Again, I congratulate Dr Kalangos on his outstanding work andhope our programs will be cooperating in the near future.

Amram J. Cohen, MD*

Department of Pediatric Cardiac SurgeryWolfson Medical CenterPO Box 5Holon 58100, Israele-mail: dawn@wolfson.health.gov.il.

Induced Ventricular Fibrillation in the Management ofAortic Arch TraumaTo the Editor:

We read with interest in the May 2001 issue of The Annals thearticle by Dr Lim and associates [1]. In summary, the authorsrecommend that penetrating cardiac injuries be repaired duringtemporary cardiac arrest. This has been achieved in their clinicalpractice by intravenous injection of adenosine.

Temporary short-lasting circulatory arrest as an adjunct torepair injuries of the heart and the aorta was first recommendedby the great Japanese surgeon Juro Wada in the 1970s [2] andreemphasized by us a few years later [3]. We found it a mosteffective and occasionally a life-saving situation, which greatlysimplified suturing holes in both the heart and the aorta. We,however, applied artificially induced ventricular fibrillation, amaneuver that could be easily accomplished by homemadefibrillators, instead of pharmacologic ventricular asystole. Hav-ing used it in a good number of patients, we found it an easy andprobably safer method than pharmacologic asystole to handlepenetrating injuries of the large vessels of the heart.

Francis Robicsek, MD, PhD

The Carolinas Heart Institute1000 Blythe BoulevardCharlotte, NC 28203

References

1. Lim R, Gill IS, Temes RT, Smith CE. The use of adenosine forrepair of penetrating cardiac injuries: a novel method. AnnThorac Surg 2001;71:1714–5.

2. Wada J. Electrically induced fibrillation in cardiac arrest andresuscitation. In: Stephenson HE Jr, ed. Cardiac arrest andresuscitation. St. Louis: CV Mosby Co, 1974:783–95.

3. Robicsek F, Matos-Cruz M. Artificially induced ventricularfibrillation in the management of through-and-through pen-etrating wounds of the aortic arch: a case report. Surgery1991;10:544–5.

ReplyTo the Editor:

We read with great interest the comments made by Dr Robicsekregarding our article [1].

We were not aware of Dr Robicsek’s and Dr Wada’s publishedreports in treating penetrating cardiac trauma with artificiallyinduced ventricular fibrillation. Both methods are probablyequally safe, but the advantage of adenosine-induced asystole is

that it renders the heart completely flaccid and much moreamenable to manipulation, especially when dealing with injuriesof the lateral wall. This indeed was our experience in both caseslisted in the publication.

Inderjit S. Gill, MDRoger Lim, MDR. Thomas Temes, MDCharles E. Smith, MD

Department of Thoracic and Cardiovascular SurgeryThe Cleveland Clinic FoundationCleveland, OH 44109-1998e-mail: gillis@ccf.org.

Reference

1. Lim R, Gill IS, Temes RT, Smith CE. The use of adenosine forrepair of penetrating cardiac injuries: a novel method. AnnThorac Surg 2001;71:1714–5.

Cellular Myoplasty: What Are We Really Trying toAchieve?To the Editor:

The article by Dr Pouzet and his colleagues in the March 2001issue of The Annals [1] adds to a rapidly expanding body ofliterature assessing the efficacy of “cellular myoplasty” in pre-venting or reversing heart failure due to postinfarction leftventricular remodeling.

The implied hypothesis is that cellular myoplasty replacescardiac myocytes, which are lost as a result of myocardialinfarction. While attractive, this idea overlooks important as-pects of myocardial structure and consequences of postinfarc-tion ventricular remodeling. Two points need clarification.

First, normal myocardium is composed of cardiac myocytesand an intracellular collagen matrix, which are intimately re-lated and necessary for effective cardiac performance. Myocar-dial infarction destroys both of these tissue types. Myocytes thatare implanted randomly into an infarct in the absence of a viablecollagen network to “harness them together” are unlikely toprovide effective contractile force.

Second, postinfarction left ventricular remodeling results inthe insidious development of heart failure over time [2]. Patientsare initially hemodynamically compensated, indicating that theyhave a sufficient number of viable myocytes to maintain ade-quate cardiac performance. Over time, the remodeling processcauses a myopathic process in normally perfused myocardiumthat leads to heart failure [3].

Given these two facts, it would seem to us that a strategyintended to prevent myocardial impairment secondary to leftventricular remodeling would be superior to one that proposesto restore ventricular function by introducing myocytes in anattempt to replace those lost due to infarction.

We hypothesize that the salutary effects attributed to cellularmyoplasty in this study are in reality due to an alteration ininfarct material properties, which ameliorate infarct expansion,therefore, limiting the myopathic effects of postinfarction leftventricular remodeling [4].

In our opinion, the rat model with its inconsistent infarcts,residual ischemic myocardium, and inability to adequately as-sess regionally contractility and geometry is not an appropriate*Doctor Cohen passed away on Aug 15, 2001.

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model to answer these questions. Better experimental modelsexist.

Robert C. Gorman, MDJoseph H. Gorman III, MD

Department of SurgeryHospital of The University of Pennsylvania3400 Spruce StPhiladelphia, Pennsylvania 19104

References

1. Pouzet B, Vilquin J-T, Hagege AA, et al. Factors affectingfunctional outcome after autologous skeletal myoblast trans-plantation. Ann Thorac Surg 2001;71:844–51.

