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J Thorac Cardiovasc Surg 1998;115:261-262
© 1998 Mosby, Inc.

LETTERS TO THE EDITOR

Batista operation for dilated cardiomyopathy: A physiologic concept

Jyotirmay Chanda, MD, Ryosei Kuribayashi, MD, Tadaaki Abe, MD

To the Editor:

We read with great interest the recent article by Dickstein, Spotnitz, and Burkhoff.Go 1 Using a multiple-compartment elastance model, the authors tried to demonstrate the overall effect of ventricular mass reduction on cardiac function.

The basic principle of the Batista operation for dilated cardiomyopathy is "not to reduce the mass" of the ventricle but to "reduce the volume of the chamber" of the dilated ventricle, thus to reduce the wall stress of the ventricle. However, the reduction of chamber volume would be achieved only at the expense of muscle excision. The ventricular chamber volume reduction in dilated cardiomyopathy was not a lay idea. It was theoretically well conceived.

Chamber enlargement will lead to increased peak systolic wall stress (by the law of Laplace), which in the postulated system then causes myocardial hypertrophy of sufficient magnitude to normalize the systolic stress.Go 2 Despite the increase in myocardial mass, the myocardial stress is always higher in patients with dilated cardiomyopathy.Go Go 2-6 Grant, Greene, and BunnellGo 7 defined a ventricle with eccentric hypertrophy as a magnified image of the normal ventricle without alteration in relative wall thickness (wall thickness/radius). This idea was supported by others.Go Go 2,3 According to this principle, the normal mass and chamber volume ratio should be maintained in dilated cardiomyopathy. The mean normal value of left ventricular mass/left ventricular end-systolic and end-diastolic volume ratios (LVM/LVESV and LVM/LVEDV) calculated from the data of Kennedy and associatesGo 8 were 4.0 and 1.3, respectively. The calculated LVM/LVESV ratio varies, but this valueGo Go 3,4 was never less than 3.0 in normal subjects. Similarly, the calculated LVM/LVEDV ratioGo Go Go 3,5,6 was never less than 0.95 in normal subjects.

The mean myocardial systolic stress in nonsurvivors and survivors with dilated cardiomyopathyGo 5 was 590 and 541 dyne/cm2, respectively, as calculated according to the following equationGo 1:


where PLV is instantaneous left ventricular pressure, Vm is the volume of the myocardium, and {sigma} is calculated systolic stress. The calculated value of mean LVM/LVESV ratio in survivors and nonsurvivors with dilated cardiomyopathyGo 5 was 1.06 and 1.36, respectively. Similarly, in another reportGo 4 concerning patients with compensated dilated cardiomyopathy, the calculated mean LVM/LVESV ratio (1.8) was higher than that (1.09) in patients with decompensated dilated cardiomyopathy. These findings suggest that ventricular mass does not increase proportionally with the increase in chamber volume, as hypothesizedGo Go Go 2,3,7 earlier, and an LVM/LVESV ratio not less than 1.8 might be considered an important prognostic value of compensatory mechanism in dilated cardiomyopathy.

The importance of ventricular mass in reduction of systolic stress can be shown by the following example. In a normal subject with a Plv (mean left ventricular systolic pressure) of 122 mm Hg, a Vlv (LVESV) of 45 ml, and an LVM of 164 gm, the calculatedGo 1 systolic stress {sigma} is 306 dyne/cmGo 2. In a patient with decompensated dilated cardiomyopathy with PLV = 105 mm Hg, VLV = 300 ml, and LVM = 480 gm, the calculatedGo 1 systolic stress would be 414 dyne/cm2. In this patient, to keep the systolic stress 306 dyne/cm2, more 338 gm (i.e., total LVM, 818 gm) of LV mass is necessary; and with the reduction of LVESV from 300 to 150 ml, LVM from 480 to 300 gm, the left ventricular systolic stress would be reduced from 414 to 359 dyne/cm2, if the PLV were to remain 105 mm Hg. Theoretically, if no muscle was excised during the reduction of LVESV from 300 to 150 ml, the value of left ventricular systolic stress {sigma} (277 dyne/cm2) would be even less than 306 dyne/cm2. These examples clearly demonstrate that in dilated cardiomyopathy, surgical intervention directed to chamber volume reduction (unfortunately at the expense of mass reduction) would decrease the myocardial wall stress and hence improve the cardiac function.

Here we wish to emphasize that although the ventricular remodeling surgery for dilated cardiomyopathy has not received enough attention in medical publications, the idea of surgical intervention is unique and physiologically well-based.

Department of Cardiovascular SurgeryAkita University School of Medicine1-1-1 Hondo
Akita 010, Japan References

  1. Dickstein ML, Spotnitz HM, 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. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest 1975;56:56-64.
  3. Hood WP Jr, Rackley CR, Rolett EL. Wall stress in the normal and hypertrophied human left ventricle. Am J Cardiol 1968;22:550-8.[Medline]
  4. Hirota Y, Shimizu G, Kaku K, Saito T, Kino M, Kawamura K. Hypertrophic nonobstructive cardiomyopathy: a precise assessment of hemodynamic characteristics and clinical implications. Am J Cardiol 1984;54:1033-8.[Medline]
  5. Douglas PS, Morrow R, Ioli A, Reichek N. Left ventricular shape, afterload and survival in idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1989;13:311-5.[Abstract]
  6. Bortone AS, Hess OM, Chiddo A, et al. Functional and structural abnormalities in patients with dilated cardiomyopathy. J Am Coll Cardiol 1989;14;613-23.
  7. Grant C, Greene DG, Bunnell IL. Left ventricular enlargement and hypertrophy. Am J Med 1965;39:895-904.[Medline]
  8. Kennedy JW, Baxley WA, Figley MM, Dodge HT, Blackmon JR. Quantitative angiography. I. The normal ventricle in man. Circulation 1966;34:272-8.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
J. Chanda and R. Kuribayashi
The Batista procedure for dilated cardiomyopathy: An analysis that goes beyond ""hand waving""
J. Thorac. Cardiovasc. Surg., August 1, 1998; 116(2): 370 - 371.
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