case of right ostial stenosis 6 months after a Carrel patchmethod using GRF glue was reported by Kiyama andassociates [3]. The authors suspected that marked pro-gression of stenosis occurred in association with injectionof GRF glue into the dissected space.

To diagnose ostial stenosis of the coronary arterieswithout cardiac catheterization is difficult. Transesopha-geal echocardiography provides useful information oncoronary blood flow to enable prompt and less invasivediagnosis. Especially in patients with an artificial valve orhistory of graft replacement, TEE is preferable to avoidinfection.

Gelatin-resorcinol-formaldehyde glue has excellenthemostatic characteristics and is widely used for dissect-ing aneurysm; however, some problems concerning GRFglue have been reported. Fukunaga and associates [4]reported nine cases of aortic root redissection after re-construction of dissecting aneurysms using GRF glue.They considered that the complications were likely to becaused by the toxic effects of formaldehyde, particularlyin cases where an excessive amount of formaldehyde waspresent that was not chemically bound to resorcin. Cor-onary ostial stenosis after complete replacement of theaortic root and reimplantation of the coronary arterieswas observed in several circumstances in which no GRFglue was used. It might be related to the suture techniqueat the coronary ostium, particularly if a small Dacrongraft is used for reimplantation. In our case, it is conceiv-able that ostial stenosis occurred as a result of inappro-priate use of GRF glue rather than a technical problem,because T1 scintigraphy, electrocardiography, and TEEshowed no abnormalities on discharge and it occurredbilaterally and simultaneously. Bingley and associates [5]reported that some months to years after the initial use ofGRF glue, tissues were extremely fibrosed at the site ofglue application, and a number of patients had redissec-tion of the aortic root where GRF glue had been applied.In our case, an excessive amount of formaldehyde couldhave induced bilateral ostial stenosis of the coronaryarteries owing to redissection of the coronary ostia ac-companied by fibrosis at the site of glue application;however, it is impossible to verify the adverse effects ofthe formaldehyde because histologic examination wasnot done. Bachet and associates [2] recommended that asfew as two or three droplets of formaldehyde are suffi-cient to polymerize 1 mL of gelatin resorcinol mixture. Toavoid ostial stenosis, the glue is injected between thedissected layers, with special care directed not to con-taminate the coronary ostia. A few drops of formaldehydeare then added to the glue by using a cannula-tippedsyringe. Thereafter, the layers should be compressed toimprove the polymerization process.

The authors thank Naoko Ishizuka, MD, Department of Cardi-ology, The Heart Institute of Japan, Tokyo Women’s MedicalUniversity, for her skillful evaluation of echocardiography.

References

1. Guilmet D, Bachet J, Goudot B, et al. Use of biological glue inacute aortic dissection. J Thorac Cardiovasc Surg 1979;77:516–21.

2. Bachet J, Goudot B, Dreyfus G, et al. The proper use of glue:a 20-year experience with the GRF glue in acute aorticdissection. J Cardiac Surg 1997;12:243–53; discussion 253–5.

3. Kiyama H, Ohshima N, Sakurada M, et al. A case of progres-sive right coronary ostial stenosis after Carrel patch methodusing gelatin-resorcin-formalin glue. Kyobu Geka 1998;51:102–5.

4. Fukunaga S, Karck M, Harringer W, et al. The use of gelatin-resorcin-formalin glue in acute aortic dissection type A. EurJ Cardiothorac Surg 1999;15:564–70.

5. Bingley JA, Gardner MAH, Stafford EG, et al. Late complica-tions of tissue glues in aortic surgery. Ann Thorac Surg 2000;69:1764–8.

A Case of Asymptomatic ThoracicAorta Mural ThrombiImran Hassan, MD, Kenton J. Zehr, MD, and WilliamK. Freeman, MD

Divisions of Cardiovascular Surgery and Cardiology, MayoClinic, Rochester, Minnesota

The natural history, prognostic significance, and optimaltherapy of asymptomatic thoracic aorta mural thrombidetected incidentally is not well defined in the literature.We report a case of asymptomatic thoracic aorta muralthrombi in a 42-year-old woman with a history of smok-ing and steroid use that was conservatively managedwith anticoagulation and had a favorable outcome.

