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Ann Thorac Surg 1996;62:321-322
© 1996 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery Regional Cardiothoracic Unit Wythenshawe Hospital Southmoor Rd Manchester M23 9LT United Kingdom
To the Editor:
We read with great interest the article by Chen and associates [1] that described a technique of measuring transmural myocardial pressure using a fluid-filled balloon. However, we have great reservations in accepting their claim that a significant reduction in systolic average transmural myocardial pressure occurred due to the essential flaw in using untransformed fast muscle in their experiments. Despite a wealth of ongoing experimental data collected from both human and animal models since the debut of dynamic cardiomyoplasty, its mechanism(s) of action still remains far from clear [2, 3]. In this respect, the evidence presented so far on the hemodynamic effects of this procedure has been conflicting [4]. This has led various groups to propose different theories of mechanisms to account for the discrepancy between the subjective improvement in functional status and quality of life and the lack of consistent demonstrable hemodynamic benefit. Systolic "squeeze" assist, passive girdling effect, reversal of chronic chamber remodeling, and a reduction in systolic and diastolic wall stress were among such proposed mechanisms.
Chen and associates demonstrated a significant reduction in systolic average transmural myocardial pressure using a fluid-filled balloon in an acute goat model of dynamic cardiomyoplasty. Techniques designed to measure intramuscular pressure in contracting muscle posed great practical challenges. Measurement of pressure within a fluid-filled balloon interposed between the myocardium and the latissimus dorsi flap eliminated this problem while permitting the direct calculation of transmural myocardial pressure. However, interpretation of their results is severely hampered by the use of untransformed latissimus dorsi muscle in a normal heart. It is a well-known fact that during fiber-type transformation, muscle loses not only its mass and power but also the speed of contraction [5]. A reduction in systolic transmural myocardial pressure and wall stress cannot be maintained if the contraction of the transformed muscle wrap is slower than that of the myocardium. This differs from the phenomenon of reduction in diastolic wall stress, which depends on an artificial ventricular hypertrophy created by the presence of the muscle wrap regardless of its contractile properties. We strongly believe therefore that the use of untransformed muscle in the setting of dynamic cardiomyoplasty research is unhelpful or even misleading. In particular, there is no place for the incorporation of untransformed muscle in an experimental design after a decade of clinical cardiomyoplasty employing only trained muscle. Further progress toward the understanding of its mechanism(s) of action can only be achieved with research that employs transformed latissimus dorsi muscle.
References
Division of Applied Sciences Harvard University Cambridge, MA 02138 and Division of Cardiac Surgery Brigham Women's Hospital Harvard Medical School 75 Francis St Boston, MA 02115
To the Editor:
We appreciate the comments of Drs Tang and Hooper and thank them. In summary, they question the interpretation of our results because untransformed latissimus dorsi muscle (LD) was applied to normal myocardium in an acute goat model of cardiomyoplasty. They believe strongly that the use of untransformed muscle in dynamic cardiomyoplasty (DCM) research is misleading and should not be used. We address their concerns.
We are unclear regarding the statement that "a reduction in systolic transmural myocardial pressure and wall stress cannot be maintained if the contraction of the transformed muscle wrap is slower than that of the myocardium." If Tang and Hooper mean "contraction" to be velocity of shortening when the heart is wrapped with LD, we disagree. The velocity of LD shortening is always slower than that of the myocardium when the net systolic transmural myocardial pressure is reduced. In such a situation, the muscle wrap is intimately applied to the epicardium, and the rate of volume change inside the wrap is equivalent to the rate of volume change inside the heart. Assuming both the wrap and the myocardium to be spherical for simplicity, we may apply the formula for volume of a sphere:
 | (1) |
where V = volume of the sphere and r = radius of the sphere. The circumference of the sphere is given by
 | (2) |
where C = the circumference. Substituting (2) into (1) and differentiating with respect to time yields the rate of change of volume inside the sphere in terms of the circumference's rate of change,
 | (3) |
where subscripts w and h refer to the muscle wrap and heart respectively; 
is the rate of volume change; and 
, as the rate of change of the sphere's circumference, is the shortening velocity of the sphere's surface. Thus, the rate of volume change inside a contracting sphere is function of not only the velocity of its contracting surface but also its circumference. By equation (3)
, the greater the circumference, the greater the volume change, even if shortening velocity is held constant. Because
 | (4) |
then by substitution equation 3 yields
 | (5) |
In addition, because
 | (6) |
then, by equation (5),
 | (7) |
Thus, in DCM, the shortening velocity of the LD muscle wrap must be less than that of the heart, because the circumference of the wrap is greater than that of the heart.
If Tang and Hooper are referring to the time for wrap excitation-contraction, the time between neural stimulation and crossbridge activity, we agree that this is a factor; however, it is not the only one. A reduction in transmural myocardial pressure (Pt) will occur if the LD applies a net pressure against the epicardium. In other words, the LD must be loaded. Whether this occurs is a complex function of the excitation-contraction times of the wrap and the cardiomyopathic heart, the wrap's initial tension, the rate of volume change inside the wrap, and the fundamental force-velocity properties of both the wrap and the cardiomyopathic heart. Which factor is the most important is unclear at this time.
Using untransformed muscle, our results suggest that DCM benefits the myocardium, in part at least, by reducing transmural myocardial pressure. There is an ongoing controversy regarding the primary mechanism of DCM, and some reports have shown no systolic augmentation. At the same time, there have also been many case reports and studies detailing augmented stroke volume and aortic pressure when directly comparing on beats with off beats in cardiomyoplasty using transformed LD muscle [1–3]. That can only happen if systolic "squeeze" assist occurred, and therefore reduced transmural myocardial pressure. Furthermore, although we know transformed muscle is slower than untransformed muscle, we also know empirically that it is not so slow that zero tension is developed within the time period of a typical cardiac cycle. This means that, properly wrapped, the transformed LD will exert a pressure on the epicardium and reduce the average Pt over the cardiac cycle.
We strongly believe that if its experimental limitations are understood and appreciated, untransformed muscle does have a role in DCM research. The point of research is not only to understand the clinical status quo but also to show future directions of the field. Given that new training methods preserving muscle strength and mass are currently being developed [4], the performance of untransformed muscle represents the goal of transformed muscle. Because we used a balloon, our model was not, strictly speaking, cardiomyoplasty. This does not mean, however, that our results do not have anything to offer on this subject. The point of our study was to introduce a method of calculating Pt, show that, despite hemodynamics that remained statistically the same, a considerable reduction in Pt occurred, and postulate that such results suggest a mechanism for DCM. Of course, to truly represent clinical cardiomyoplasty, the best animal model would use transformed muscle applied to a dilated cardiomyopathic heart (whose myocardium would contract markedly differently than healthy myocardium); however, if one were to say all models other than this were misleading, then essentially all past experimental work in the field would be invalid.
References
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