Symptoms are invariably due to hemodynamic deterio-ration or pulmonary edema. The reported interval be-tween injury and surgical intervention is highly variable,from hours to decades. In the present case, completeavulsion of the anterolateral papillary muscle causedmassive mitral incompetence, pulmonary edema, andrapid hemodynamic deterioration. Similarly, in manypatients reported to have required mitral valve opera-tions within 2 weeks of their trauma, there was completerupture of either [7, 15, 17, 23] or both [21] papillarymuscles. Although the nature of the damage to the valveand subvalvular structures dictates the best mode ofrepair, there is no consenus in the literature as to thepreferred treatment of a given lesion in this group ofpatients. Mitral valve replacement is the most commontreatment reported. Although reconstruction of the sub-valvular apparatus might be preferable, the most expe-ditious procedure is sometimes necessary. Because of theextremely compromised circulation and poor conditionof the patient described, reconstruction of the valve wasnot attempted and a prosthetic valve was implanted.Transoesophageal echocardiography was invaluable inthe diagnosis of papillary muscle rupture.

References

1. Parmley LF, Manion WC, Mattingly TW. Nonpenetratingtraumatic injury of the heart. Circulation 1958;18:371–96.

2. McLaughlin JS, Cowley RA, Smith G, Matheson NA. Mitralvalve disease from blunt trauma. J Thorac Cardiovasc Surg1964;48:261–71.

3. Bailey CP, Vera CA, Hirose T. Mitral reguritation fromrupture of chordae tendinae due to “steering wheel” com-pression. Geriatrics 1969;24:90–105.

4. Goggin MJ, Thompson FD, Jackson JW. Deceleration traumato the heart and great vessels after road-traffic accidents. BrMed J 1970;2:767–9.

5. Weldon CS, Krause AH, Parker BM, Clarke RE, Roper CL.Clinical recognition and surgical management of acute dis-ruption of the mitral valve. Ann Surg 1972;175:1000–16.

6. Manhas DR, Hessel EA, Winterscheid LC, Dillard DH,Merendino KA. Repair of mitral incompetence secondary toruptured chordae tendinae. Circulation 1971;43:688–97.

7. Bryant LR, Modin-Uddin K, Dillon ML, Hinshaw MA, UtleyJR. Cardiac valve injury with major chest trauma. Arch Surg1973;107:279–83.

8. Bircks W, Korfer R. Traumatic mitral incompetence. J Car-diovasc Surg 1978;19:557–61.

9. Anyanwu CH. Mitral incompetence and ventricular septaldefects following non-penetrating injury. Thorax 1976;31:113–7.

10. Harada M, Osawa M, Kosukegawa K, Usuda T, Nakamura K.Isolated mitral valve injury from nonpenetrating cardiactrauma. Report of a case with successful repair. J CardiovascSurg 1977;18:459–64.

11. Rashid A, Chandraratna PAN, Hildner FJ, Samet P, YahrWZ, Greenberg J. Papillary muscle rupture following non-penetrating chest trauma: report of a case with hemody-namic and serial echocardiographic findings and successfulsurgical treatment. Heart Lung 1978;7:647–51.

12. Reginato E, Speroni F, Riccardi M, Verunelli F, Eufrate S.Post-traumatic mitral regurgitation and ventricular septaldefect in the absence of left pericardium. Thorac CardiovascSurg 1980;28:213–7.

13. Kratz JM, Sade RM, Usher BW. Traumatic disruption of thefibrous skeleton of the heart, with injury of the tricuspid and

mitral valves, aortic annulus, and ventricular septum. Car-diovasc Dis Bull Texas Heart Inst 1980;7:288–90.

14. Araki J, Koizumi S. Emergency surgical repair of massivemitral regurgitation due to ruptured chordae tendinae byblunt chest trauma. Thorac Cardiovasc Surg 1982;30:46–7.

15. Mazzucco A, Rizzoli G, Faggian G, et al. Acute mitralregurgitation after blunt chest trauma. Arch Intern Med1983;143:2326–9.

16. Devineni R, McKenzie FN. Acute mitral insufficiency result-ing from blunt chest trauma. J Thorac Cardiovasc Surg 1983;85:797–8.

17. Cuadros CL, Hutchinson JE, Mogtader AH. Laceration of apapillary muscle and the aortic root as a result of blunttrauma to the chest. J Thorac Cardiovasc Surg 1984;88:134–40.

