Ann Thorac Surg 1997;64:670-677
© 1997 The Society of Thoracic Surgeons
Original Article: Cardiovascular
Right Latissimus Dorsi Cardiomyoplasty Improves Left Ventricular Energetics
Lishan Aklog, MD,
Frederick Y. Chen, MD, PhD,
BrianJ. deGuzman, MD,
MichaelP. Murphy, MD,
WendelJ. Smith, MD,
RitaG. Laurence, BS,
RobertF. Appleyard, PhD,
Lawrence H. Cohn, MD
Division of Cardiac Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
Accepted for publication March 7, 1997.
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Abstract
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Background. The mechanism by which cardiomyoplasty appears to enhance left ventricular (LV) function is not well understood. We applied the time-varying elastance model to study the effect of cardiomyoplasty on LV function, ventriculovascular coupling, and LV energetics in an acute canine model.
Methods. Right latissimus dorsi cardiomyoplasty was performed in 5 dogs. The end-systolic pressure-volume relation was generated by using brief caval occlusions. End-systolic elastance, effective arterial elastance, stroke work, internal work, total mechanical work, and stroke work efficiency (stroke work/total mechanical work) were calculated from these pressure-volume data. Myocardial oxygen consumption and overall mechanical efficiency (stroke work/myocardial oxygen consumption) were predicted using the myocardial oxygen consumption-total mechanical work relation.
Results. Skeletal muscle contraction significantly increased end-systolic elastance, an index of contractility. Although stroke work did not change significantly, the increase in end-systolic elastance led to a 29% decrease in total mechanical work, a 50% decrease in internal work, and an increase in stroke work efficiency from 53% to 66%. This was consistent with the observed 29% decrease in effective arterial elastance/end-systolic elastance, an indicator of ventriculovascular coupling that is related inversely to stroke work efficiency. Predicted myocardial oxygen consumption decreased by at least 22%, and predicted overall mechanical efficiency increased at a minimum from 16.1% to 18.4%.
Conclusions. These results support the theory that cardiomyoplasty unloads the LV by decreasing LV volumes and increasing contractility. These effects appear to improve LV energetics by decreasing total mechanical work without significantly affecting stroke work, resulting in improved stroke work efficiency. The decrease in total mechanical work strongly suggests a decrease in myocardial oxygen consumption and an increase in overall mechanical efficiency.
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Introduction
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Despite more than a decade of clinical and laboratory investigation, dynamic cardiomyoplasty remains a promising but poorly understood surgical modality in the treatment of chronic heart failure. Proponents point to multiple retrospective reports that consistently document significant improvements in functional status [1–3]. Of these, many also document modest improvements in ejection fraction and a few report an improvement in actuarial survival. Critics, however, point to the lack of prospective randomized data and the difficulty in establishing definitive objective evidence of enhanced ventricular function, clinically or in the laboratory.
Early experimental work used traditional, relatively load-dependent indices of left ventricular (LV) function. These studies generally showed modest, inconsistent changes in these parameters [4–6]. However, recent studies by our laboratory and others have used load-insensitive indices of contractility, such as peak systolic elastance, to demonstrate clearly an improvement in LV function and a decrease in LV volumes with skeletal muscle contraction [7–10].
These findings are consistent with the concept, proposed by Chiu [11] and others [12], that cardiomyoplasty acts, in part, by unloading the LV. This presumably leads to decreased wall stress, decreased oxygen consumption, and improved energetic efficiency. Although one study has suggested a decrease in peak ventricular wall stress [5], the direct effect of cardiomyoplasty on ventricular energetics has not been established.
In this study, we used the time-varying elastance model and the relation between myocardial oxygen consumption (MVO2) and total mechanical work (PVA), developed by Suga and colleagues [13], to assess the effects of skeletal muscle contraction on ventricular energetics and ventriculovascular coupling in an acute canine model.
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Material and Methods
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Five adult male mongrel dogs (25 to 30 kg) were used in this study and were cared for according to the standards set forth in the National Institutes of Health's "Guide for the Care and Use of Laboratory Animals" (NIH publication 85-23, revised 1985).
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Surgical Preparation and Instrumentation
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General anesthesia was induced using thiopental and was maintained with halothane and nitrous oxide. Right latissimus dorsi cardiomyoplasty was performed through a median sternotomy as previously described [8], using a cuffed electrode around the thoracodorsal nerve, a Medtronic (Minneapolis, MN) SP 2083 sensing lead on the right ventricle, and a Medtronic SP1005 Cardiomyostimulator.
