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Ann Thorac Surg 1996;62:1245-1247
© 1996 The Society of Thoracic Surgeons

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Correspondence

Suggestions for Overcoming the Weak Points of Cardiomyoplasty

Sinai Samaritan Medical Center, PO Box 342, Milwaukee, WI 53201-0342

To the Editor:

We wish to share some suggestions that could help overcome the weak points of cardiomyoplasty that have compromised the early and long-term results of this operation to date—shortcomings nicely summarized by Magovern and Simpson in their article entitled "Clinical Cardiomyoplasty: Review of the Ten-Year United States Experience" [1]. As a preface, we respectfully offer the reminder that the first cardiomyoplasty in the United States was performed at Allegheny General Hospital [2] and that this hospital now has the largest series of dynamic cardiomyoplasties in this country. Thus, with little more than an adumbration of the complexities of dynamic cardiomyoplasty, Magovern and Simpson have directed attention to the four problems that are the very keystones to the eventual use of dynamic cardiomyoplasty to extend and improve the lives of those afflicted with a failing heart:

1. Magovern and Simpson point out that "the 40% operative mortality clearly demonstrated that the procedure was inappropriate for patients lacking the reserve to survive a major cardiac operation and the 8-week period necessary for LDM [latissimus dorsi muscle] training."
   
2. In addition, "some patients who survived longer than 1 year exhibited deterioration in cardiac function or reversal of early hemodynamic gains to baseline levels. It is possible that the LDM cannot sustain forceful contraction at a stimulus ratio of 1:2 with the LDM training and maintenance protocol now mandated for Food and Drug Administration–sanctioned studies."
   
3. Regarding muscle ischemia after mobilization, "isolation of the LDM on its neurovascular bundle creates an immediate ischemic insult to this area, which may be exacerbated by muscle edema. The muscle can produce new vascular patterns if allowed to adapt more slowly to its new role in a two-stage cardiomyoplasty procedure based on the concept of `vascular delay'."
   
4. As for a weak LDM in some cardiomyoplasty patients, "the advantages of reclaiming up to 30% of LDM function are a strong argument for instituting this procedure in our patients. It may be possible to enhance LDM strength by pharmacologic manipulation."
   

We are grateful to Magovern and Simpson for bringing into sharp focus the following four essential areas that we have been investigating since 1989:

1. How can we help patients during the first 8 weeks after cardiomyoplasty?
   
2. How can we change the stimulation protocol to allow the muscle to rest more than it works?
   
3. How can we prevent ischemia-reperfusion damage after muscle mobilization and accelerate angiogenesis?
   
4. How can we enhance the LDM contractile force of a chronically debilitated failing heart?
   

In our former work in Russia and, since 1993, with a research team also devoted to developing an artificial heart in Milwaukee, our investigations have enabled us to crystallize this four-pronged search for answers into a unified physiologic-pharmacologic approach to therapeutic angiogenesis after cardiomyoplasty. With thanks to Drs Magovern and Simpson for presenting this opportunity, we would like to briefly review our work and to suggest the following to fellow investigators.

1. To help patients during the first 8 weeks after cardiomyoplasty, we have been investigating in Milwaukee the use of the wrapped LDM for several minutes of cardiac assist several times every day immediately after the cardiomyoplasty operation. The LDM is mobilized in adult sheep and the electrical stimulation protocol is started immediately after the operation, using single impulses at a rate of only 15 beats per minute. Along with muscle training, we use a strong burst of impulses (5 V, 30 Hz, 6 impulses per burst) for a short period of time (20 to 40 minutes) every day to contract the LDM in a manner that mimics cardiac assist. To avoid muscle damage, we use a "work-rest regimen" whereby the muscle is contracted for 1 minute followed by 1 minute of rest in an alternating pattern. At 6, 11, and 16 days, we perform a fatigue test for 42 minutes using 15 beats/min in a work-rest regimen (5 V, 30 Hz, 20 g/kg preload, 6 impulses per burst) and study the contractile force of the LDM.
   We have found no fatigue during these tests and no muscle damage after testing upon histologic examination, because the muscle is allowed to rest longer than it works. We therefore propose the use of this variation of skeletal muscle training (at only 15 beats/min) together with cardiac assist in a work-rest regimen, which can be started if necessary as soon as 1 day after cardiomyoplasty. Of course, cardiac assist may be limited to hour on the first day, but our data show that it may be increased to 60 minutes by day 16, and repeated two to three times each day [3].
   