2. St John Sutton M, Pfeffer MA, Moye L, et al. Cardiovasculardeath and left ventricular remodeling two years after myo-cardial infarction: baseline predictors and impact of long-term use of Captopril: information from the survival andventricular enlargement (SAVE) trial. Circulation 1997;96:3294–9.

3. Narula J, Dawson MS, Singh BK, et al. Noninvasive charac-terization of stunned, hibernating, remodeled and nonviablemyocardium in ischemic cardiomyopathy. J Am Coll Cardiol2000;36:1913–9.

4. Kelley ST, Malekan R, Gorman JH III, et al. Restraining infarctexpansion preserves left ventricular geometry and functionafter acute anteroapical infarction. Circulation 1999;99:135–42.

ReplyTo the Editor:

We thank Drs Gorman and Gorman for their letter, whichindeed addresses two distinct issues. The first pertains to themechanism by which skeletal myoblast transplantation (a termthat should be preferred to “cellular myoplasty”) improvespostinfarct left ventricular function. We totally agree that limi-tation of remodeling due to the elastic properties of the im-planted cells acting as a structural scaffold is likely to play animportant role, and this hypothesis is further supported by ourmost recent experimental data in sheep, which show a signifi-cant reduction of end-diastolic left ventricular volumes in themyoblast-transplanted group (manuscript in preparation). How-ever, the limited functional efficacy of fibroblasts compared withsmooth muscle cells or fetal cardiomyocytes [1] suggests that thebenefits of cell transplantation may also involve an improve-ment of systolic performance, which is more directly related tothe contractile properties of the implanted cells.

The second issue addressed by this letter pertains to the ratmodel used in our study [2]. It is true that coronary arteryligation may result in infarcts of different sizes. This factor,however, can be easily addressed by increasing the sample size.In our study, the baseline (postinfarct, pretransplant) left ven-tricular ejection fractions were 32.6 � 1.8% in controls (n � 23)and 30.3 � 1.7% in myoblast-injected rats (n � 21), and the closesimilarity between these two values provides compelling evi-dence for the appropriate comparability of the initial infarctareas. On the other hand, we agree that regional contractility isdifficult to assess echocardiographically in the rat heart. How-ever, such was not the objective of the present study, which wasspecifically designed to assess to what extent the initial impair-ment of left ventricular function and the number of injectedmyoblasts altered the posttransplant functional outcome. “Bet-ter experimental models” always exist and we have actually

used a sheep model of myocardial infarction to study regionalfunction after myoblast transplantation (manuscript inpreparation).

Bruno Pouzet, MDPhilippe Menasche, MD, PhD

Department of Cardiovascular SurgeryHopital Bichat46 rue Henri Huchard75877 Paris Cedex 18, France

References

1. Sakai T, Li R-K, Weisel RD, et al. Fetal cell transplantation: acomparison of three cell types. J Thorac Cardiovasc Surg 1999;118:715–25.

2. Pouzet B, Vilquin J-T, Hagege AA, et al. Factors affectingfunctional outcome after autologous skeletal myoblast trans-plantation. Ann Thorac Surg 2001;71:844–51.

Right Ventricle to Pulmonary Artery Connection Afterthe Ross Procedure: Is it Really a Concern?To the Editor:

With great interest, I read the article by Ehud Raanani andassociates [1]. In this article, the authors touch on two majorissues. The first is the specific issue of the fate of the pulmonaryhomograft in the pulmonary position after the Ross procedure.The second is trying to identify predictors of late pulmonaryhomograft stenosis, which is a more general issue.

I agree with the authors that pulmonary homograft stenosisdoes exist following the Ross procedure. However, I do not feelthat it represents a significant clinical problem. In our ownexperience of 292 Ross procedures, only 6 patients requiredsurgical intervention for pulmonary stenosis (2%). This goesalong with the authors’ own experience of 1 patient requiringchange of the homograft twice; 6 other patients were balloondilated, with 5 “moderate” reductions in gradient and 1 failurethat subsequently required surgery.

Looking at this problem, I and my colleagues specificallystudied 233 patients with detailed echocardiography. We found28 patients (12%) with gradients greater than 40 mm Hg; thosewho required reoperation or balloon intervention were from thisgroup, except for 1 patient who needed a tricuspid valve repairand, at surgery, was determined to have significant pulmonarystenosis. Very few patients developed electrocardiographic signsof right ventricular hypertrophy, dilation, or systolic dysfunc-tion. What the authors reported about the stenosis being diffuse,rather than discrete, in the whole length of the homograft withcalcification, is consistent with our findings. However, we havefew patients with additional PR.

Our surgical approach has been to augment the area ofpulmonary stenosis with a transannular bovine pericardialpatch, which has been very successful thus far. We believe thePR will be well tolerated. The reason for this is our belief thatthese patients are already at a disadvantage, the most likelyreason for development of the stenosis is immunologic, and thata second homograft will probably have the same fate.

As regards the second issue of risk factors for developingpulmonary stenosis, we believe that this is a complex issue sincethere are many variables that can enter the equation. The authors’attempt to identify predictors is commendable, but I doubt that

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