obstructive lung disease. Chest Surg Clin North Am 1995;5:575–602.

7. Ash SR, Carr DJ, Diaz-Buxo JA. Peritoneal access devices. In:Nissenson AR, Fine RN, Gentile DE, eds. Clinical dialysis, 3rded. Norwalk, CT: Appleton and Lange, 1995:307–9.

8. Almassi GH, Haasler G. Chemical pleurodesis in the pres-ence of persistent air leak. Ann Thorac Surg 1989;47:786–7.

Left Ventricular Outflow TractObstruction After Mitral ValveReplacementDidier De Canniere, MD, PhD, Jean-Luc Jansens, MD,Philippe Unger, MD, PhD, and Jean-Louis Le Clerc,MD

Department of Cardiac Surgery, Erasme University Hospital,Brussels, Belgium

We describe a patient with left ventricular outflow tractobstruction after mitral valve replacement preserving theanterior subvalvular apparatus. Postoperative trans-esophageal echocardiography demonstrated systolic nar-rowing of the left ventricular outflow tract by a bulgingseptum and systolic anterior motion of the preservedanterior mitral leaflet. Septal myectomy and transaorticmitral apparatus resection enabled us to relieve the leftventricular outflow tract obstruction. This suggests thatseptal hypertrophy might be a relative contraindicationto the preservation of the anterior mitral subvalvularapparatus in mitral replacement.

(Ann Thorac Surg 1997;64:1805–6)© 1997 by The Society of Thoracic Surgeons

A 73-year-old man with a history of recurrent epi-sodes of cardiac failure and severe chronic obstruc-

tive pulmonary disease was admitted for increasing dys-pnea. Electrocardiogram showed 2/1 atrioventricularblock. Transesophageal echocardiography demonstrated41 mitral and trivial tricuspid regurgitation. Severe an-nular calcification and posterior leaflet retraction contra-indicated valvular repair. Severe left ventricular hyper-trophy was reported without further comment. The leftventricular ejection fraction was 0.60.

At cardiac catheterization pulmonary artery pressureand pulmonary artery occlusion pressure were 78/35 and33 mm Hg, respectively, and cardiac index was 2.6 L zmin21 z m22. The mitral valve was replaced by a porcineCarpentier-Edwards 29-mm SAV bioprosthesis (BaxterXenomedica, Horw, Switzerland) with preservation ofthe anterior and posterior subvalvular mitral apparatusafter the anterior leaflet had been split to the annulus asdescribed by Miki and associates [1]. The procedure was

uneventful, and the patient was weaned from bypass withslight inotropic support (2 mg z kg21 z min21 dobutamine).The operation was ended by the placement of a VDDpacemaker through the left subclavian vein. Temporarypacing wires on the right atrium provided electrostimula-tion of the atria, and the ventricular contraction was syn-chronized on this event by the endocardiac VDD system.

During the first hour the hemodynamic situation dete-riorated rapidly in the intensive care unit; a progressivedecrease in cardiac index and systemic pressure occurredleading to an increase in inotropic support. Transesoph-ageal echocardiography was performed. Systolic narrow-ing of the left ventricular outflow tract was observedbetween a bulging septum (18 mm) and the remaindersof the anterior mitral leaflet (Fig 1). The decrease ininotropic support and the insertion of an intraaorticballoon pump somewhat ameliorated the situation.

The patient was returned to the operating room. Car-diopulmonary bypass was resumed, a septal myectomywas performed as described by Morrow [2], and theanterior mitral apparatus was resected through the aor-totomy. The aorta was cross-clamped for 12 minutes andthe patient was weaned uneventfully from bypass. Intra-operative transesophageal echocardiography confirmedthe disappearance of the left ventricular outflow tractobstruction, and no gradient was measured between theleft ventricle and the aorta. The patient experiencedbronchopulmonary complications and was discharged onpostoperative day 52.

Comment

Systolic anterior motion of the mitral valve, leading to leftventricular outflow tract obstruction, is a classic complica-tion after mitral valve repair [3]. Two risk factors areassociated with the occurence of systolic anterior motion:the excess of valvular tissue and the presence of a bulgingseptum [4, 5]. Recent data from the literature highlight thefunctional importance of preserving the subvalvar mitralapparatus during mitral valve replacement [6].

Accepted for publication Aug 1, 1997.

Address reprint requests to Dr De Canniere, Department of CardiacSurgery, Erasme University Hospital, Route de Lennik, 808, 1070 Brussels,Belgium (e-mail: ddc@skynet.be). Fig 1. Systolic narrowing of the left ventricular outflow tract.

1805Ann Thorac Surg CASE REPORT DE CANNIERE ET AL1997;64:1805–6 SEPTAL MYECTOMY AFTER MITRAL REPLACEMENT

© 1997 by The Society of Thoracic Surgeons 0003-4975/97/$17.00Published by Elsevier Science Inc PII S0003-4975(97)01115-6

We report the case of a patient with mitral valvedisease and septal hypertrophy in whom systolic anteriormotion and left ventricular outflow tract obstructiondeveloped after mitral valve replacement with preserva-tion of the mitral subvalvar apparatus. This conditionwas successfully treated by transaortic septal myectomyand resection of the anterior subvalvar apparatus. Thepresent case suggests that preservation of the anteriorleaflet during mitral valve replacement might be delete-rious if marked septal hypertrophy is present. If preser-vation is mandatory, a solution of partial resection of theanterior leaflet as described by David [7] or Rose and Oz[8] might be preferred. Careful preoperative transtho-racic echocardiography detection of septal hypertrophyand perioperative transesophageal echocardiographyshould enable the surgeon to anticipate this complicationand thus select the appropriate surgical approach.

