarct and hemorrhage transformation. We encoun-
3
tered only two reported instances of stroke and one of hemorrhage in patients with CRAO after IAT [8]. In the EAGLE trial, two (4.7%) of 42 patients subjected to IAT suffered intracranial hemorrhages [1] , whereas Ahn et al. [9] reported a 25.8% rate of embolic infarction after IAT. Most of their subjects were asymptomatic, and only one patient experienced hemianopsia due to an occipital lobe infarct. However, IAT apparently does not worsen the 23% rate of embolic infarct ordinarily attached to angiography (diagnostic or interventional) [14]. A technical issue impacting success of IAT is appropriate microcatheter selection, particularly size and distal shape. Diameter of the OA is 1.54 0.04 mm (mean SD) and 1.31 0.05 mm in men and women, respectively [15]. As such, microwires 0.014 in and microcatheters of 0.0165-in distal inner diameter are sized appropriately for OA navigation and thrombolysis. In terms of catheter shape, an S-shaped distal tip may be used primarily to accommodate arterial curvature [12]. However, if OA originates immediately past carotid siphon, selecting OA orifice with an S-shaped microcatheter may be technically difficult. In our patient, a microcatheter with straight tip easily sufficed for thrombolysis.
CONCLUSIONS
CRAO is a rare complication after percutaneous ASD closure. Prompt revascularization through IAT may enable immediate restoration of blood flow in select patients. Timely diagnosis of CRAO and prompt intervention are essential to reduce ischemic injury of retina and mitigate loss of vision
ACKNOWLEDGMENT
The authors are very grateful to Professor Gi Beom Kim for his help in this study. REFERENCES 1. Schumacher M, Schmidt D, Jurklies B, et al. EAGLE-Study Group Central retinal artery occlusion: Local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010;117:1367–1375. 2. Beck J, Raabe A, Lanfermann H, et al. Tissue at risk concept for endovascular treatment of severe vasospasm after aneurysmal subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2004;75:1779–1781. 3. Masura J, Gavora P, Podnar T. Long-term outcome of transcatheter secundum-type atrial septal defect closure using Amplatzer septal occluders. J Am Coll Cardiol 2005;45:505–507. 4. Krumsdorf U, Ostermayer S, Billinger K, et al. Incidence and clinical course of thrombus formation on atrial septal defect and
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
4
5.
6.
7.
8.
9.
Jeon et al. patient foramen ovale closure devices in 1,000 consecutive patients. J Am Coll Cardiol 2004;43:302–309. Yorgun H, Canpolat U, Kaya EB, Aytemir K, Oto A. Thrombus formation during percutaneous closure of an atrial septal defect with an Amplatzer septal occluder. Texas Heart Inst J 2011;38: 427–430. Ruge H, Wildhirt SM, Libera P, et al. Images in cardiovascular medicine. Left atrial thrombus on atrial septal defect closure device as a source of cerebral emboli 3 years after implantation. Circulation 2005;112:e130–e131. Dardas PS, Ninios V, Mezilis N, et al. Cryptogenic stroke after percutaneous closure of an atrial septal defect. Hellenic J Cardiol 2012;53:155–159. Noble J, Weizblit N, Baerlocher MO, Eng KT. Intra-arterial thrombolysis for central retinal artery occlusion: A systematic review. Br J Ophthalmol 2008;92:588–593. Ahn SJ, Kim JM, Hong JH, et al. Efficacy and safety of intraarterial thrombolysis in central retinal artery occlusion. Invest Ophthalmol Visl Sci 2013;54:7746–7755.
10. Richard G, Lerche RC, Knospe V, Zeumer H. Treatment of retinal arterial occlusion with local fibrinolysis using recombinant tissue plasminogen activator. Ophthalmology 1999;106: 768–773. 11. Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004; 78:723–736. 12. Hwang G, Woo SJ, Jung C, et al. Intra-arterial thrombolysis for central retinal artery occlusion: Two cases report. J Korean Med Sci 2010;25:974–979. 13. Kim JJ, Fischbein NJ, Lu Y, et al. Regional angiographic grading system for collateral flow: Correlation with cerebral infarction in patients with middle cerebral artery occlusion. Stroke 2004;35:1340–1344. 14. Bendszus M, Koltzenburg M, Burger R, et al. Silent embolism in diagnostic cerebral angiography and neurointerventional procedures: A prospective study. Lancet 1999;354:1594–1597. 15. Lang J, Kageyama I. The ophthalmic artery and its branches, measurements and clinical importance. Surg Radiol Anat 1990;12:83–90.
