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Ann Thorac Surg 2007;83:1539-1541
© 2007 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Friedrich-Schiller-University Jena, Jena, Germany
b Department of Cardiology, Friedrich-Schiller-University Jena, Jena, Germany
c Department of Cardiology, HELIOS Klinikum Erfurt, Erfurt, Germany
Accepted for publication November 3, 2006.
* Address correspondence to Dr Krieg, Klinik für Herz und Thoraxchirurgie, Friedrich-Schiller-Universität Jena, Jena, 07743 Germany. (Email: peter.krieg{at}med.uni-jena.de).
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Prior history of this 62-year-old man included a stroke 14 years ago without any known residual neurologic symptoms and a second stroke 8 months ago, affecting both middle cerebral arteries. A left heart catheter showed no acute occlusion or stenosis of any coronary artery but a transesophageal echocardiography (TEE) demonstrated a PFO. A PFO occlusion with an Amplatzer occlusion device (AGA Medical Corporation) was carried out, and the patient was discharged on aspirin and clopidogrel with marked improvement of his neurologic symptoms (ie, disturbances of word finding and of lower extremities coordination).
Eight months later he was admitted to an angiology department due to pain in his legs after walking a distance of about 200 m.
Angiography revealed bilateral thromboembolic occlusion of the lower leg arteries and thrombolysis was started. Protein C, protein S, antithrombin III, and activated protein C-ratio were all within normal ranges. A few days later he suddenly developed an ST-elevation myocardial infarction of the posterior wall.
The right coronary artery was completely occluded due to thrombotic material as revealed by left heart catheter. Immediate catheter thrombectomy resulted in thrombolysis in myocardial infarction study group (TIMI) flow 2, and the patient was put on glycoprotein IIb/IIIa-receptor blocker for 48 hours and continuous heparin with complete resolution of his symptoms. The TEE detected a 3-cm thrombus attached to the Amplatzer device on the left atrial disc (Fig 1) and a cerebral computed tomography demonstrated a new ischemic lesion. Six days later, still on heparin, there was a deterioration of his neurologic status with increasing stupor, sudden anisocoria, and systemic hypotension. A new cerebral computed tomography added no information, but a new TEE showed an increased size of the left atrial thrombus. An electrocardiogram demonstrated an atrioventricular block III with a resulting heart rate of 43 bpm. Therefore the patient was transferred to our hospital by helicopter for surgical therapy. He arrived in the evening awake with a mild-to-moderate right-sided hemiparesis, blurred speech, and cold legs. His mean arterial pressure was 45 to 50 mm of mercury on 24 mg per hour of dobutamine, and he was immediately transferred to the operating room. After opening the thorax, the right ventricle was found to be dilated and not contracting. The patient was put on total cardiopulmonary bypass and the right atrium was opened. The Amplatzer device was located and taken out with the adherent thrombus (Fig 2). The atrial septal defect was closed with a pericardial patch and the right atrium was closed. A saphenous vein graft was anastomosed to the right coronary artery in standard fashion. Reperfusion was started and the heart started beating in sinus rhythm without electrocardiographic signs of ischemia. After cardiopulmonary bypass was stopped the circulation was sufficient with mild support of catecholamines. The intraoperative TEE demonstrated no residual thrombus and no residual shunt across the atrial septal defect closure. After completion of the operation the patient was transferred to the intensive care unit with stable sinus rhythm and an adequate cardiopulmonary status. He was extubated on the first postoperative day. A postoperative echocardiography demonstrated a still markedly dilated right ventricle with reduced right ventricular function. The left ventricle showed a small reduction of global function with disturbances of posterior septal wall motion. The maximal postoperative troponin I was 30 ng/mL on postoperative day 1 (preoperatively, 3.7 ng/mL). He was discharged on postoperative day 15. By that time his speech was back to normal, his initial hemiparesis noted on admission had markedly improved, and according to his own judgement, his initial memory disturbances were not noticeable anymore.