Instrumentation included Millar catheter pressure transducers (Millar Instruments, Houston, TX) in the left ventricle and aortic root, an electromagnetic flow probe (Carolina Medical Electronics, King, NC) around the aortic root, and an 8F volume conductance catheter (Webster Laboratories, Baldwin Park, CA) in the LV connected to a Leycom Sigma 510F Conductance Catheter System (Cardiodynamics, Rijnsberg, the Netherlands). All signals were sent to a Simultrace Physiologic Monitoring System (PPG Biomedical Systems, Pleasantville, NY), displayed for real-time analysis, and transferred to a minicomputer, where they were digitized at 200 Hz and stored for future analysis. The stimulator parameters were programmed as follows: amplitude, two times palpation threshold (3 to 5 V); burst frequency, 30 Hz; pulse width, 210 microseconds; pulse train duration, 185 milliseconds; synchronization delay, 50 milliseconds; and synchronization ratio, 1:1.
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Data Collection
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Pressure–volume data were collected with the stimulator on and off, as previously described [8]. Each data run consisted of at least two volume calibration episodes and two caval occlusion episodes. The volume calibration episodes were performed by injecting hypertonic saline into the pulmonary artery. The caval occlusion episodes were performed to generate the end-systolic pressure-volume relations (ESPVRs). Muscle fatigue was avoided by limiting stimulation to periods of 20 seconds or less, separated by at least 5 minutes of rest.
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Data Analysis
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Data analysis was performed using the computational program MATLAB (The Mathworks, Natick, MA).
MARKING BEATS.
End-diastole and begin-ejection were identified for each beat by the inflection point of the LV pressure and aortic flow tracings, respectively. End-ejection was identified by the point where aortic flow fell to zero. These points were confirmed by the inflection point and dicrotic notch of the aortic pressure tracing.
VOLUME CALIBRATION.
Conductance catheter calibration parameters were calculated separately for each data run. The volume gain (1/
) was calculated from steady-state hemodynamic data using the aortic flow signal as a standard. The volume offset (Vc) was calculated using the data from the hypertonic saline injections.
STEADY-STATE DATA.
Steady-state hemodynamic parameters were calculated after averaging the first five steady-state beats of each episode. Mean aortic pressure, cardiac output, systemic vascular resistance, end-diastolic volume (Ved), end-systolic volume (Ves), stroke volume (SV), end-diastolic pressure (Ped), stroke work (SW), and ejection fraction were among the parameters calculated from these data.
END-SYSTOLIC PRESSURE-VOLUME RELATION.
The ESPVR was calculated from the pressure-volume loops recorded during transient bicaval occlusion using an iterative algorithm as previously described [8]:
 | (1) |
The slope of this relation, Ees, is the end-systolic elastance, a load-independent index of contractility, Pes is the end-systolic pressure, Ves is the end-systolic volume, and V0 is the volume-axis intercept of this relationship.
ARTERIAL ELASTANCE.
The effective arterial elastance (Ea) was defined as the slope of the line connecting the end-systolic and end-diastolic points of a given pressure-volume loop. This can be expressed as the ratio of Pes and SV:
 | (2) |
The ratio Ea/Ees is an index of ventriculovascular coupling.
ENERGETICS.
The PVA, SW, and internal work (IW) performed by the LV were calculated from a steady-state beat according the techniques described by Suga and associates [13]. The PVA is the area between the ESPVR, the end-diastolic pressure-volume relation (EDPVR), and the systolic portion of the pressure-volume loop, and it represents the total mechanical work performed by the ventricle. The SW is the area within the pressure-volume loop and the IW is the portion of the PVA that lies outside the pressure-volume loop:
 | (3) |
This relation is illustrated in Figure 1
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Fig 1. . Schematic diagrams showing the components of the time-varying elastance model and the myocardial oxygen consumption (MVO2)–total mechanical work (PVA) relation. (Ea = effective arterial elastance; EDPVR = end-diastolic pressure-volume relation; Ees = end-systolic elastance; ESPVR = end-systolic pressure-volume relation; IW = internal work; SW = stroke work.
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Stroke work efficiency (EffSW) is defined as follows:
 | (4) |
and represents the portion of the total mechanical work performed by the LV that goes toward generating SW. This also has been referred to as the external work or energy transfer efficiency.