18. Al Kasab S, Westaby S, Al Zaibag MA, Habbab M, Gunawar-dena KA, Al Fagih MR. Traumatic papillary muscle dysfunc-tion: attempted mitral-valve repair and eventual prostheticreplacement. Eur Heart J 1988;9:1030–3.

19. Neiman J, Hui WKK. Posteromedial papillary muscle rup-ture as a result of right coronary artery occlusion after bluntchest injury. Am Heart J 1992;123:1694–9.

20. Zabeneh RI, Venkataramani A, Zabeneh SS, Norwood SH.Blunt chest trauma causing isolated single papillary muscledysfunction and mitral regurgitation. Chest 1993;104:986–7.

21. Cho MC, Kim DW, Hong JM, Ahn JH, Hong JS. Leftventricular and papillary muscle rupture following bluntchest trauma. Am J Cardiol 1995;76:424–6.

22. Smedira NG, Zikri M, Thomas JD, Lauer MS, Kelleman JJ,McCarthy PM. Blunt traumatic rupture of a mitral papillarymuscle head. Ann Thorac Surg 1996;61:1526–8.

23. Wilke A, Kruse T, Hesse H, Bittinger A, Moosdorf R, MaischB. Papillary muscle injury after blunt chest trauma. J Trauma1997;43:360–1.

An Unusual Case of BioprostheticMitral Valve ThrombosisBoban Thomas, MD, Francesc Carreras, MD, XavierBorras, MD, and Guillem Pons-Llado, MD

Service of Cardiology, Hospital de la Santa Creu i Sant Pau,Barcelona, Spain

Bioprosthetic valve thrombosis and related embolism areconsidered extremely unlikely, thus allowing most pa-tients to avoid long-term anticoagulation. There is, how-ever, limited experience in the diagnosis and treatment ofsuch a condition. We present the case of a patient with aporcine mitral bioprosthesis who presented with acutethrombosis with unusual echocardiographic features. Afavorable outcome was observed after conventional anti-coagulant treatment.

(Ann Thorac Surg 2001;72:259–61)© 2001 by The Society of Thoracic Surgeons

Accepted for publication May 9, 2000.

Address reprint request to Dr Carreras, Servei de Cardiologia, Hospitalde Sant Pau, Sant Antoni M. Claret, 167, 08025 Barcelona, Spain; e-mail:fcarreras@hsp.santpau.es.

259Ann Thorac Surg CASE REPORT THOMAS ET AL2001;72:259–61 MITRAL BIOPROSTHETIC VALVE THROMBOSIS

© 2001 by The Society of Thoracic Surgeons 0003-4975/01/$20.00Published by Elsevier Science Inc PII S0003-4975(00)02497-8

Tissue bioprosthetic valves are used extensively be-cause long-term anticoagulation can be avoided as

the risk of thrombotic complications after 3 monthspostoperatively is low [1]. Once anticoagulant treatmenthas been withdrawn, however, thrombosis should beconsidered as a potential cause of prosthetic malfunction.To detect this complication transesophageal echocardiogra-phy can be used as the features of prosthetic thrombosis inbiologic valves have been described previously [2].

An 82-year-old man, operated on at our institution,received Carpentier-Edwards (Irvine, CA) bioprostheticvalves in the aortic (pericardial tissue, model 2900, size23) and mitral (porcine tissue model 6650, size 27) posi-tions for severe aortic and mitral regurgitation. A routinepostoperative Doppler echocardiographic study esti-mated a mean mitral pressure gradient of 4 mm Hg anda pressure half time of 128 msec; the function of the aorticprosthesis was also normal. When the patient was innormal sinus rhythm, the left atrium was not dilated(39 mm) and the size and function of the left ventriclewere within normal limits, so he was advised to stopanticoagulation 3 months postoperatively. A routineechocardiographic study 1 year after the operationshowed normal prosthetic function. The patient re-mained well for another 3 months, after which dyspneadeveloped over a period of 48 hours. He was admitted tothe hospital with a clinical picture of acute pulmonaryedema and atrial fibrillation with a rapid ventricularresponse. The patient was treated with diuretics, andconversion to sinus rhythm occurred after administrationof intravenous amiodarone, which improved his clinicalcondition. A transthoracic echocardiogram with the pa-tient in sinus rythm revealed signs of mitral prostheticobstruction (mean mitral gradient, 20 mm Hg; pressurehalf time, 382 msec) and a mildly dilated left atrium(52 mm). A transesophageal echocardiography studyshowed homogeneously thickened (5 mm) prostheticmitral leaflets (Fig 1) without valve regurgitation. Thisfinding suggested the presence of a thrombus adhered tothe ventricular aspect of the leaflets. A chronic degener-ative process of the tissue leaflets or a pannus was not