(Ann Thorac Surg 2001;72:1735–7)© 2001 by The Society of Thoracic Surgeons

Since the initial description by Weismann and Tobin[1] in 1958, aortic mural thrombus has been accepted

as a definite clinical entity and a source of arterialthromboembolism [1]. The mural thrombus is usuallylocated in the abdominal aorta but infrequently it canoccur in the thoracic aorta [2]. The true incidence ofthoracic aorta thrombus is unknown, but is probablyunderestimated. In a series of 10,671 autopsies from theUniversity of California Los Angeles Medical Centerfrom 1955 to 1983, the incidence of mural thrombus in thenonaneurysmal thoracic aorta was 0.09% [1]. However,with the development of transesophageal echocardiogra-phy, and its widespread application, the clinical diagno-sis of thoracic aorta thrombi has become more readilyidentified as a source of peripheral arterial emboli [3].

A 42-year-old woman, with a history of depression,presented after an overdose of verapamil, lorazepam,

Accepted for publication Jan 13, 2001.

Address reprint requests to Dr Zehr, Division of Cardiothoracic Surgery,Mayo Clinic, 200 First St, SW, Rochester, MN 55905; e-mail: zehr.kenton@mayo.edu.

1735Ann Thorac Surg CASE REPORT HASSAN ET AL2001;72:1735–7 ASYMPTOMATIC AORTIC THROMBI

© 2001 by The Society of Thoracic Surgeons 0003-4975/01/$20.00Published by Elsevier Science Inc PII S0003-4975(01)02612-1

and hydrocodone/acetaminophen. Her past medical his-tory was significant for treated hypertension and she hada five-pack year smoking history. She was treated withsteroids in the past for an uncharacterized rheumatoidsyndrome and had been on birth control pills throughouther life. On her second hospitalization day she requiredintubation after developing adult respiratory distresssyndrome presumably caused by aspiration. She re-mained hemodynamically stable with a sinus rhythmrate of 70 per minute and a blood pressure nadir of100/60 mm Hg. A computed tomographic scan was per-formed to rule out pulmonary emboli. Although she hadno evidence of pulmonary emboli, three mural thrombiwere noted in the transverse aortic arch (Fig 1). Atransesophageal echocardiography confirmed the pres-ence of mobile hypoechoic masses in the aortic archconsistent with mural thrombi, along with the absence ofunderlying aortic dissection, penetrating ulcer, or wallhematoma. Because of her tenuous pulmonary status shewas treated with systemic anticoagulation instead of bysurgical intervention. After 36 hours of anticoagulationwith heparin, she developed a lower gastrointestinalhemorrhage and the heparin was discontinued. Sheremained neurologically intact without evidence of pe-ripheral emboli, and with subsequent improvement ofher pulmonary status she was extubated. Coagulationstudies that included evaluation for antithrombin III,protein C or protein S deficiency, Lupus anticoagulant,anticardiolipin antibody, dysfibrinogenemia and pro-thrombin 20210 G-A mutation, did not demonstrate ahypercoagulable condition. Therefore, she was anticoag-ulated with warfarin sodium. A transesophageal echocar-diography 2 weeks after diagnosis showed minimal re-sidual thrombus, and at 14 months a computedtomographic scan showed resolution of the muralthrombi (Fig 2). She was doing well with no untowardsequela at her most recent follow-up at 16 months.

Comment

The optimal management of asymptomatic thoracic aortamural thrombi has not been clearly established [4]. Most

of the literature addressing treatment options pertains topatients with peripheral or visceral embolic events. Insuch situations, systemic anticoagulation has been con-sidered the mainstay of treatment [2]. However, the risksassociated with anticoagulation and the risk of recurrentembolism cannot be accurately estimated because of thelimited number of reported patients. Recently, there havebeen several reports regarding successful operativethrombectomy of lesions in the thoracic aorta [2–4]. Mostof these operations require cross clamping of the aortaand circulatory arrest if an operation in the region of theaortic arch is contemplated, with a potential for signifi-cant morbidity and mortality. Keen and colleagues [5]have reported a 33% mortality at 30 days in 12 patientswho underwent operations on the suprarenal aorta forthrombus associated with atheroembolism.

