A lthough the concept of substituting cardiac muscle with skeletal muscle goes back several decades, significant advance could not have been made without first resolving two major biological constraints associated with this approach. Both the myocardium and the skeletal muscle are composed of striated contractile muscle fibers. However, they have considerable structural and functional differences (Table 1). In terms of harvesting the power produced by the skeletal muscle to assist the heart, these differences created two practical problems. The first is the fatigability of the skeletal muscle when stimulated to contract at a frequency equivalent to that of the heart. Most skeletal muscles are composed of a mixture of type I, slowand fatigue-resistant fibers with type II, fast-twitch and fatigueprone fibers. The latter are highly anaerobic and the biochemical apparatus is geared for rapid, strong contractions rather than for sustained repetitive contractions. Another problem is related to the difference in the contractile pattern in response to a single-pulse electrical stimulation. The myocardium, which is a syncytial tissue, contracts in an all-or-none fashion; once the electrical current strength reaches a threshold level, the whole myocardmm contracts with full force and in a sustained manner. In contrast, the skeletal muscle, even following transformation described below, is composed of many individual motor units, and a single electrical impulse often depolarizes only a number of such motor units with limited contractile force and duration. In retrospect, the solution to the problem of skeletal muscle fatigability can be traced back to the work ofBuller et al’ in 1960 when they examined the interaction between motor neurons and muscles in relation to the characteristic speeds of their responses. Cross-innervation experiments established the fact that the composition of fiber types in a fully developed muscle can be altered, introducing the concept of the “plasticity of muscles.” Subsequent studies by Salmons,* Pette,3 and others ushered in the technique of transforming the skeletal muscle into a highly fatigue-resistant, purely type I fiber muscle by means of low frequency electrical stimulations. These experiments, carried out in muscle biology laboratories in the late 1960s and early 1970s were applied by Macoviak et al’ to the arena of cardiomyoplasty in the late 1970s. Since then, extensive molecular and functional studies have been performed to elucidate and characterize the phenomenon of skeletal muscle transformation.5 In the meantime a few investigators attempted to generate greater power from skeletal muscle in response to electrical stimulation. Notable among these efforts was that of Spotnitzh in the mid 1970s who clearly showed that sufficient power can be generated from a skeletal muscle when burst stimuli were applied instead of a single-pulse electric current. However, it was also recognized that a strong tetanic contraction, although extremely powerful, induces rapid fatigue and loss of power within a short period of time. In the late 1970s we advanced the idea that a well-defined pulse train, synchronized with, and falling within a specific segment of cardiac cycle, may both augment the power output and at the same time prevent the rapid onset of fatigue in a skeletal muscle. In 1980 Drinkwater’ reported on the first synchronizable burst stimulator, and this, in combination with the capability to transform skeletal muscle to confer fatigue-resistance, removed the two biological constraints to use of the skeletal muscle for the purpose of assisting a failing heart and thus making this approach possible and practical. Both the direct and indirect functional substitution approaches, namely dynamic cardiomyoplasty and biomechanical cardiac assist, have made considerable progress in recent years, with the former reaching the early clinical trial stage. These advances and the current state of the art are well-represented in the preceding articles in this issue. To our knowledge, by June 1990 more than 100 patients worldwide have undergone dynamic cardiomyoplasty. In the earlier patients, terminally ill cases were operated on, and this was reflected in the high operative mortality rate. There is an emerging consensus that a previous muscle transformation period is not essential, and gradual “working transformation” of the muscle after it has been wrapped around the heart is feasible. Transforming stimulation is usually started 1 to 2 weeks postoperatively to allow for the recovery of blood flow to the muscle flap, and to allow for adhesion between the muscle graft and the epicardium as well as to the surrounding tissue, so that lateral displacement of the heart would not produce a detrimental effect when the muscle is stimulated to contract forcefully.
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Aug 1, 1996
S R Jones + 3
Open Access