Suga and associates [13] demonstrated a linear relation between PVA and MVO2 that remains relatively constant under a wide range of hemodynamic conditions. The MVO2-intercept of this relation is the unloaded MVO2, and the reciprocal of its slope is the contractile efficiency. A typical MVO2-PVA relation in a normal dog has an unloaded MVO2 of about 0.4 J/beat* and a contractile efficiency of about 40% [13]. Assuming that this relation is not altered, PVA data can be used to predict the effect of skeletal muscle contraction on MVO2:
 | (5) |
Overall mechanical efficiency (Effmech) was defined as follows:
 | (6) |
and represents the overall efficiency of transforming chemical energy (O2) into useful mechanical work (SW). Overall mechanical efficiency was estimated using the predicted MVO2.
STATISTICS.
The mean and SEM were calculated for each variable over all good episodes for a given data run. Results were compared with the stimulator off and on. Statistical significance was calculated using a paired t-test.
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Results
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Hemodynamic Parameters
The effect of skeletal muscle contraction on LV contractility (Ees), Ves, and Ved has been reported previously [8] and is shown in Figure 2A (Ees) and Table 1. End-systolic elastance increased by 78% (p = 0.004). End-systolic volume and Ved decreased by 30% and 19%, respectively (p = 0.008 and 0.012, respectively). The effect of skeletal muscle contraction on other hemodynamic parameters, including heart rate, mean arterial pressure, cardiac output, systemic vascular resistance, SV, Pes, and Ped is shown in Table 1. None of these variables changed consistently or significantly.
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Fig 2. . Effect of skeletal muscle contraction on ventriculovascular coupling (A through C) and energetic parameters (D through G). Thin lines and open circles show data points for individual animals; thick lines and solid squares show the change in mean value. Error bars show the standard error of the mean for each variable. (Ea = effective arterial elastance; Ea/Ees = ventriculovascular coupling; Ees = end-systolic elastance; EffSW = stroke work efficiency; IW = internal work; PVA = total mechanical work; SW = stroke work.)
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Ventriculovascular Coupling
The effect of skeletal muscle contraction on Ea and ventriculovascular coupling (Ea/Ees) is shown in Figures 2B and 2C
, and are summarized in Figure 3A and Table 1. Although Ea increased by 21%, this result was not statistically significant. The much larger increase in Ees, however, led to a 29% decrease in Ea/Ees (p = 0.012), indicating improved ventriculovascular coupling.
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Fig 3. . Effect of skeletal muscle contraction on ventriculovascular coupling (A) and left ventricular energetics (B). All data points are shown as a percentage of the off state except EffSW and Effmech, for which the actual efficiencies are shown. ( Ea = effective arterial elastance; Ees = end-systolic elastance; Effmech = overall mechanical efficiency; EffSW = stroke work efficiency; IW = internal work; MVO2 = predicted myocardial oxygen consumption; PVA = total mechanical work; SW = stroke work.)
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Ventricular Energetics
The effects of skeletal muscle contraction on SW, IW, PVA, and EffSW are shown in Figures 2D through 2G, and are summarized in Figure 3B and Table 1. Although SW fell slightly by 12%, presumably secondary to decreased Ved, this result was not statistically significant. However, PVA and IW fell significantly by 29% (p = 0.011) and 50% (p = 0.004), respectively. This led to a significant improvement in EffSW, from 52.6% to 66.4% (p = 0.001).
The reported inverse relation between Ea/Ees and EffSW was investigated and is shown in Figure 4. Pooled data from all animals were fitted to a linear regression between 1/EffSW and Ea/Ees:
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Fig 4. . Inverse relation between ventriculovascular coupling (Ea/Ees) and stroke work efficiency (EffSW) data points from this study. Each pair of points represents the results from a single animal with the stimulator off (open circles) and on (solid circles). The points were fitted to an inverse linear regression, which is represented in the upper, heavy curve. The lower, lighter curve shows the relation predicted by the Burkhoff-Sagawa model.
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 | (7) |
The regression results were m = 0.35, b = 1.05 and r2 = 0.785. Rearranging equation 7 with these values results in the following:
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Myocardial oxygen consumption and Effmech were predicted using a typical MVO2-PVA relation from the data of Suga and colleagues [13] (contractile efficiency = 40%, unloaded MVO2 = 0.4 J). Using equations 5 and 6, skeletal muscle contraction is predicted to decrease MVO2 by at least 22% and to increase Effmech at a minimum from 16.1% to 18.4%. These results are shown in Figure 3B and Table 1.
