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J Thorac Cardiovasc Surg 1998;116:1084-1086
© 1998 Mosby, Inc.

LETTERS TO THE EDITOR

Heart reduction surgery can reconstitute the residual stress-strain state of the left ventricle

To the Editor:

Left ventricular (LV) reduction is a new surgical therapeutic option that has been devised and advanced by Batista and his associates ¹ for the treatment of end-stage dilated cardiomyopathy. Resection of a large portion of the free wall of the LV muscle mass results in significant reduction in the LV cavity size and may improve ejection fraction. The ultimate goal of the procedure is to reduce the diameter of the left ventricle to restore a "more optimal" physiologic volume/mass relationship. ^1,2 Regrettably, the scientific foundation for this operation is devoid of laboratory data. Only recently has there been an attempt to formulate a physiologic rationale for this operation ² using a multiple-compartment elastance model to simulate the global effects of volume reduction on cardiac pump mechanics. The observed clinical benefits (improved ejection fraction, enhanced elastance) of ventricular mass reduction were based on sound theoretic argument. ² What remains is how to explain the apparent increase in ventricular performance that results from variable removal of the myocardium.

Many of the mechanisms of action attributed to volume reduction are rooted in long-standing belief that emphasizes wall stress as the offending cause and the target variable to be surgically manipulated. ^1,3 However, equating normalization in chamber size with reduction in wall stress may be expedient but not necessarily the principal mode by which this procedure restores myocardial function. ^1,3

On closer examination, the argued claim of reduction in active wall stress is unfounded on both theoretic grounds and clinical findings, as demonstrated by a near doubling in end-systolic elastance after the volume reduction procedure. It is hard if not impossible to reconcile the enhanced contractile function with significant attenuation of active wall stress. An equally compelling alternative argument for the observed improvement in contractile function and cardiac energetic efficiency can be formulated. This argument is centered about the concept of residual wall stress-strain state of the myocardium.

A fundamental property of the heart is its ability to engage all regions and transmural layers of myocytes in a collective and nearly uniform pattern of contraction. A common basic property of many solid and hollow organs is persistence of residual strain (and hence stress) when all external loads (cavity pressure) are removed. In elastic structures such as blood vessels and heart chambers, this property can be readily observed when a radial cut is made to equatorial cross-sectional rings, revealing the zero-stress configuration, ⁵ manifesting an opening in the muscle ring (Fig. 1). In general, the residual strain distribution ^4,5 in the heart is such that it exhibits a compressive circumferential stress in the inner layer of the ventricle and a principally tensile stress in the subepicardium (Fig. 2). As a point of reference, one would expect a greater increase in the residual stress, that is, greater opening angle, to accompany concentric hypertrophy. Conversely, a dilated, volume-overloaded heart would exhibit a decrease in its tendency to "spring open" (Fig. 1), leading to a state devoid of residual stress. A potential benefit of an elastically preloaded ventricular configuration is that it gives rise to a gradient in transmural sarcomere length at the onset of diastole that normalizes as the ventricle fills. ⁵ Naturally arising pre-strain may help redistribute the transmural gradient in LV wall stress such that myocytes located in a different region are "loaded" optimally, resulting in greater efficiency of contraction. ⁶

View larger version (24K): [in this window] [in a new window]   Fig 1. Cylindrical model (A) of the left ventricle at zero-stress state. The resulting opening angle, in response to a longitudinal cut, is indicative of the residual pre-strain and associated stored compressive/tensile stresses. Volume reduction surgery in effect mimics the stress-stress state by resecting a sliver (B) of muscle. Transformation of the "open" unstressed state to closed pre-stressed configuration is a natural by-product of the procedure.

View larger version (19K): [in this window] [in a new window]   Fig 2. Idealized plots of transmural (endocardium-epicardium) residual strain and stress. Arrows describe the increasing degree of deformation (pre-strain angle of opening) at zero-stress predicted for a cylindrical model of the heart (Fig 1). Note that the strain/stress are compressive (-) in the subendocardial layer and tensile in the subepicardial layer. (Adapated from Fung YC. Biomechanics-Circulation. New York: Springer-Verlag; 1980. p 80. Reproduced with permission.)

The volume reduction procedure has the potential to reestablish the strain-stress state of the LV chamber by surgically mimicking and reconstituting the zero-stress state. By staging and recreating what would be the equivalent of a zero-stress opening arc (Fig. 1) seen in healthy hearts, surgical remodeling can recreate, within limits, the residual strain/ stress state of the dilated resized heart. A natural by-product of resecting a variable sliver of the LV free wall (Fig. 1) is that when the LV chamber is reconstructed the resulting end-effect is reduced diameter, giving rise to a relatively thickened LV wall, necessitating compression of the subendocardial layers and stretching of the subepicardial layers. Importantly, transmural distribution of residual stress is expected to affect not only the passive and active ventricular properties but also a number of related attributes of cardiac function, such as preload-recruitable stroke work, myocardial energetics, and coronary flow dynamics. The restitution of residual strain-stress may prove to be applicable and contribute to the efficacy of cardiomyoplasty. In particular, recent preliminary data suggest that the benefits (reverse remodeling) observed may be related to passive constants (girdling) of the heart and not to systolic augmentation per se. Clearly the intended benefits of restoring the residual strain/stress are disease-specific and may not be amenable to surgically achieving the ideal in terms of the regional and global structure conformation that may be required. Depending on the prevailing LV geometry and chamber size, the reconstructed heart may not reach the desired degree of pre-strain. This may explain, in part, the variable results achieved clinically thus far. ³ It must be recognized that this proposed conceptual framework and theoretical approach remain unproven, requiring basic laboratory supporting data. Moreover, the analysis presented is confined to circumferential strain-stress consideration. A 3-dimensional mapping of the residual (end-systolic) regional strains would provide important additional information that may help "optimize" the planed surgical remodeling (resection size, shape) of the heart, beyond that of performing a "simple" excision.

J. Yasha Kresh, PhD, FACC
Andrew S. Wechsler, MD, FACS
Departments of Cardiothoracic Surgery and Medicine
Allegheny University of the Health Sciences
Philadelphia, PA 19102

12/8/93477

References

1. Batista RJV, Verde J, Nery P, Bocchino L, Takeshita N, Bhayana JN, et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634-8. [Abstract/Free Full Text]
   
2. Dickstein ML, Spotnitz HL, 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]
   
3. McCarthy PM, Starling RC, Wong J, Scalia GM, Buda T, Vargo RL, et al. Surgery for acquired heart disease: early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997;114:755-65. [Abstract/Free Full Text]
   
4. Omens JH, Fung YC. Residual strain in rat left ventricle. Circ Res 1990;63:37-45.
   
5. Fung YC. Biodynamics-circulation. New York. Springer; 1997. p. 73-81.
   
6. Kresh JY, Armour JA. The heart as a self-regulating system: integration of hemodynamic mechanisms. Technol Health Care 1997;5:159-69. [Medline]
   

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