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Ann Thorac Surg 1996;61:640-645
© 1996 The Society of Thoracic Surgeons

Original Article: Cardiovascular

Influence of Prolonged Ventricular Assistance on Myocardial Histopathology in Intact Heart

Masayuki Kinoshita, MD, Hisateru Takano, MD, PhD, Shigeko Takaichi, PhD, Yoshiyuki Taenaka, MD, PhD, Takeshi Nakatani, MD, PhD

Departments of Artificial Organs and of Etiology and Pathology, National Cardiovascular Center, Research Institute, Osaka, Japan

Accepted for publication September 22, 1995.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. The unloading effect of ventricular assistance on the injured myocardium may adversely affect the compensatory hypertrophy of the residual intact myocardium because myocardial protein synthesis is partly controlled by cardiac work. The influence of prolonged ventricular assistance on normal myocardium was evaluated from a pathologic point of view.

Methods. A ventricular assist device was chronically implanted in 5 goats using left atrium–aorta bypass. The pumping ratio was fixed at 70 beats/min. Left ventricular biopsy samples were taken before and 1 month after assistance.

Results. Although the volume densities of myocytes and interstitial tissue in the myocardium showed no significant changes after 1 month of support, the myocyte volume density to nuclear volume density ratio and the interstitial tissue volume density to nuclear volume density ratio decreased significantly (p < 0.01 and p < 0.05, respectively). A cross-sectional area of myocyte showed decreases of 20.9% to 49.5%, whereas the nuclear cross-sectional area showed no significant changes. In addition, myofibrillar volume density in the cytoplasm decreased from 54.9 ± 2.3% to 49.1 ± 4.4%.

Conclusions. The results indicate that long-term ventricular assistance in the intact heart leads to myocardial atrophy. This suggests that in the damaged heart subjected to prolonged unloading by ventricular assistance, there is the possibility of limiting compensatory hypertrophic changes in the residual intact myocardium.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
See also page 645.

In a failing heart, the major factors for restoration of adequate pump function are the metabolic recovery of the injured myocardial cells and the compensatory hypertrophy of the residual intact myocardium. The hemodynamic and mechanical effects of a ventricular assist device (VAD) on a failing heart are to improve the myocardial oxygen supply–demand balance and to unload the ventricle, consequently saving the myocardium with reversible injury [1, 2]. However, these effects may adversely affect another recovery mechanism, ie, the compensatory hypertrophy of the residual intact myocardium, because myocardial protein synthesis is partly controlled by the cardiac work load [3] and may be suppressed under the unloading conditions imposed by the VAD. A decrease in cardiac protein synthesis can be achieved in the setting of a reduced cardiac work load by lowering peripheral demands [4, 5]. Therefore, it can be hypothesized that a reduction in left ventricular work load for a long period with a VAD may suppress the myocardial adaptation mechanism in the setting of heart failure and even cause myocardial atrophy in the residual intact myocardium.

To answer questions concerning the effects of prolonged ventricular unloading on residual intact myocardium, it is necessary to test the hypothesis with an intact heart to clarify the basic effects of long-term unloading of the left ventricle. The purpose of this study was to examine the long-term effect of ventricular assistance on the intact myocardium from the pathologic point of view and to determine whether prolonged ventricular assistance causes myocardial atrophy.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Five adult goats weighing 22.0 to 43.0 kg (mean weight, 32.2 ± 9.5 kg) were used for the experiment. All animals were cared for by a veterinarian in accordance with the ``Principles of Laboratory Animal Care'' formulated by the National Society for Medical Research and the ``Guide for the Care and Use of Laboratory Animals'' prepared by the National Academy of Sciences and published by the National Institutes of Health (NIH publication 85-23, revised 1985).

Operative Procedure
After intramuscular injections of atropine sulfate (0.5 mg) and ketamine hydrochloride (10 mg/kg), the animals were intubated and anesthetized with 1% to 2% halothane and 50% nitrous oxide mixed with oxygen. Under sterile conditions, a thoracotomy was performed through the left fifth intercostal bed. Control transmural myocardial biopsy samples were obtained from three different sites in the left ventricular anterior wall with a biopsy needle (Tru-Cut, 14 gauge x 11.4 cm; Travenol Laboratories Inc, Deerfield, IL). Two samples, one for light and one for electron microscopic observations, were taken from each site.

After intravenous administration of heparin sodium (300 U/kg), a pneumatic diaphragmatic type of VAD (National Cardiovascular Center VAD) was placed between the left atrium and the descending aorta; the device was powered with a drive unit (Toyobo Co, Ltd, Osaka, Japan). Details of this device have been described elsewhere [6]. Electromagnetic flowmeters (Nihon Kohden Co, Ltd, Tokyo, Japan) were put around the pulmonary artery and the outlet woven Dacron graft of the VAD to measure pulmonary artery flow and pump flow through the device. Fluid-filled catheters were inserted into the internal thoracic artery and the left ventricle to measure pressure. The chest was closed in layers with a temporary tube thoracostomy, and the VAD pump was fixed paracorporeally on the chest wall.

After the operation, pumping conditions were set in fixed mode to yield a maximum bypass ratio (pump flow/pulmonary artery flow) with pumping of 70 beats/min. The animals were kept in a specially designed cage for a month.