Comment
Although a large body of clinical and laboratory data has been published on cardiomyoplasty over the past decade, this procedure remains an enigma. Despite multiple retrospective studies documenting significant functional improvement and a possible survival benefit [1–3], wide acceptance of this procedure has been hampered by a lack of controlled, prospective clinical data and inconsistent laboratory results.
Chiu [11], Lee and Wechsler [14], and others long have theorized that cardiomyoplasty may exert significant conformational effects on the dilated myocardium that unload the LV. This unloading effect would account for the dichotomy between the functional improvements seen in clinical cardiomyoplasty and the difficulty documenting improved LV function in earlier reports using load-dependent indices such as cardiac output and ejection fraction [4–6]. Recently, several studies from our laboratory and others [7–10] clearly have documented improved LV function and decreased LV volumes using load-insensitive indices.
These investigators also have hypothesized that this unloading effect would translate into decreased wall stress and decreased MVO2—a "myocardial sparing effect." Although direct confirmation of this effect has been lacking, indirect evidence of decreased MVO2 has been reported. Lee and co-workers [5] showed a 13% decrease in calculated mean systolic wall stress, the primary determinant of MVO2, with skeletal muscle contraction. Kawaguchi and associates [15] used an artificial external compression device to mimic cardiomyoplasty in an isolated, cross-circulated heart model, and showed a decrease in PVA and MVO2 with cardiac compression.
Ventricular Energetics
Suga's [13] time-varying elastance model and the associated MVO2-PVA relation has been used extensively to study ventricular energetics in a wide variety of laboratory and clinical conditions. These relations are diagrammed in Figure 1. Briefly, they showed that, in the pressure-volume plane, the area between the ESPVR, the EDPVR, and the systolic portion of the pressure-volume loop represents the PVA generated during a cardiac cycle. The portion of the PVA within the pressure-volume loop is the SW, and the portion that lies outside the loop is the IW as shown in equation 3. The IW is thought to represent the work generated by conformational changes during isovolumic contraction and relaxation that does not contribute to the ejection of the SV against arterial pressure.
They also showed that PVA is related linearly to MVO2. For a given contractile state, this MVO2-PVA relation has been shown to be constant under a wide range of hemodynamic conditions. The MVO2-intercept of this relation is the unloaded MVO2 and represents the oxygen requirements of basal myocardial metabolism and excitation-contraction coupling. The reciprocal of the slope of this relation is the contractile efficiency, which is the efficiency of converting excess MVO2 (the portion above unloaded MVO2) into mechanical contraction. The contractile efficiency is thought to represent primarily the efficiency of cross-bridge cycling, and it appears to be independent of contractile state [13].
From this analysis, one can determine the efficiency of transforming chemical energy (O2) into useful mechanical work (SW), the Effmech using equation 6. This transformation can be divided conceptually into two steps (Fig 5). First, excess MVO2 is transformed into PVA. The efficiency of this transformation is the contractile efficiency. Only a portion of the PVA goes toward useful SW. The EffSW, therefore, can be defined as in equation 4. This also has been referred to as the energy transfer efficiency.
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Fig 5. . Energetic efficiencies associated with chemomechanical energy transformation in the myocardium. (E-C = excitation-contraction.)
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The results of this study document improved LV energetics during skeletal muscle contraction with right latissimus dorsi cardiomyoplasty performed in an acute canine model. As we reported previously [8], turning the stimulator on significantly increased Ees and decreased LV volumes in all animals. The decrease in Ved led to a small, statistically insignificant decrease in SW. Although SW fell slightly, the increase in Ees led to a much larger decrease in IW and, therefore, in PVA. Hence, a larger portion of the PVA went toward useful SW, resulting in improved EffSW (see Fig 3B). Therefore, it appears that skeletal muscle contraction can generate the same SW with significantly less total mechanical work.
Ventriculovascular Coupling and Stroke Work Efficiency
The ratio of Ea to Ees is an index of ventriculovascular coupling and has been shown to be related inversely to EffSW. Theoretic work by Burkhoff and Sagawa [16] defined the relation between SW, Ea, Ees, Ved, and V0 as follows:
 | (9) |
They showed that at a given Ved and contractile state, SW is maximized when Ea/Ees = 1, and that Effmech is maximized when Ea/Ees = 0.5. This model later was extended to analyze the relation between Ea/Ees and EffSW, first by Nozawa and colleagues, [17] and later by Little and Cheng [18]. These investigators showed an inverse relation, which they approximated as follows:
 | (10) |
This study documents improved ventriculovascular coupling with skeletal muscle contraction in cardiomyoplasty. Although the Ea showed a small, statistically insignificant increase, the much larger increase in Ees resulted in a significant decrease in Ea/Ees (see Fig 2C). Given equation 9, one initially might suspect that this decrease in Ea/Ees, closer to the optimal value of Ea/Ees = 1, would translate into a significant increase in SW. However, the significant fall in end-diastolic volume (especially relative to the volume-axis intercept of the end-systolic pressure-volume relation) tends to decrease SW, resulting in no significant overall change in SW. In fact, equation 9 accurately predicts the small decrease in SW seen with skeletal muscle contraction.