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Case Report Intra-Arterial Thrombolysis of Central Retinal Artery Occlusion Following Percutaneous Atrial Septal Defect Closure Jin Pyeong Jeon,1 MD, Young Dae Cho,2* MD, and Moon Hee Han,2 MD Use of percutaneous devices for atrial septal defect (ASD) closure is growing, given the minimally invasive nature and the long-term durability of this approach. The reported rate of thrombus formation after catheter closure is 1.2%. Thrombotic risk varies according to closure device and Dacron-covered nitinol Amplatzer devices carry a 0-0.3% rate of thrombus formation; but central retinal artery occlusion (CRAO) is rarely implicated as an adverse event. Herein, we report the first successful intraarterial thrombolytic treatment of CRAO developing after ASD closure via Amplatzer device. VC 2015 Wiley Periodicals, Inc. Key words: central retinal artery occlusion; thrombolysis; atrial septal defect
INTRODUCTION
CASE
A consensus by authorities on optimal treatment of central retinal artery occlusion (CRAO) has yet to evolve. The European Assessment Group for Lysis in the Eye (EAGLE) [1] trial failed to demonstrate that intraarterial thrombolysis (IAT) is superior to conservative treatment in managing CRAO. Heterogeneity in degree of ischemic damage sustained and time intervals from onset of symptoms to treatment (mean, 11.89 5.67 hr) have hampered outcome assessments. However, ischemia of the penumbra zone may be alleviated through reperfusion therapy [2], thus indicating that early restoration of retinal blood flow has merit in this setting. Percutaneous device usage is increasingly elected for atrial septal defect (ASD) closure due to the minimally invasive nature and the long-term durability of this approach [3]. Related complications generally include cardiac perforation, aorta-to-right arterial fistula, device malposition or embolization, and thrombus formation [3,4]. Although the reported rate of thrombus development after catheter closure of ASD is 1.2% [4], CRAO is rarely implicated as an adverse event. Herein, we describe an instance where CRAO following transcatheter ASD closure by Amplatzer device was successfully resolved through IAT.
A 21-year-old woman was admitted for closure of a moderate-grade ASD. Maximal ASD diameter by transesophageal echocardiography (TEE) was 14.3 mm. A 17-mm Amplatzer septal occluder (AGA medical Corp, Golden Valley, MN) was deployed as usual for transcatheter occlusion. Aspirin (200mg daily oral dose) and heparin (750 units/hr as intravenous infusion) were administered after the procedure. No visible thrombus was evident in proximity to the device by
C 2015 Wiley Periodicals, Inc. V
1
Department of Neurosurgery, Hallym University College of Medicine, Chuncheon, Korea 2 Department of Radiology, Seoul National University College of Medicine, Seoul, Korea Conflict of interest: Nothing to report. *Correspondence to: Young Dae Cho, M.D., Department of Radiology, Seoul National University College of Medicine, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea. Email: [email protected] Received 10 March 2015; Revision accepted 14 June 2015 DOI: 10.1002/ccd.26100 Published online 00 Month 2015 in Wiley Online Library (wileyonlinelibrary.com)
2
Jeon et al.
