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a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California
b Department of Cardiothoracic Surgery, El Camino Hospital, Mountain View, California
c Department of Cardiovascular Disease, El Camino Hospital, Mountain View, California
d Department of Anesthesiology, El Camino Hospital, Mountain View, California
Accepted for publication May 29, 2007.
* Address correspondence to Dr Pelletier, Department of Cardiothoracic Surgery, Stanford University Medical Center, 300 Pasteur Dr, Falk CVRB, Stanford, CA 94305 (Email: marcp{at}stanford.edu).
| Abstract |
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| Introduction |
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A previously healthy 35-year-old Asian woman underwent primary repair of a secundum type ASD without complication. Three years postoperatively, although she remained asymptomatic, a routine follow-up echocardiography demonstrated a round, pedunculated, right atrial mass with a stalk and characteristics suggestive of a myxoma (Fig 1). Further imaging of the mass by preoperative magnetic resonance imaging and transesophageal echocardiography was also highly consistent with an atrial myxoma (Fig 2).
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Histology revealed the mass to be an organized thrombus (Fig 3). The patient had an uneventful postoperative course and was discharged home on postoperative day 5. A postoperative hypercoagulability screening panel was negative. The patient was started on both aspirin (81 mg/day) and warfarin to maintain a 2 to 3 international normalized ratio for 3 months. The postoperative echocardiogram at 3 months was normal.
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| Comment |
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Given the rarity of thrombus formation after primary ASD repair, coupled with the patients longstanding asymptomatic postoperative course, further imaging was obtained by transesophageal echocardiography and magnetic resonance imaging. Both modalities suggested the more common diagnosis of an atrial myxoma. Myxomas remain the most common cause of atrial tumors and are often discovered incidentally, as was the mass in our patient [5]. Moreover, given the reported rapid rates of the growth of a myxoma after surgical intervention (eg, development of a 4 x 6 cm myxoma within 8 months), development of an approximately 2-cm2 mass between interval echocardiograms seemed a reasonable possibility [6].
The case highlights the importance of considering the possibility of thrombus long after primary repairs of the ASD. Furthermore, the workup revealed limitations of current imaging modalities to discern between organized clot and atrial myxoma. Although acoustic density has been used to distinguish between thrombus and myxoma [5], such evaluation did not help in this case. Cardiac computed tomography might have provided more detailed information, but was not performed given the low index of suspicion for thrombus and unequivocal findings by echocardiography and magnetic resonance imaging.
If preoperative tissue diagnosis had been possible, alternative treatment options for atrial thrombus including thrombolysis, anticoagulation, and catheter-based retrieval might also have been considered. Catheter-based retrieval is a relatively novel development, with a limited number of case reports describing this approach [7, 8]. Recent data from meta-analyses and Dinckal and colleagues [4] case report support the use of thrombolytics and anticoagulation therapy [4, 8]. However, a well-controlled trial evaluating these approaches against the open surgical approach remains to be conducted. It should also be pointed out that the majority of data evaluating treatment of atrial thrombus come from patients suffering from large embolized clot loads from deep venous thrombosis (ie, "emboli in transit") or transmural thrombi generated secondary to turbulent atrial flow states (eg, atrial fibrillation). Whether these techniques can be used for postoperative thrombi is unclear. This consideration is especially apt, as the nature of a developing thrombus at a suture line might be more or less resistant to anticoagulation therapy compared with a relatively fresh, embolized thrombus caught in the atrium. This point is well illustrated in this case, whereupon intraoperative examination, the thrombus was found to be a well formed, hard mass with a reasonable pedicle attaching it to the atrial wall. The hard consistency and histologic appearance of the thrombus suggested that a response to lytic or anticoagulation therapy would be highly unlikely.
One final aspect of this case involves the appropriateness of anticoagulation therapy after primary ASD repair. For catheter-based therapy and patch repair of ASDs, patients are routinely anticoagulated until endothelialization of the foreign material is believed to be complete (ie, typically 3 months). However, in the case of primary repairs of PFOs or ASDs, most centers refrain from postoperative anticoagulation. Given the findings from this case and the others discussed, such anticoagulation strategies may deserve review.
For future cases of primary ASD repair, it may be prudent to anticoagulate patients for approximately 3 months, as has been previously suggested [4]. Also this case illustrates the importance of early echocardiography follow-up after intracardiac repair. This approach may help to identify postoperative thrombi earlier, providing a therapeutic window for anticoagulation or lytic therapy. A combination of preoperative hypercoagulability screening, postoperative anticoagulation, and routine interval assessment by echocardiography may provide the optimal strategy.
In conclusion, thrombus formation at the site of primary ASD or PFO repair is an uncommon postoperative complication that has the potential for embolic sequelae. The present case demonstrates the importance of postoperative interval imaging to detect potential thrombi prior to manifestation by embolic event. A short course of routine postoperative anticoagulation might also be considered in patients undergoing primary ASD repair.
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This article has been cited by other articles:
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F. Filsoufi, J. Chikwe, J. G. Castillo, and J. Sanz Multimodal Imaging Characterization of Intracardiac Thrombus and Myxoma Ann. Thorac. Surg., June 1, 2008; 85(6): 2162 - 2162. [Full Text] [PDF] |
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A. Y. Sheikh and M. P. Pelletier Reply Ann. Thorac. Surg., June 1, 2008; 85(6): 2162 - 2163. [Full Text] [PDF] |
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