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J Thorac Cardiovasc Surg 2002;123:582-583
© 2002 The American Association for Thoracic Surgery

Letters to the Editor

Cellular myoplasty: What are we really trying to achieve?

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

University of Pennsylvania Medical School
Philadelphia, PA 19104

To the Editor:

The article by Rajnoch and associatesGo 1 and the associated editorial by Weisel and colleaguesGo 2 in the May 2001 issue of the Journal add to a rapidly expanding body of literature assessing the efficacy of "cellular cardiomyoplasty" in preventing or reversing heart failure due to postinfarction left ventricular remodeling.

The implied hypothesis is that cellular cardiomyoplasty replaces cardiac myocytes that have been lost as a result of a myocardial infarction. Although attractive, this idea is relatively naive given what is known about normal myocardium and ventricular remodeling. Two points need clarification.

First, normal myocardium is composed of cardiac myocytes and an intracellular collagen matrix, which are intimately related and necessary for effective cardiac performance. Myocardial infarction destroys both of these tissue types. Myocytes that are implanted randomly into an infarct in the absence of a viable collagen network to "harness them together" are unlikely to provide effective contractile force.

Second, postinfarction left ventricular remodeling results in the insidious development of heart failure over time.Go 3 Patients are initially hemodynamically compensated, indicating that they have a sufficient number of viable myocytes to maintain adequate cardiac performance. Over time, the remodeling phenomenon results in a myopathic process in normally perfused myocardium that leads to heart failure.Go 4

Given these two facts, it seems to us that a strategy intended to prevent myocardial impairment resulting from left ventricular remodeling would be superior to one that proposes to restore ventricular function by haphazardly introducing myocytes in an attempt to replace those lost as the result of an infarction.

We hypothesize that the salutary effects attributed to cellular cardiomyoplasty in this studyGo 1 are in reality the result of an alteration in infarct material properties, which prevented infarct expansion, therefore limiting the myopathic effects of postinfarction left ventricular remodeling.Go 5

The surgical armamentarium for the treatment of patients with heart failure is replete with operations that seemed like good ideas initially but, when introduced clinically, provided inconsistent results. Before yet another procedure is introduced, we should fully understand the problem we are trying to solve and what we can realistically hope to accomplish with the operation.

12/8/120722doi:10.1067/mtc.2002.120722

References

  1. Rajnoch C, Chachques JC, Berrebi A, Bruneval P, Benoit M-O, Carpentier A. Cellular therapy reverses myocardial dysfunction. J Thorac Cardiovasc Surg. 2001;121:871-8.[Abstract/Free Full Text]
  2. Weisel RD, Li RK, Mickle DA, Yau TM. Cell transplantation comes of age. J Thorac Cardiovasc Surg. 2001;121:835-6.[Free Full Text]
  3. St John Sutton M, Pfeffer MA, Moye L, et al. Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival And Ventricular Enlargement (SAVE) trial. Circulation. 1997;96:3294-9.[Abstract/Free Full Text]
  4. Narula J, Dawson MS, Singh BK, Amanullah A, Acio ER, Chaudhry FA, et al. Noninvasive characterization of stunned, hibernating, remodeled and nonviable myocardium in ischemic cardiomyopathy. J Am Coll Cardiol. 2000;36:1913-9.[Abstract/Free Full Text]
  5. Kelley ST, Malekan R, Gorman JH 3rd, Jackson BM, Gorman RC, Suzuki Y, et al. Restraining infarct expansion preserves left ventricular geometry and function after acute anteroapical infarction. Circulation. 1999;99:135-42.[Abstract/Free Full Text]



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