Fig. 1. Central retinal artery occlusion. (A) Unremarkable diffusion MRI. (B) Angiography of left internal carotid artery showing patent small–caliber ophthalmic artery (OA) (arrow). (C) Ethmoidal and lacrimal branches of left ECA devoid of chorodial blush. (D) Selective microcatheter angiography of OA shows faint arterial supply to inferior orbit. (E) Selective angiography of OA after intra-arterial (IA) thrombolytic uroki-
nase infusion confirms restoration of posterior ciliary artery and muscular arteries (arrows). (F) Photography of fundus after IA thrombolysis—note ischemic, edematous retina with cherry-red spot and preservation of retina supplied by ciliary artery. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
echocardiography. Twenty-eight hours later, the patient suffered sudden loss of left eye vision. Serial neurologic and ophthalmologic examinations documented a defect of left visual filed, with minimal preservation of central vision. Visual acuity was diminished 20/50 and was restricted to light perception. Examination of the fundus showed cherry-red spots and edema of left maculae, consistent with CRAO. Acute cerebral infarction was ruled out by diffusion-weighted magnetic resonance imaging (Fig. 1A). Cerebral angiography was performed (170 min after onset of symptoms) using a GE biplane angiographic system (GE Healthcare, Milwaukee, WI). The left internal carotid artery was patent, showing no occlusion of the small-caliber (0.9 mm) ophthalmic artery (OA) (Fig. 1B); but ethmoidal and lacrimal ocular branch arteries of the external carotid artery (ECA) were devoid of choroidal blush (Fig. 1C). Selective angiography via a microcatheter (Excelsior SL-10; Boston Scientifics Corp, Natick, Massachusetts, USA) revealed faint arterial supply to inferior orbit, whereas the central retinal artery was not completely occluded
(Fig. 1D). Urokinase (500,000 units; Green Cross pharmacy, Yongin, Korea) thrombolytic therapy was slowly infused through the catheter in a 75-min period. Selective angiography thereafter indicated restoration of posterior ciliary and muscular arteries (Fig. 1E), associated with prompt recovery of central and temporal portions of left visual filed after IAT. Photography of fundus after IAT showed note ischemic, edematous retina with cherry-red spot and preservation of retina supplied by ciliary artery (Fig. 1F). Goldmann perimetry testing 3 months later demonstrated improved (20/ 30) visual acuity, with a left visual field defect at inferonasal quadrant. DISCUSSION
Thrombus formation after catheter closure of ASD is a rare complication that may result in serious embolic injury. Five patients (1.2%) reported by Krumsdorf et al. [4] developed thrombi after catheter ASD closure. Such thrombi may present acutely in the periprocedural period [5] or emerge as late developments
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Intra-Arterial Thrombolysis of CRAO
up to 3 years after implantation [6]. Paroxysmal atrial fibrillation and persistent atrial septal aneurysm may accompany thrombus formation [4]. Thrombotic risk varies according to closure device. Dacron-covered nitinol Amplatzer devices carry a 0–0.3% rate of thrombus formation in patients with ASD and foramen ovale (at 4 weeks and 6 months, respectively). Although cerebral thromboembolic events are occasionally seen with Amplatzer device closure of ASD [7], CRAO has yet to be implicated. Currently, there is controversy surrounding comparative efficacies of IAT and conservative treatment in managing CRAO. A systemic review [8] concluded that IAT produced better outcomes than conventional treatment in terms of preserving vision. However, analysis of non-randomized and retrospective studies, without attention to degree of CRAO and time intervals for intervention, may be fundamentally flawed. Differences in preservation of visual function prior to delivery of IAT likely reflect variability in extent of ischemic damage that will impact treatment outcomes. One particular study has shown that early reperfusion via IAT may preferentially benefit patients with incomplete CRAO [9], compared with those suffering subtotal and total CRAO. On the other hand, the therapeutic time window for reperfusion of CRAO remains unclear. According to the literature, IAT has been performed after a lag of up to 50 hr [8,10], although Hayreh et al. [11] saw irreversible retinal damage in rhesus monkey models after 240 minutes. Few prospective studies have investigated an optimal time interval in humans, but a window of 6–12 hr is generally considered the limit for IAT [12]. Finally, Hwang et al. [12] have suggested that instances of CRAO involving milder degrees of arterial occlusion and shorter intervention delays may in fact yield better visual outcomes. We attribute the rapid symptomatic improvement of our patient after IAT to timely reperfusion (within 3 hr after symptom onset) and salvage of the ciliary artery, preserving minimal central vision. Another important factor in these circumstances is the contribution of collateral flow in maintaining tissue viability. Kim et al. [13] determined that the extent of collateral circulation seen on baseline angiography correlated with infarct volume and National Institute of Health Stroke Scale (NIHSS) scores in patients with acute middle cerebral artery occlusion. Most studies of CRAO have not addressed regional collateral flow, which may well be a confounding factor in prior studies that skews results. In our patient, choroidal blush (from ECA) was lacking (Fig. 1C). Hence, timely reperfusion via OA is especially urgent in situations where collateral circulation is poor. The major safety concerns of IAT are cerebral infarct and hemorrhage transformation. We encoun-
3
tered only two reported instances of stroke and one of hemorrhage in patients with CRAO after IAT [8]. In the EAGLE trial, two (4.7%) of 42 patients subjected to IAT suffered intracranial hemorrhages [1] , whereas Ahn et al. [9] reported a 25.8% rate of embolic infarction after IAT. Most of their subjects were asymptomatic, and only one patient experienced hemianopsia due to an occipital lobe infarct. However, IAT apparently does not worsen the 23% rate of embolic infarct ordinarily attached to angiography (diagnostic or interventional) [14]. A technical issue impacting success of IAT is appropriate microcatheter selection, particularly size and distal shape. Diameter of the OA is 1.54 0.04 mm (mean SD) and 1.31 0.05 mm in men and women, respectively [15]. As such, microwires 0.014 in and microcatheters of 0.0165-in distal inner diameter are sized appropriately for OA navigation and thrombolysis. In terms of catheter shape, an S-shaped distal tip may be used primarily to accommodate arterial curvature [12]. However, if OA originates immediately past carotid siphon, selecting OA orifice with an S-shaped microcatheter may be technically difficult. In our patient, a microcatheter with straight tip easily sufficed for thrombolysis.
