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Ann Thorac Surg 1997;64:1525-1526
© 1997 The Society of Thoracic Surgeons


Correspondence

Vascular Delay and Cardiomyoplasty

John M. Alvarez, FRACS

Department of Cardiothoracic Surgery, Monash Medical Centre, 246 Clayton Rd, Clayton 3168, Melbourne, Victoria, Australia.

To the Editor:

I read with great interest the article by Carroll and associates [1] stressing the importance of a period of vascular delay before the performance of the cardiomyoplasty procedure. I would like to make the following comments.

This elegant article clearly demonstrates that the current way the cardiomyoplasty procedure is performed can cause extensive, albeit unpredictable damage to the distal two thirds of the latissimus dorsi muscle (LDM). In this experiment, in those LDMs that did not have a period of vascular delay, 4 of 9 LDM muscle wraps (44%) had ruptured due to frank muscle necrosis involving the distal two thirds of the LDM. Of the remaining 5 LDMs able to be measured, the reduction in perfusion and in circumferential and longitudinal force generation of the key middle and distal thirds of these muscles was markedly inferior to those that had a period of vascular delay.

This is altogether not surprising to any who have dissected this muscle. I would attest that most of the distal half of a substantial number of these muscles look very "blue and unhealthy" compared with the proximal "pink and healthy" half.

Carroll and associates state that "although the efficiency of vascular delay in improving muscle flap survival is not in doubt, the exact mechanism is still not fully understood." I may be able to shed some light as to why the muscles that have undergone a period of vascular delay perform so much better, at least at the experimental level.

My colleagues and I [2] have also performed, in the sheep, a similar experiment of "vascular delay." In 6 sheep we endoscopically divided all intercostal perforators supplying the LDM; after a period of 14 days, the LDM was then formally dissected and angiograms were obtained via the thoracodorsal artery.

At the same time the opposite (nonligated intercostal perforators) LDM was fully dissected and thoracodorsal artery angiograms were also obtained. Hence this LDM served as the control. Figure 1Go convincingly demonstrates that the period of vascular delay allows striking new vessel development to occur between the thoracodorsal pedicle vascular networks and the vascular networks of the intercostal perforators such that the TDA is now capable of fully providing a vascular supply to the entire muscle. Histologic examinations of the middle and distal half of those LDMs that had a period of "vascular delay" revealed no evidence of myocyte necrosis.



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Fig 1. . Angiogram of the latissimus dorsi muscle via the thoracodorsal artery (TDR). The muscle on the right has had the intercostal perforators (ICP) endoscopically ligated; after a 2-week delay extensive, new vascular collaterals (arrows) have developed between the territory from the TDR pedicle and the intercostal perforators (ICP) vascular territories. The muscle on the left (the contralateral control with no division of ICP or vascular delay) has no such collateral channels.

 
In addition, 4 sheep had a formal surgical dissection of the LDM such that its only vascular supply was via the thoracodorsal artery. These LDMs were left in situ, closely mimicking what is done clinically (barring it being transposed into the chest). Gross extensive necrosis of the distal half of the LDM occurred in all cases. The crux of these experiments is that those LDMs that have undergone a period of vascular delay are spared a significant ischemic injury that can cause extensive muscle necrosis. As Carroll and colleagues correctly point out, it is this distal two thirds of the muscle that is wrapping the heart and therefore ostensibly the most critical part of the LDM.

Hence, I wholeheartedly concur with Carroll and associates that if the cardiomyoplasty operation is to be properly assessed and not discarded prematurely it will need to be performed as a staged procedure that will ensure at least a wholly viable muscle available for cardiac assist. Whether this fully vascularized, wholly preserved LDM can actually produce effective myocardial assist remains, however, to be demonstrated.

References

  1. Carroll SM, Carroll CMA, Stremel RW, Heilman SJ, Tobin GR, Barker JH. Vascular delay of the latissimus dorsi muscle: an essential component of cardiomyoplasty. Ann Thorac Surg 1997;63:1034–40.[Abstract/Free Full Text]
  2. Alvarez JM, Carter M, McKie G. Endoscopic ligation of the intercostal arterial perforators to the latissimus dorsi muscle with a timed delay allows the thoracodorsal vascular pedicle to supply the entire muscle's vascular bed. Asia Pacific Heart J (in press).