It appears that the improved EffSW seen in this study can be attributed directly to improved ventriculovascular coupling resulting from an increase in Ees. The pooled data confirm an inverse relation between Ea/Ees and EffSW (see Fig 4) that is very similar to the predicted relation in equation 10:
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| (11) |
This curve is slightly higher than the predicted curve. This probably is due to several assumptions in the Burkhoff-Sagawa model, namely, that Ped is negligible and that the mean ejection pressure is approximately equal to Pes. These assumptions may not be reflected precisely in our experimental model, and they may account for the small difference in these curves.
Prediction of Myocardial Oxygen Consumption
Although MVO2 was not measured directly in this study, the MVO2-PVA relation can be used to make inferences regarding the effect of skeletal muscle contraction on MVO2. We first must realize that the calculated PVA in this model represents the contribution of both skeletal and cardiac muscles to contraction. Although the relative contributions of the heart (PVAh) and skeletal muscle (PVAsm) to total mechanical work (PVAtot) cannot be determined directly from these data, the heart's contribution to the PVA can be expressed as follows:
 | (12) |
It is reasonable to assume that the skeletal muscle wrap is performing some work when it contracts (ie, that PVAsm is greater than zero). Therefore, with skeletal muscle contraction:
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Because PVAtot fell by 29%, we can infer that PVAh fell by at least as much. The PVAh actually can be calculated directly by generating pressure-volume loops using the transmural pressure (Ptm) across the ventricular wall. In a recent report from our laboratory, Chen and associates [19] used a fluid-filled balloon interposed between skeletal muscle and the LV to document a 26% to 53% decrease in Ptm with skeletal muscle contraction, despite no change in SV. The actual decrease was a function of the volume of fluid in the balloon, which altered the baseline stretch (preload) on the skeletal muscle. In a recently published follow-up report, we documented how the decrease in mean Ptm resulted in a similar decrease in PVAh [20].
Although we must await direct measurements of MVO2 to be certain, it is still worth considering the implications of these results on the effect of cardiomyoplasty on MVO2. Let us first assume that the skeletal muscle does not alter the fundamental MVO2-PVA relation of the heart. This is a reasonable assumption, at least in the acute setting, because the wrap only interacts with the heart mechanically. The components of the MVO2-PVA relation (unloaded MVO2 and contractile efficiency) are believed to represent fundamental biologic properties of the myocardium that are independent of the mechanical state of the ventricle. It is difficult to imagine how the skeletal muscle wrap could alter these processes acutely. If the MVO2-PVA relation remains unchanged, the fall in PVAh would translate directly into a decrease in MVO2 by moving down and to the left along the MVO2-PVA relation (Figs 6A and 6B, part A). Using a typical MVO2-PVA relation from Suga's data [13], we can predict the effect of skeletal muscle contraction on MVO2 and Effmech. The minimum 29% decrease in PVAh would translate into at least a 22% decrease in MVO2. This in turn would lead to a minimum increase in Effmech from 16.1% to 18.4%.
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Fig 6. . Predictions of the effect of skeletal muscle contraction on myocardial oxygen consumption (MVO2) using the MVO2-total mechanical work (PVA) relation. Off and On PVA data points are plotted on a typical MVO2-PVA relation (thick line). The effect of shifting the relation or changing its slope are shown in panels A and B, respectively. Point A assumes no change in the MVO2-PVA relation with skeletal muscle contraction. Points B and C show the effects on MVO2 of altering the slope and intercept of this relation.