CONCLUSIONS
CRAO is a rare complication after percutaneous ASD closure. Prompt revascularization through IAT may enable immediate restoration of blood flow in select patients. Timely diagnosis of CRAO and prompt intervention are essential to reduce ischemic injury of retina and mitigate loss of vision
ACKNOWLEDGMENT
The authors are very grateful to Professor Gi Beom Kim for his help in this study. REFERENCES 1. Schumacher M, Schmidt D, Jurklies B, et al. EAGLE-Study Group Central retinal artery occlusion: Local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010;117:1367–1375. 2. Beck J, Raabe A, Lanfermann H, et al. Tissue at risk concept for endovascular treatment of severe vasospasm after aneurysmal subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2004;75:1779–1781. 3. Masura J, Gavora P, Podnar T. Long-term outcome of transcatheter secundum-type atrial septal defect closure using Amplatzer septal occluders. J Am Coll Cardiol 2005;45:505–507. 4. Krumsdorf U, Ostermayer S, Billinger K, et al. Incidence and clinical course of thrombus formation on atrial septal defect and
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
4
5.
6.
7.
8.
9.
Jeon et al. patient foramen ovale closure devices in 1,000 consecutive patients. J Am Coll Cardiol 2004;43:302–309. Yorgun H, Canpolat U, Kaya EB, Aytemir K, Oto A. Thrombus formation during percutaneous closure of an atrial septal defect with an Amplatzer septal occluder. Texas Heart Inst J 2011;38: 427–430. Ruge H, Wildhirt SM, Libera P, et al. Images in cardiovascular medicine. Left atrial thrombus on atrial septal defect closure device as a source of cerebral emboli 3 years after implantation. Circulation 2005;112:e130–e131. Dardas PS, Ninios V, Mezilis N, et al. Cryptogenic stroke after percutaneous closure of an atrial septal defect. Hellenic J Cardiol 2012;53:155–159. Noble J, Weizblit N, Baerlocher MO, Eng KT. Intra-arterial thrombolysis for central retinal artery occlusion: A systematic review. Br J Ophthalmol 2008;92:588–593. Ahn SJ, Kim JM, Hong JH, et al. Efficacy and safety of intraarterial thrombolysis in central retinal artery occlusion. Invest Ophthalmol Visl Sci 2013;54:7746–7755.
10. Richard G, Lerche RC, Knospe V, Zeumer H. Treatment of retinal arterial occlusion with local fibrinolysis using recombinant tissue plasminogen activator. Ophthalmology 1999;106: 768–773. 11. Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004; 78:723–736. 12. Hwang G, Woo SJ, Jung C, et al. Intra-arterial thrombolysis for central retinal artery occlusion: Two cases report. J Korean Med Sci 2010;25:974–979. 13. Kim JJ, Fischbein NJ, Lu Y, et al. Regional angiographic grading system for collateral flow: Correlation with cerebral infarction in patients with middle cerebral artery occlusion. Stroke 2004;35:1340–1344. 14. Bendszus M, Koltzenburg M, Burger R, et al. Silent embolism in diagnostic cerebral angiography and neurointerventional procedures: A prospective study. Lancet 1999;354:1594–1597. 15. Lang J, Kageyama I. The ophthalmic artery and its branches, measurements and clinical importance. Surg Radiol Anat 1990;12:83–90.
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