Because the natural history and prognostic significanceof asymptomatic thoracic aorta thrombi are not knownand the data regarding the treatment of thrombi present-ing with peripheral arterial emboli is inconclusive, themanagement of these asymptomatic lesions is unclear.Pasierski and colleagues [4] reported a patient with anasymptomatic aortic arch thrombus that was treated withanticoagulation and subsequently resolved without anyclinical evidence of peripheral embolism. They suggesteda benign course if the thrombi were without associatedemboli at presentation. They recommended anticoagula-tion as the appropriate treatment in these cases. Weapplied a similar approach with a favorable outcome.

When considering therapeutic options for thoracicaorta thrombi, it is necessary to view them as a hetero-geneous group rather than a single entity, each having adifferent clinical course and prognosis depending uponits nature and etiology. Karalis and colleagues [6] re-ported a 73% incidence of embolic events among patientswith pedunculated and highly mobile aortic thrombi, asopposed to only 12% when those thrombi were layeredand immobile. Similarly, aortic lesions can cause eithermacro emboli or atheroembolization (micro emboli). Thelatter have shown to be optimally treated by surgicalresection, while the former is best managed by anticoag-

Fig 1. Contrast computed tomographic scan at presentation. Tho-racic aorta with thrombus.

Fig 2. Contrast computed tomographic scan at 6 months. Completeresolution of thoracic aorta mural thrombus.

1736 CASE REPORT HASSAN ET AL Ann Thorac SurgASYMPTOMATIC AORTIC THROMBI 2001;72:1735–7

ulation [3]. Although most thoracic thrombi are seen withatherosclerotic disease, several other etiologies havebeen described, including aneurysms, dissections,trauma, malignancy, hypercoagulable states (polycythe-mia and antithrombin III deficiency) and systemic fungalinfections [7].

Perler and colleagues [8] reported two young femalepatients with aortic mural thrombosis and questionedwhether arteriosclerosis was indeed the underlying eti-ology. They speculated the existence of a distinct clinicalentity involving aortic thrombosis in young females dueto intimal hyperplasia and thrombosis secondary to ste-roid use and cigarette smoking. Recently Lozano andcolleagues [2] reported recurrent embolism from a float-ing thrombus in the thoracic aorta in a 46-year-old femaleon long-term steroids. Our case did have a history ofcigarette use and past treatment with steroids.

It is apparent that in certain situations aortic thrombimay be better treated with surgical intervention thananticoagulation and vice versa, although there is noobjective data to support either contention. At the sametime the risks for catastrophic embolization despite anti-coagulation, the mortality and morbidity associated withsurgical removal, and the risk of recurrence with eithermethod in asymptomatic patients is unknown. The treat-ment of thoracic aorta thrombi should therefore be basedupon the nature and etiology of the lesions and theattendant risks of treatment to the individual patient. Inthis case, where cardiopulmonary bypass would havebeen poorly tolerated, the patient was best served byusing conservative therapy.

As a consequence of the widespread availability oftransesophageal echocardiography thoracic aortathrombi will continue to be diagnosed with increasedfrequency, particularly in asymptomatic patients. Furtherstudies and reports are needed to outline the naturalhistory of these thrombi and outcomes of various thera-peutic interventions in order to define the optimal treat-ment strategy.

References

1. Machleder HI, Takiff H, Lois JF, Holburt E. Aortic muralthrombus: an occult source of arterial thromboembolism. JVasc Surg 1986;4:473–8.

2. Lozano P, Gomez FT, Julia J, M-Rimbau E, Garcia F. Recur-rent embolism caused by floating thrombus in the thoracicaorta. Ann Vasc Surg 1998;12:609–11.