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Devuyst and colleagues [3] described 30 patients younger than 60 years of age with stroke and PFO who had surgical closure. There were no complications in the perioperative period and after 2 years there was no TIA or recurrent stroke and no new cerebral lesion as determined by magnetic resonance imaging. On the other hand, postoperative TEE demonstrated a residual shunt in 2 patients with single as opposed to double continuous suture line techniques.
In a study by Homma and colleagues [4], 28 patients with cryptogenic stroke underwent surgical closure of the PFO. None of the patients younger than 45 years of age experienced any recurrent neurologic event, but 4 patients aged 45 years or more suffered recurrence (one stroke and three TIAs). The authors concluded that surgical closure of a PFO does not consistently prevent recurrence of ischemic events and that recurrence is more common in older patients, although a PFO is easily repaired by surgery in patients with cryptogenic stroke.
Dearani and colleagues [1] retrospectively analyzed 91 patients with previous cerebrovascular ischemic events who underwent surgical PFO closure. There was no operative mortality. Follow-up totalled 176.3 patient-years; mean follow-up was 2.0 years. No one had a cerebral infarction and 8 patients had a TIA during follow-up, with one caused by temporal arteritis. Transesophageal echocardiography demonstrated all closures to be intact in these patients. The overall freedom from TIA recurrence during follow-up was 92.5 ± 3.2% at 1 year and 83.4 ± 6.0% at 4 years. Having multiple neurologic events before PFO closure was the only significant risk factor for TIA or cerebral infarction recurrence after closure by univariate analysis (p = 0.05). The authors concluded that surgical closure of a PFO can be performed with minimal morbidity and mortality. In addition the authors concluded that PFO closure may decrease the risk of recurrent stroke or TIA and may avoid lifelong anticoagulation in the young adult if there is no other indication, and that recurrent cerebrovascular ischemic events after surgery should prompt further evaluation to identify causes other than paradoxical embolism.
Percutaneous transcatheter closure is reported as being safe and effective with efficacy ranging from 86% to 100%, and recurrent neurologic and peripheral embolic events are reported as 0% to 3.8% per year [5, 6]. In a study by Krumsdorf and colleagues [7] of 1,000 consecutive patients undergoing atrial septal defect and PFO closure using transcatheter devices, 2.5% of PFO patients had thrombus formation within the atria. Nevertheless, none of the thrombi developed on an Amplatzer device as opposed to five other devices used in this study. In a study by Anzai and colleagues [8] describing 66 patients with transcatheter closure there were no thrombi on Amplatzer devices as opposed to the CardioSEAL device (NMT Medical Inc, Boston, MA) with 22% of thrombus formation. In a study by Hung and colleagues [6], the annual risk of recurrent stroke or TIA after device placement was 3.2%, whereas Windecker and colleagues [5] reported a 2.5% annual risk for TIA and a 0.9% risk for peripheral emboli.
In our 62-year-old patient without any known coagulopathy, a 3-cm thrombus developed within the left atrium on the Amplatzer PFO occluder. This thrombus was resistant to intensive anticoagulation with heparin and a glycoprotein IIb/IIIa-antagonist and resulted in recurrent major adverse cardiac, peripheral, and neurologic thromboembolic events making early surgery mandatory. Fibrinolysis was contraindicated with respect to the recurrent neurologic symptoms.
The fact that there are differences concerning the incidence of thrombus formation depending on the kind of closure device used [7] shows that a completely safe transcatheter closure device is not yet available, even though the Amplatzer devices have shown to be among the least susceptible to thrombus formation. Currently there should be still a high grade of suspicion for thrombus formation in patients with an Amplatzer device.
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This article has been cited by other articles:
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  J. Bonatti, N. Bonaros, S. Muller, and T. Bartel Completely endoscopic removal of a dislocated Amplatzer atrial septal defect closure device Interactive CardioVascular and Thoracic Surgery, February 1, 2008; 7(1): 130 - 132. [Abstract] [Full Text] [PDF]
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