 

Reply

Richard W. Stremel, PhD, John H. Barker, MD, PhD

Department of Physiology & Biophysics and Division of Plastic and Reconstructive Surgery, Department of Surgery, University of Louisville, Health Science Center A-1115, Louisville, Ky 40292.

To the Editor:

We appreciate the kind words and comments from Mr Alvarez and appreciate knowing that the very old technique of vascular delay [1] is still the subject of investigation around the world. Our group has studied and used vascular delay of skin and muscle flaps for several years. The technique used in this study was bipedicle vascular delay of the latissimus dorsi muscle (LDM), developed by Dr Gordon Tobin and colleagues [2, 3].

We must correct an over-interpretation, dealing with the magnitude of muscle necrosis, presented in Mr Alvarez's letter. In our most recent study [4], the frank necrosis of the nondelayed LDM was limited to the distal region. The middle region was often fibrosed and less muscular, but was present and not necrosed. We would estimate that the distal third of the LDM is at risk when acutely lifted for cardiomyoplasty (CMP). However, the point we and Mr Alvarez make is that this region of necrosis is clearly reduced by vascular delay. The potential benefit of a whole, vital, well-perfused muscle to assist the myocardium in CMP is obvious.

We have investigated the mechanism of "vascular delay" for several years and agree with the Melbourne group that vascular delay leads to a reorganization of the architecture of the vascular channels within the LDM [2, 5]. We have also investigated the mechanism of this reorganization of the vascular channels. We and others have shown that muscle stimulation and training enhances vascularity. We have also studied the role of basic fibroblast growth factor in the vascular changes associated with delay. Administration of basic fibroblast growth factor to a sublethally ischemic LDM significantly increases the perfusion and contractile characteristics of the muscle compared with its appropriate control [6].

Mr Alvarez ends his letter with the appropriate conclusion (we believe) that vascular delay should become an essential component of the CMP, but leaves the question of whether using this "...fully vascularized, wholly preserved LDM..." in CMP will actually improve myocardial assist. Our colleagues in cardiothoracic surgery at the University of Louisville have performed these very experiments [7]. The results, in dogs, are compelling! Figure 1Go shows an example response for aortic flow in 1 dog 2 weeks after a CMP operation that was preceded by a 2-week vascular delay period. In this study, the left ventricle was depressed by injecting large microspheres into the left main coronary artery. The hemodynamic changes induced by stimulation of the vascularly delayed LDM are highly significant compared with the nonassisted hemodynamics and to the hemodynamic changes effected by simple CMP without vascular delay. These very recent data strongly support the notion that vascular delay is an essential component of CMP, if myocardial assist and hemodynamic improvement are the goals of CMP.



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Fig 1. . Example of aortic blood flow measurements in an animal with cardiomyoplasty and vascular delay. Latissimus dorsi muscle stimulation (s) in synchrony with left ventricular contraction (every seventh beat in this example) significantly increases aortic flow [7].

 

References

  1. Tagliacozzi G. De curtoroum chirurgia per insitionem. Venezia: Gaspare Bindonum, Jr, 1597.
  2. Keelen PC, Barker JH, Frank JM, Anderson GL, Tobin GR. The effects of delay on necrosis in latissimus dorsi pedicle flaps in hairless mice. Eur Surg Res 1993;25:192.
  3. Carroll SM, Heilman SJ, Stremel RW, Tobin GR, Barker JH. Vascular delay improves latissimus dorsi muscle perfusion and muscle function for use in cardiomyoplasty. Plast Reconstr Surg 1997;99:1329–37.[Medline]
  4. Carroll SM, Carroll CMA, Stremel RW, Heilman SJ, Tobin GR, Barker JH. Vascular delay of the latissimus dorsi muscle: an essential component of cardiomyoplasty. Ann Thorac Surg 1997;63:1034–40.
  5. Barker JH, van Aalst VC, Keelen PC, et al. Vascular delay in skeletal muscle: a model for microcirculatory studies. Plast Reconstr Surg (in press).[Medline]
  6. Carroll CMA, Carroll SM, Overgoor MLE, et al. Augmentation of skeletal muscle flap perfusion and function by vascular delay and the exogenous administration of basic fibroblast growth factor (bFGF). Plast Reconstr Surg (in press).[Medline]
  7. Ali AT, Chiang BY, Slater AD, Dowling RD, Santamore WP. Is vascular delay superior to chronic stimulation of the latissimus dorsi muscle in dynamic cardiomyoplasty? Int J Cardiovascu Med Sci 1997;1:30.




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