number of cells reaching the myocardium is too insignificant toimpart functional improvement to host myocardium. Further,we believe that quantification of the migrating donor cells mightalso provide a clue regarding the efficiency of the host’s ownbone marrow cells to migrate and supplement the ability of themyocardium to regenerate. Consistent with previously pub-lished data [2] the study provides impetus to the belief that inthe event of myocardial injury, bone marrow stem cells undergodifferentiation to initiate and perform the repair process.

In the light of this report [1] and other recent studies, thecurrent understanding of immune tolerance needs to be re-viewed more carefully.

Husnain Kh. Haider, MPharm, PhD

Department of Cardiothoracic and Vascular SurgeryNational University of SingaporeSingapore 117597, Singaporee-mail: khhaider@hotmail.com

Yel Lei, MDShujia Jiang, MD

10-Medical DriveNational University of SingaporeSingapore-117597, Singapore

Peter K. Law, PhD

1770 Moriah Woods BlvdSuite 18Cell Therapy, IncMemphis, TN 38117-7126

Eugene K. W. Sim, FRCS

Department of Cardiac, Thoracic and Vascular SurgeryNational University Hospital5 Lower Kent Ridge RdSingapore 119074, Singaporee-mail: sursinkw@nus.edu.sg

References

1. Saito T, Kuang J-Q, Bittira B, Al-Khaldi A, Chiu RC-J. Xeno-transplant cardiac chimera: immune tolerance of adult stemcells. Ann Thorac Surg 2002;74:19–24.

2. Orlic D, Kajstura J, Chimenti S, et al. Mobilized bone marrowcells repair the infarcted heart improving function and sur-vival. Proc Natl Acad Sci USA 2001;98:10344–49.

ReplyTo the Editor:

Dr Haider and colleagues wrote that “the authors based theirobservation solely on the expression of x-gal staining, whichwould have been more conclusive with evidence of the absenceof immune cell infiltration at the site of the graft.” In fact, thatcan be seen in our Figure 4 [1]. One day after ligation of the leftanterior descending coronary artery [LAD], the infarct siteunderwent necrosis with inflammatory cell infiltration as ex-pected. Because LAD was occluded, the recruited bone marrowstromal cells (MSCs) initially reached the viable zone around theinfarcted area by way of collaterals (Figs 4C, 4D). This zoneclearly showed the absence of cellular infiltration attacking thelabeled mouse MSCs. In our follow-up control study (unpub-lished data), we injected differentiated cutaneous fibroblastsfrom the same mouse donor into the rat heart and confirmed a

rapid cellular infiltration response against the implanted cellsand elimination of the labeled fibroblasts within several days.These observations are consistent with our interpretation thatthe MSCs possess unique immune tolerance, as we discussed inour report [1].

It was not feasible to accurately quantitate the number of cellsreaching the myocardium because of their distribution withinthe myocardium. Furthermore, as we demonstrated, the labeledcells did not all differentiate into neo-cardiomyocytes, but alsobecame cells of other phenotypes. A technique that can reliablyquantitate not only the labeled cells in the myocardium but alsothe number of differentiated cells of specific phenotype and theirtopological distribution would be highly valuable, as establish-ment of a dose–response relationship (ie, number of cells versusfunctional improvement) would be very important clinically.

Finally, our choice of the cellular xenotransplant model tostudy myocardial regeneration is not meant to imply that xeno-transplantation is preferable to allotransplantation clinically.Our intent was to “push the envelope” to see how the MSCswould respond in this immunologically even more hostileenvironment.

Takayuki Saito, MD, PhD

Department of Cardiovascular SurgerySchool of Medical Sciences1 Kawasumi, Mizuho-kuNagoya, Japane-mail: saitotjk@hotmail.com

Ray C.-J. Chiu, MD, PhD

Division of Cardiac SurgeryThe Montreal General Hospital, MUHC1650 Cedar Ave, Suite C9-169Montreal, PQ H3G 1A4, Canadae-mail: rchiu@po-box.mcgill.ca

Reference

1. Saito T, Kuang J-Q, Bittira B, Al-Khaldi A, Chiu RC-J. Xeno-transplant cardiac chimera: immune tolerance of adult stemcells. Ann Thorac Surg 2002;74:19–24.

Treatment of Persistent Chylothorax With SomatostatinTo the Editor:

We read with special interest the case report by Pettitt andcolleagues [1]. In their treatment of persistent postoperativechylothorax after surgery for congenital heart disease, they usedan intravenous infusion of somatostatin in the neonate. Subse-quently, the patient’s chest tube drainage stopped withoutsignificant adverse effects. We would like to add a few commentson some aspects of their case report.

The authors mentioned that their patient showed no apparentadverse effects except for some transient cutaneous flushing.However, they also documented an elevation of liver functiontests with vomiting in 1 patient, and flu-like symptoms inanother patient. Fortunately, the side effects in their cases werenot fatal. Unfortunately, we have experienced significant com-plications associated with the use of somatostatin.

Our patient had asplenia syndrome with total anomalouspulmonary venous connection (TAPVC) and underwent re-pair of the TAPVC and pulmonary artery banding at 1 monthof age. As her cyanosis recurred, she underwent a total

340 CORRESPONDENCE Ann Thorac Surg2003;76:337–42

© 2003 by The Society of Thoracic Surgeons 0003-4975/03/$30.00Published by Elsevier Inc

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