References

1. Miki S, Ueda Y, Tahata T, Okita Y. Mitral valve replacementwith preservation of chordae tendineae and papillary mus-cles. Ann Thorac Surg 1995;60:225–6.

2. Morrow AG. Hypertrophic subaortic stenosis: operativemethods utilized to relieve left ventricular outflow obstruc-tion. J Thorac Cardiovasc Surg 1978;76:423–30.

3. Perier P, Hagen T, Stumpf Y. Septal myectomy for leftventricular outflow obstruction after mitral valve repair. AnnThorac Surg 1994;57:1328–30.

4. Jiang L, Levine RA, King ME, Weyman AE. An integratedmechanism for systolic anterior motion of the mitral valve inHCMO based on echocardiographic observations. Am Heart J1987;113:633–44.

5. Lee KS, Stewart WJ, Lever HM, Underwood PL, CosgroveDM. Mechanism of outflow tract obstruction causing failedmitral valve repair. Circulation 1993;88:24–9.

6. DeAndra A Jr, Komeda M, Nikolic SD, Daughters GT, IngelsNB, Miller DC. Left ventricular function, twist, and recoil aftermitral valve replacement. Circulation 1995;92:458–66.

7. David TE. Mitral valve replacement with preservation ofchordae tendineae: rationale and technical considerations.Ann Thorac Surg 1986;41:680–2.

8. Rose EA, Oz MC. Preservation of anterior leaflet chordaetendineae during mitral valve replacement. Ann Thorac Surg1994;57:768–9.

INVITED COMMENTARY

In patients with left ventricular hypertrophy, iatrogenicleft ventricular outflow tract obstruction may occur aftermitral valve replacement. The outflow obstruction mostfrequently results from implantation of a high-profile,large-diameter prosthesis. If the prosthesis is not ori-ented properly, a strut may obstruct the outflow tract. Ina patient with a calcified annulus, such as the onedescribed in this report, a 29-mm prosthesis may beexcessively large. In addition, sparing the chordae by split-ting and reattaching the segments of the anterior leafletmay have contributed to the obstruction in this case. Ahypertrophied posteromedial papillary muscle with fi-brosed chordae may be a contraindication to this technique.

Although no reference was made to idiopathic hyper-trophic subaortic stenosis as a preoperative finding, id-

iopathic hypertrophic subaortic stenosis may also havecontributed to the outflow obstruction in this patient.When mitral valve replacement is used to relieve idio-pathic hypertrophic subaortic stenosis, the anterior mi-tral leaflet should be removed, the posteromedial papil-lary muscle excised, and a small-diameter, low-profilemechanical prosthesis inserted.

Denton A. Cooley, MD

Texas Heart InstitutePO Box 20345, MC 3-258Houston, TX 77225-0345

Postoperative Myocardial IschemiaCaused by Chest TubeCompression of Vein GraftRolf Svedjeholm, MD, PhD, and Erik Håkanson, MD,PhD

Departments of Cardiothoracic Surgery and CardiothoracicAnesthesia, Linkoping Heart Center, University Hospital,Linkoping, Sweden

Here we report an unexpected and possibly overlookedcause of postoperative myocardial ischemia: a chest tubecompressing a vein graft. After the position of the chesttube was adjusted, graft flow was reestablished, rightventricular contractility returned, and myocardial infarc-tion was probably prevented. The literature on chest tubecomplications is briefly reviewed and experience fromour institution is reported.

(Ann Thorac Surg 1997;64:1806–8)© 1997 by The Society of Thoracic Surgeons

A variety of complications have been described inassociation with closed chest tube insertion. How-

ever, data on complications from mediastinal chest tubesinserted in association with cardiac operations are lim-ited. Here we report an unexpected and possibly over-looked cause of postoperative myocardial ischemia: achest tube compressing a vein graft. The literature onchest tube complications is briefly reviewed and experi-ence from our institution is reported.

The patient, a 77-year-old man with hypertension, elevatedserum lipid levels, rheumatoid arthritis, and angina for 3years was hospitalized for myocardial infarction. Subse-quently unstable angina developed and a semiurgent cor-onary angiogram was performed. The angiogram showedan 80% left main stenosis, occlusion of the left anterior

Accepted for publication August 8, 1997.

Address reprint requests to Dr Svedjeholm, Department of Cardiotho-racic Surgery, Linkoping Heart Center, University Hospital, S-581 85Linkoping, Sweden (e-mail: rolf.svedjeholm@thx.us.lio.se)

1806 CASE REPORT SVEDJEHOLM AND HÅKANSON Ann Thorac SurgMYOCARDIAL ISCHEMIA CAUSED BY CHEST TUBE 1997;64:1806–8

© 1997 by The Society of Thoracic Surgeons 0003-4975/97/$17.00Published by Elsevier Science Inc PII S0003-4975(97)01005-9