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Significant changes in the MVO2-PVA relation would have to occur to negate this decrease in MVO2. It would require nearly doubling the unloaded MVO2 to 0.77 J/beat or decreasing the contractile efficiency to 28% (see Figs 6A and 6B, part B). These are well beyond the variation in these parameters reported in the literature by Suga [13] and others under a wide range of physiologic conditions. Significant shifts in unloaded MVO2 do occur with inotropic agents such as dobutamine, and are thought to result from increased oxygen costs of calcium cycling during excitation-contraction coupling. The shift generally is proportional to the resulting increase in Ees. Although we have shown an increase in Ees with skeletal muscle contraction, this presumably results from external mechanical effects and not from acute changes in intrinsic myocardial processes such as excitation-contraction coupling. Therefore, it seems unlikely that it would alter unloaded MVO2 acutely. Any decrease in unloaded MVO2 or increase in contractile efficiency would only decrease MVO2 even further (see Figs 6A and 6B, part C).
The long-term effect of cardiomyoplasty on the MVO2-PVA relation almost certainly is more complicated, especially when applied to the failing heart. Using a rapid-ventricular-pacing model of heart failure, Wolff and colleagues [21] showed that dilated cardiomyopathy alters the MVO2-PVA relation by increasing contractile efficiency. They suggested that this may result from a shift in metabolic substrate utilization from free fatty acids to glucose, or from transformation to fetal isoforms of myosin-adenosine triphosphatase in response to increased wall stress and chronic depletion of energy stores. Chiu [11] and others have suggested that the unloading and oxygen-sparing effects of cardiomyoplasty may halt or even partially reverse the progressive decline in LV function that characterizes dilated cardiomyopathy. An attractive hypothesis is that the improved ventricular energetics would begin to reverse the shift in myosin-adenosine triphosphatase isoforms and restore the MVO2-PVA relation back toward normal. Long-term experiments will be necessary to investigate this hypothesis.
Limitations
The primary limitations of this study that could affect its applicability to clinical cardiomyoplasty are that we used untrained muscle in dogs with normal LV function. We used brief periods of stimulation separated by periods of rest to prevent muscle fatigue. However, even without fatigue, skeletal muscle transformation using current protocols has been shown clearly to decrease the rate and magnitude of force generation and to produce progressive muscle fibrosis [22]. Furthermore, chronic heart failure is characterized by abnormalities in skeletal muscle function. These effects certainly could diminish the positive results we have reported, and one should be cautious in extrapolating these results to the clinical realm. However, recent efforts to overcome these effects with novel stimulation protocols and pharmacologic manipulation of the skeletal muscle (anabolic steroids, angiogenic factors) have produced encouraging results. These efforts eventually may produce long-lasting, fatigue-resistant skeletal muscle with power equal to, or even greater than, the untrained skeletal muscle used in these experiments.
Another factor that may affect the clinical applicability of these results is the fact that we used the right latissimus dorsi muscle, whereas most clinical cases of cardiomyoplasty have used the left. Proponents of each side, in the past, have presented theoretic reasons to prefer one side over the other. However, it now appears more likely that, as long as a complete wrap can be performed, the muscle used and its orientation are of secondary concern. The pressure–volume loops that we generated using the right latissimus dorsi muscle [8] do not differ significantly from those shown in studies using the left latissimus dorsi muscle [23, 24].
Finally, it is not clear how well these results can be generalized to the failing heart. As mentioned previously, dilated cardiomyopathy is characterized by significant derangements in ventricular energetics. However, there is some evidence that the dilated ventricle may extract greater benefit from skeletal muscle contraction. Using their artificial cardiac compression device in an isolated heart model, Kawaguchi and co-workers [25] showed that dynamic cardiac compression showed greater mechanical enhancement in dilated ventricles when compared with normal ventricles. Whether these results can be extrapolated to more clinically relevant situations will require further research.
Conclusion
In summary, these results support the hypothesis that cardiomyoplasty unloads the LV by decreasing ventricular volumes and increasing contractility. These two effects appear to improve LV energetics by decreasing PVA without significantly affecting SW, resulting in improved EffSW. The improved EffSW appears to be directly attributable to improved ventriculovascular coupling. The fact that PVA decreased strongly suggests a decrease in MVO2 and Effmech. Complete MVO2-PVA analysis with direct measurements of MVO2 will be necessary to characterize fully the effect of cardiomyoplasty on LV energetics.
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Acknowledgments
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We thank the Cardiac Assist Systems Division of Medtronic Inc, especially Michael Colson, Pierre Grandjean, and David Franciscelli, for graciously providing essential equipment and technical assistance. In addition, we give special thanks to Mr Charles A. and Mrs Elfriede A. Collis and to Mr David L. Brook for providing generous financial support to the laboratory.
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Footnotes
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Address reprint requests to Dr Cohn, Division of Cardiac Surgery, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115.
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References
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Abstract
Introduction