considered, given the normal features of the previousechocardiographic study. Moreover, pannus growth inmitral bioprostheses presents predominantly on the flowsurface as a circumferential rim that extends onto thevalve cusps and usually is associated with structuralabnormalities and mitral regurgitation [3].

Because experience with thrombolytic therapy forthrombotic occlusion of bioprosthetic valves is limitedand the clinical condition of the patient improved afterconversion to sinus rhythm, initial treatment with throm-bolytic agents or surgery was not considered. Intrave-nous unfractionated heparin at a therapeutic dose (par-tial thromboplastin time, 2 to 3 times the control) wasstarted. A repeat transthoracic echocardiogram andtransesophageal echocardiography 1 week later showeda normal transvalvular mean gradient (4 mm Hg), pres-sure half time of 146 msec, decreased left atrial size(41 mm), and dramatically reduced leaflet thickness(1.2 mm) (Fig 2). Long-term warfarin treatment wasindicated, and the patient had an uneventful clinicalcourse without further signs of prosthetic dysfunction onechocardiography for 1 year after the acute episode.

Comment

Freedom from the need for anticoagulation makes bio-prosthetic valves an attractive option. However, the po-tential for thrombus formation and valve dysfunctiondoes remain, as mild abnormalities in blood rheologyfavoring thrombosis have been described in patients withbioprostheses [4].

Some aspects of this case are remarkable. From theclinical perspective, there was an apparent lack of pre-cipitating factor of the thrombotic process, as the patienthad no underlying coagulation abnormality, left ventric-ular dysfunction, or low cardiac output, which are pro-cesses known to cause bioprosthetic thrombosis [5]. Al-though it cannot be excluded that the valve thrombosiscould have been a consequence of the episode of parox-ysmal atrial fibrillation, it is more probable that the

Fig 1. Transesophageal echocardiographic view showing abnormaldiffuse valve thickening of a biologic mitral prosthesis.

Fig 2. Image of the valve, in the same view as in Figure 1, obtainedafter resolution of the thrombus with antithrombotic therapy. Leafletthickening has disappeared, thus excluding a degenerative process.

260 CASE REPORT THOMAS ET AL Ann Thorac SurgMITRAL BIOPROSTHETIC VALVE THROMBOSIS 2001;72:259–61

arrhythmia was secondary to the increased left atrialpressure caused by the prosthetic obstruction. Also in-teresting was the rapidly evolving left heart failure,which is seen more commonly in acute thrombotic ob-struction of mechanical valves. In fact, some reportedpatients with bioprosthetic thrombosis presented withinsidious symptoms of heart failure [2].

Second, the echocardiographic appearance of the pros-thetic thrombosis in our case was unusual, with a layeredthrombus adhered to the ventricular aspect of the valveleaflets causing a uniform increase in valve thickness(Fig 1). The restricted motion of the leaflets resulted intransient stenosis. Other reports have shown the classicfindings of a pedunculated mass on the free edge of theleaflets with an otherwise normal thickness of the valvetissue [2].

Finally, the resolution of the case also deserves com-ment. Although thrombolytic therapy is an establishedfirst-line therapy for high-risk patients with prostheticvalve thrombosis [6], conventional anticoagulant treat-ment with heparin was instituted as a first therapeuticattempt in our case according to the experience describedby others [7] and resulted in an early complete resolutionof the process (Fig 2). Heparin therapy has been recom-mended in patients with prosthetic valve thrombosis andfunctional class I or II [8], and cases with good outcomeafter heparin treatment have been reported [2, 7].

References

1. Stein PD, Alpert JS, Dalen JE, Horstkotte D, Turpie AG.Antithrombotic therapy in patients with mechanical andbiological prosthetic heart valves. Chest 1998;114(Suppl 5):602S-10S.