3. Lau LS, Blanchard DG, Hye RJ. Diagnosis and managementof patients with peripheral macroemboli from thoracic aorticpathology. Ann Vasc Surg 1997;11:348–53.

4. Pasierski T, Jasek S, Firek B, Przybylski A, Szwed H, SadowskiZ. Resolution of an aortic mobile mass with anticoagulationwithout evidence of arterial embolism. Clin Cardiol 1996;19:151–2.

5. Keen RR, McCarthy WJ, Shireman PK, et al. Surgical man-agement of atheroembolization. J Vasc Surg 1995;21:773–800.

6. Karalis DG, Chandrasekaran K, Victor MF, Ross JJ Jr, MintzGS. Recognition and embolic potential of intraaortic athero-sclerotic debris. J Am Coll Cardiol 1991;17:73–8.

7. Agolini SF, Shah KT, Goodreau JJ, McLoughlin Jr TM, SinclairMC. Splenic infarction caused by a large thoracic aorticthrombus. J Vasc Surg 1997;26:1069–72.

8. Perler BA, Kadir S, Williams GM. Aortic mural thrombus inyoung women: premature arteriosclerosis or separate clinicalentity? Surgery 1991;110:912–6.

Pneumococcal Aortic ValveEndocarditis CausingAortopulmonary Artery FistulaSantiago A. Endara, MD, Michael A. Corkeron,FFICANZCA, Al Mutazz Diqer, FRACS, Angus J. Neal,MBBS, and Dong Kang, MD

Departments of Cardiothoracic Surgery and Intensive CareMedicine, Townsville General Hospital, Townsville,Queensland, Australia

We report a case of an aortic-pulmonary artery fistulasecondary to acute bacterial endocarditis and aortic rootabscess formation. The patient presented with general-ized symptoms and an initial pneumococcal pneumonia,then developed respiratory and cardiac failure necessi-tating ventilation and inotropic agents. An echocardio-gram showed a vegetation in the aortic valve, an abscessinvolving the aortic root, and suggested a fistula betweenthe aorta and main pulmonary artery, which was con-firmed at emergent operation. Despite a complicatedearly postoperative course the patient has made a fullrecovery.

(Ann Thorac Surg 2001;72:1737–8)© 2001 by The Society of Thoracic Surgeons

Aortopulmonary artery fistula is a rare and potentiallycatastrophic complication of bacterial endocarditis.

We describe such a case.

A 43-year-old woman with no significant prior medicalhistory came to a regional hospital in North Queensland,Australia, in September 1999, with a 3-day history ofmalaise, fever, diarrhea, nausea, vomiting, and abdomi-nal pain. Chest roentgenogram showed bilateral infil-trates consistent with pneumonia. She was initiallytreated with intravenous cephalothin. Retrospective re-view of the films taken at this stage confirmed theimpression of a pneumonic process and at that time werenot suggestive of acute respiratory distress syndrome orcardiogenic pulmonary edema. Blood cultures revealedStreptococcus pneumoniae, and the antibiotic was changedto intravenous benzylpenicillin. After showing initialimprovement the patient developed severe respiratorydistress and was transferred to our institution.

Shortly after arrival to our hospital the previous find-ings were confirmed. Additionally she was noted to havea third heart sound without an audible murmur andbilateral pleural effusions. There were no peripheral

Accepted for publication Aug 18, 2000.

Address reprint requests to Dr Endara, Department of CardiothoracicSurgery, Townsville General Hospital, Eyre St, North Ward, Townsville,Queensland, 4810, Australia; e-mail: endaras@health.qld.gov.au.

1737Ann Thorac Surg CASE REPORT ENDARA ET AL2001;72:1737–8 PNEUMOCOCCAL AORTOPULMONARY FISTULA

© 2001 by The Society of Thoracic Surgeons 0003-4975/01/$20.00Published by Elsevier Science Inc PII S0003-4975(00)02412-7