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J Thorac Cardiovasc Surg 1998;116:369-370
© 1998 Mosby, Inc.

Letters To The Editor

The Batista procedure for dilated cardiomyopathy: An analysis that goes beyond "hand waving"

Charles R. Bridges, MD, ScD

To the Editor:

Considerable confusion exists regarding the physiologic basis of the Batista procedure, both in the literature and in the content of national presentations discussing this procedure. A typical example of this confusion results when the Laplace relationship for a sphere is quoted:
(1)


Here h is the wall thickness, {sigma} is the wall stress, P is the transmural pressure, and R is the cavitary radius. It is typically stated that since systolic pressure is relatively constant, the Batista procedure, by removing mass, results in a decrease in radius and a proportionate decrease in stress. These assertions are of course valid. It is then asserted that the procedure has a physiologic benefit through a reduction in stress. This latter assertion is where the argument leaves the realm of science and enters the realm of imprecise reasoning ("hand waving"). A reduction in stress does not equate with a physiologic benefit per se. A simple counterexample makes the point. If half of the ventricle of a normal person were resected, a reduction in stress would result. However, removing mass from a normal ventricle would certainly not improve its function! Of course, the Batista operation is beneficial only for dilated ventricles. I would then ask precisely how dilated must the ventricle be? From a rigorous mathematical point of view, the answer has not yet been provided. What is needed and what has been lacking to date is an adequate theory to allow one to predict when and whether resection of ventricular muscle will lead to an increase in function. Dickstein and associatesGo 1 correctly point out that here function must be defined by using absolute indices such as cardiac output, stroke volume, or exercise capacity, not by using relative indices such as ejection fraction.

In a recently published letter to the Editor of this Journal, Chanda, Kuribayashi, and AbeGo 2 give several examples of situations in which reduction of ventricular mass leads to a reduction in calculated systolic wall stress. These examples confirm their hypothesis that removal of ventricular mass in dilated cardiomyopathy will lead to a decrease in wall stress. In an example of the somewhat specious reasoning alluded to above, these authors conclude that "in dilated cardiomyopathy, surgical intervention directed to chamber volume reduction . . . would decrease the myocardial wall stress and hence improve the cardiac function." Although their examples are somewhat contrived, it is clear that wall stress will be reduced but not at all clear that cardiac function will improve. The actual value of the wall stress calculated by these authors in each of their examples is incorrect by a factor of 103. The stress should be calculated with units of (dyne x 103)/cm2 or kdyne/cm2. The stress calculated in each of their examples should be corrected by replacing dyne/cm2 with kdyne/cm2.

Thus the conclusions of Chanda, Kuribayashi, and AbeGo 2 that "the idea of [the Batista procedure] is unique and physiologically well-based" is overly optimistic and certainly not warranted on the basis of their calculations. The fact that systolic stress decreases with ventricular resection ought to be self-evident because it follows directly from the Laplace relationship. Conversely, the conclusion of Dickstein and associatesGo 1 that "overall pump function is depressed ... after heart reduction surgery" is based on an analysis, albeit detailed, of a single set of geometric and functional left ventricular parameters "appropriate for a 70 kg man with dilated cardiomyopathy." Their analysis cannot exclude the possibility that there exists another entire set of functional and geometric parameters for which the Batista procedure does lead to an improvement in function. Another simple counterexample makes the point. It is clear that, in nature, muscle fibers can only generate a certain maximum amount of force per unit surface area; let us call this {sigma}max. It is also clear that to generate a non-zero stroke volume in a living mammal, intraventricular pressure must exceed a minimally acceptable systemic systolic pressure, for example, Pmin {approx}60 mm Hg. On the basis of equation 1, it is clear that for a sufficiently dilated ventricle
(2)


It follows that stroke volume approaches zero! In this limiting case, resection of ventricular mass, by reducing R while keeping h constant, will obviously increase stroke volume to a non-zero value. In fact, if ventricular dysfunction were occurring purely on a geometric basis (due to dilatation with normal intrinsic fiber contractility), an appropriate ventricular resection such that R/h were corrected to normal, would lead to a return to normal function!

These examples demonstrate that the analysis of Chanda, Kuribayashi, and AbeGo 2 is overly optimistic and the analysis of Dickstein and coworkersGo 1 is overly pessimistic about the potential beneficial effects of the Batista procedure. There are extreme theoretical cases in which the Batista procedure clearly will lead to an increase in function in absolute terms. There are other extremes in which function will be worsened. In both cases stress will be reduced. Therefore stress reduction alone does not imply any particular acute effect on function. A more careful analysis is needed that examines the set of circumstances in between these two extremes. An appropriate theory should allow for a quantitative prediction of when and whether a beneficial effect of the Batista procedure should be expected.

Department of SurgeryHospital of the University of Pennsylvania, 3400 Spruce St., 6 Silverstein Building, Philadelphia, PA 19104-4283

References

  1. Dickstein ML, Spotnitz HM, Rose EA, Burkhoff D. Heart reduction surgery: an analysis of the impact on cardiac function. J Thorac Cardiovasc Surg 1997;113:1032-40.[Abstract/Free Full Text]
  2. Chanda J, Kuribayashi R, Abe T. Batista operation for dilated cardiomyopathy: a physiologic concept. J Thorac Cardiovasc Surg 1998;115:262-2.[Free Full Text]




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