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Ann Thorac Surg 2002;73:342-343
© 2002 The Society of Thoracic Surgeons

Correspondence

Cellular myoplasty: what are we really trying to achieve?

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

a Department of Surgery, Hospital of The University of Pennsylvania, 3400 Spruce St, Philadelphia, Pennsylvania 19104, USA

To the Editor

The article by Dr Pouzet and his colleagues in the March 2001 issue of The Annals [1] adds to a rapidly expanding body of literature assessing the efficacy of "cellular myoplasty" in preventing or reversing heart failure due to postinfarction left ventricular remodeling.

The implied hypothesis is that cellular myoplasty replaces cardiac myocytes, which are lost as a result of myocardial infarction. While attractive, this idea overlooks important aspects of myocardial structure and consequences of postinfarction 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 [2]. Patients are initially hemodynamically compensated, indicating that they have a sufficient number of viable myocytes to maintain adequate cardiac performance. Over time, the remodeling process causes a myopathic process in normally perfused myocardium that leads to heart failure [3].

Given these two facts, it would seem to us that a strategy intended to prevent myocardial impairment secondary to left ventricular remodeling would be superior to one that proposes to restore ventricular function by introducing myocytes in an attempt to replace those lost due to infarction.

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

In our opinion, the rat model with its inconsistent infarcts, residual ischemic myocardium, and inability to adequately assess regionally contractility and geometry is not an appropriate model to answer these questions. Better experimental models exist.

References

  1. Pouzet B., Vilquin J.-T., Hagège A.A., et al. Factors affecting functional outcome after autologous skeletal myoblast transplantation. Ann Thorac Surg 2001;71:844-851.[Abstract/Free Full Text]
  2. St John Sutton M., Pfeffer M.A., 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;96:3294-3299.[Abstract/Free Full Text]
  3. Narula J., Dawson M.S., Singh B.K., et al. Noninvasive characterization of stunned, hibernating, remodeled and nonviable myocardium in ischemic cardiomyopathy. J Am Coll Cardiol 2000;36:1913-1919.[Abstract/Free Full Text]
  4. Kelley S.T., Malekan R., Gorman J.H., III, et al. Restraining infarct expansion preserves left ventricular geometry and function after acute anteroapical infarction. Circulation 1999;99:135-142.[Abstract/Free Full Text]




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