2. Oliver JM, Gallego P, Gonzalez A, Dominguez FJ, Gamallo C,Mesa JM. Bioprosthetic mitral valve thrombosis: clinical pro-file, transesophageal echocardiographic features, and fol-low-up after anticoagulant therapy. J Am Soc Echocardiogr1996;9:691–9.

3. Butany J, Yu W, Silver MD, David TE. Morphologic findingsin explanted Hancock II porcine bioprostheses. J Heart ValveDis 1999;8:4–15.

4. Koppensteiner R, Moritz A, Schlick W, et al. Blood rheologyafter cardiac valve replacement with mechanical prosthesesor bioprostheses. Am J Cardiol 1991;67:79–83.

5. Hagley MT, Lopez-Candales A, Phillips KJ, Daily BB, Kou-choukos NT. Thrombosis of mitral valve bioprostheses inpatients requiring circulatory assistance. Ann Thorac Surg1995;60:1814–6.

6. Manteiga R, Carlos Souto J, Altes A, et al. Short-coursethrombolysis as the first line therapy for cardiac valve throm-bosis. J Thorac Cardiovasc Surg 1998;115:780–4.

7. Moujir F, Martın-Duran R, Vazquez de Prada JA, Trugeda A,Figueroa A, Olalla JJ. Disfuncion por trombosis en bioprotesisde Hancock mitral resuelta con heparina. Rev Esp Cardiol1989;42:219–21.

8. Lengyel M, Fuster V, Keltai M, et al. Guidelines for man-agement of left-sided prosthetic valve thrombosis: a rolefor thrombolytic therapy. Consensus Conference on Pros-thetic Valve Thrombosis [Review] J Am Coll Cardiol 1997;30:1521– 6.

Implantable CardioverterDefibrillator Patch Erosion in aHeart Transplant PatientSuneel Chilukuri, BA, James P. Herlihy, MD, G. AliMassumkhani, MD, J. Michael Duncan, Jr, MD, andO. H. Frazier, MD

Pulmonary Medicine and Critical Care, St. Luke’s EpiscopalHospital, Baylor College of Medicine, Houston, Texas

A 57-year-old man who had received an automatic im-plantable cardioverter defibrillator and subsequent or-thotopic heart transplant presented to medical attentionfor hemoptysis. The hemoptysis was caused by themigration of the left ventricular patch of the automaticimplantable cardioverter defibrillator, which had beenleft in place at the time of orthotopic heart transplant.The patch had eroded into the left lung. We recommendthat implantable cardioverter defibrillators be removedcompletely at the time of heart transplantation to preventsubsequent complications.

(Ann Thorac Surg 2001;72:261–3)© 2001 by The Society of Thoracic Surgeons

The automatic implantable cardioverter defibrillator(AICD) was first introduced in 1980 for the treat-

ment of refractory ventricular tachycardia and fibrilla-tion. Since that time, many studies have confirmed itseffectiveness, and hence its use has rapidly increased. Asignificant number of candidates for implantable cardio-verter defibrillators (ICD) have cardiomyopathy as theetiology of their arrhythmia and are therefore also can-didates for orthotopic heart transplantation (OHT). Al-though experience placing transplants in patients whohave an ICD in place is limited, the number of suchpatients is growing. Here, we report a case of a majorcomplication resulting from an ICD patch left in place atthe time of OHT.

A 57-year-old man who had had an ICD placed 7 yearspreviously and an OHT 6 years previously presented tothe hospital for hemoptysis. In 1991, the patient had hadrepeated episodes of monomorphic ventricular tachycar-dia, for which an internal defibrillator was placed. AVentak Model 1550 (Cardiac Pacemakers, St. Paul, MN)ICD was implanted through a standard left anteriorthoracotomy approach, with intrapericardial patches se-cured over the right atrium and on the posterolateral and

Accepted for publication May 16, 2000.

Address reprint requests to Dr Herlihy, Pulmonary Medicine and CriticalCare, St. Luke’s Episcopal Hospital, Medical Clinic of Houston, 6624Fannin, Suite 1700, Houston, TX 77030; e-mail: herlihy@mchllp.com.

261Ann Thorac Surg CASE REPORT CHILUKURI ET AL2001;72:261–3 ICD PATCH EROSION

© 2001 by The Society of Thoracic Surgeons 0003-4975/01/$20.00Published by Elsevier Science Inc PII S0003-4975(00)02566-2