2. Because the LDM works nonstop in the cardiac assist regimen (or every other cardiac contraction), two related problems arise: the LDM must be allowed to rest, and the cardiac muscle must be allowed to work on its own. The longer the traumatized skeletal muscle works without rest, the weaker it becomes. The longer the cardiac muscle relies on the LDM for assistance, the weaker it becomes. In Moscow, to modify the electrical stimulation protocol so that the skeletal muscle rested more than it worked, we investigated the reduction of LDM stimulation as follows: Ten patients were studied 2 to 4 years after cardiomyoplasty using different stimulation regimens. A Russian-built stimulator (EKS 445) was used that allowed us to change the cardiosynchronization ratio from 1:1 to 1:8. Measurement of cardiac index, stroke volume index, and cardiac output showed that the best results were obtained with the 1:4 ratio, and we followed this stimulation regimen in many of our Russian patients. Therefore, to avoid LDM fatigue, we propose the use of a carefully stepped electrical stimulation protocol for all patients after cardiomyoplasty [4].
   
3. To prevent ischemia-reperfusion damage to the vascular network after muscle mobilization and to accelerate angiogenesis, we have hypothesized that we could protect the native vascular network and thereby minimize local ischemia-reperfusion lesions in ischemic LDM by use of autologous biological glue as a drug delivery depot. In our investigation model in Milwaukee, the following three glue compositions were used: pure glue, glue containing aprotinin (a proteinase inhibitor), and glue containing pyrrolostatin (a lipid peroxidation inhibitor).
   The anterior border of the LDM of adult sheep was completely isolated and the LDM divided into two parts: one with an undisturbed blood supply and the other in an ischemic state. These layers were separated by adipose tissue; ie, a flap of subcutaneous adipose tissue was dissected free, leaving the proximal part connected to the remaining adipose tissue. All three layers were sutured together to form four discrete pockets. One pocket was left free of glue as a control, the second contained pure biological glue, the third contained biological glue with aprotinin, and the fourth contained biological glue with pyrrolostatin.
   After 1 month, we studied the progress of angiogenesis in the four pockets. In the control pocket (no glue), we found a few vessels between the muscle fibers and partially degenerated areas in the ischemic muscle. In the pocket with biological glue alone, we found numerous small capillary structures. In the pockets containing aprotinin or pyrrolostatin, we found extensive neovascularization represented by an increased number of capillaries and the presence of larger vascular structures. We concluded that application of biological glue promoted good hemostasis and created a firmly attached, but flexible, interface (very important for mobile tissue like myocardium). These results led us to suggest that pharmaceuticals can considerably reduce ischemia-reperfusion damage in LDM after mobilization and increase late angiogenesis, thus preparing the LDM for more efficient contractile work. We are conducting further studies to determine if enhanced angiogenesis through the creation of this fibrin interface will improve the results of cardiomyoplasty [5].
   
4. Also in Milwaukee, to enhance LDM contractile force, we used an anabolic steroid in an experimental animal model to produce a thicker and stronger muscle than could be produced by using electrical stimulation alone. By means of an implanted osmotic pump, we continuously administered an anabolic steroid locally into adult sheep LDM for 8 weeks while it was simultaneously electrically stimulated. After 8 weeks the LDM had lost no contractile force, but had became stronger than at the start of the combined protocol—30% to 40% stronger than with electrical stimulation alone [6].
   On the basis of the findings of these investigations, we propose the following approaches to cardiomyoplasty to help to overcome its weak points: (1) the use of pharmaceuticals added to biological glue applied to mobilized LDM to prevent ischemia-reperfusion damage, (2) the use of biological glue with added autologous endothelial cells to serve as an interface between the LDM and myocardium to accelerate and enhance angiogenesis, (3) the use of an anabolic steroid locally in the LDM (when this muscle is very weak) to increase its contractile force, and (4) the use of a modified electrical stimulation protocol begun immediately after cardiomyoplasty, which includes a work-rest regimen of stimulation to allow for immediate partial cardiac assist if needed.
   

References

1. Magovern GJ Sr, Simpson KA. Clinical cardiomyoplasty: review of the ten-year United States experience. Ann Thorac Surg 1996;61:413–9.[Abstract/Free Full Text]
2. Magovern GJ, Heckler FR, Park SB, et al. Paced skeletal muscle for dynamic cardiomyoplasty. Ann Thorac Surg 1988;45:614–9.[Abstract]
3. Chekanov VS, Tchekanov GV, Rieder MA, et al. Is it possible to perform immediate cardiac assist using untrained latissimus dorsi muscle in a work-rest regimen? ASAIO J 1995;41:M489–94.[Medline]
4. Chekanov VS, Krakovsky AA, Buslenko NS, et al. Cardiomyoplasty: review of early and late results. Vasc Surg 1994;28:481–8.
5. Chekanov VS, Nikolaychik VV, Tchekanov GV, Rieder MA. Cardiomyoplasty: overcoming weak points. ASAIO J 1996; 42:42.
6. Chekanov VS, Tchekanov GV, Rieder MA, et al. Force enhancement of skeletal muscle used for dynamic cardiomyoplasty and as skeletal muscle ventricle. ASAIO J 1995;41:M499–507.[Medline]

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