After a month VAD support, the animals were anesthetized to obtain myocardial samples with the heart beating. The biopsy method and the number of samples were the same as for the controls. The animals were then sacrificed.

Specimen Preparations
The midportion of the transmural samples were prepared as follows: The samples for the light microscopic studies were fixed in 10% formaldehyde, dehydrated, and embedded in paraffin, and sections 3 µm thick were stained with hematoxylin and eosin. Specimens for the electron microscopic studies were fixed in 3% glutaraldehyde, postfixed in 1% osmium tetroxide, dehydrated, and embedded in epoxy resin. Ultrathin sections were stained with uranyl acetate and lead citrate.

Morphometric Methods
Four kinds of morphometric studies at three levels of magnification were conducted under light microscopy (Nikon Co, Ltd, Tokyo, Japan) and electron microscopy (H-600; Hitachi Co, Ltd, Tokyo, Japan).

Myocyte And Interstitial Tissue Volume Densities (Light Microscopy x400).
With an ocular micrometer including 121 cross hairs per square centimeter, volume densities of myocytes (Vm) and interstitial tissue (Vi) in the myocardium were measured by the point-count method of Weibel and Bolender [7]. Measurements were made in 60 fields randomly selected from the three biopsy specimens from the three different sites. A total of 7,260 points and an area of 3.75 x 10-2 cm2 were examined.

NUCLEAR VOLUME DENSITY (LIGHT MICROSCOPY x1,000).
Relative volume densities of nuclei (Vn) in the myocardium were measured by the point-count method using the same ocular micrometer. This measurement was performed in 300 fields randomly selected from the three specimens. A total of 36,300 points and an area of 3.0 x 10-2 cm2 were examined.

CROSS-SECTIONAL AREA OF MYOCYTE AND NUCLEUS (LIGHT MICROSCOPY x1,000).
A cross-sectional area of a myocyte containing a round-shaped nuclear cross-section was computed with a digitizer (KD3800; Graphtec Co, Ltd, Tokyo, Japan). The area of each cross-sectioned nucleus was also measured by the same method. These measurements were performed with 100 photomicrographs of cardiomyocytes taken randomly from the three specimens.

MYOFIBRILLAR AND MITOCHONDRIAL VOLUME DENSITIES (ELECTRON MICROSCOPY x8,000).
The relative volume densities of myofibrils and mitochondria in the cytoplasm were measured by the point-count method. This analysis was carried out with 30 electron micrographs randomly selected from the three specimens at the final magnification of x8,000 using an overlay with 108 points per 436 cm2. A total of 3,240 points and an area of 2.04 x 104 µm2 were examined.

Statistical Analysis
Values relating to volume densities are expressed as primary data, and the 100 measurements of the cross-sectional area of a myocyte and nucleus in each sample are shown as the mean ± the standard deviation. Statistical evaluations were done using a paired t test to compare the values obtained before VAD support and those obtained after VAD support. A p value of less than 0.05 was considered significant.


   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
Hemodynamic Observations
All animals tolerated the surgical implantation and postoperative course. Though the pumping condition was fixed for 30 days, the bypass ratio in each animal varied moment by moment, being approximately 60% to 80% in all animals. Left ventricular pressure was lower than aortic pressure in some beats throughout the experiment because of the assistance (Fig 1Go).



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  		Fig 1. . Representative pressure tracings during ventricular assist pumping: electrocardiogram (ECG); left ventricular pressure (LVP); and aortic pressure (AoP).

 
Light Microscopic Studies
Representative photomicrographs from 1 animal before and after VAD assistance are shown in Figure 2Go. The myocyte cross-sectional area is smaller in the later study.



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  		Fig 2. . Photomicrographs from 1 animal (A) before and (B) after support with ventricular assist device. The cross-sectional area of the myocyte after support appeared smaller than that seen before support.

 
The Vm and Vi values are summarized in Table 1Go. The initial Vm data ranged from 62.3% to 72.2% (mean value, 66.2% ± 3.8%), and the data obtained after VAD assistance ranged from 65.0% to 71.4% (mean value, 68.7% ± 2.7%). The Vm and Vi values did not change significantly during the 30 days of VAD support.


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  		Table 1. . Myocyte and Interstitial Tissue Volume Densitiesa
 
The Vn and the ratios Vm to Vn and Vi to Vn are shown in Table 2Go. The Vn increased significantly from a mean value of 1.20% ± 0.35% to a mean of 1.82% ± 0.75% (p < 0.05), and the Vm to Vn and Vi to Vn ratios showed significant decreases from a mean value of 58.6% ± 15.9% to a mean of 43.1% ± 16.7% (p < 0.01) and from a mean value of 29.7% ± 8.1% to a mean of 19.4% ± 7.1% (p < 0.05), respectively.


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  		Table 2. . Nuclear Volume Density and Relative Volume of Myocardial Tissue to Nuclei
 
The cross-sectional areas of a myocyte and nucleus are summarized in Table 3Go. Prior to assistance, both areas had linear correlations with body weight (Fig 3Go). The mean myocyte area was 422.2 ± 156.2 µm2 before assistance and 270.1 ± 89.2 µm2 after assistance (p < 0.01). The rate of individual decrease between the values measured before and after assistance ranged from 20.9% to 49.5% (mean rate, 34.6% ± 11.0%). The nuclear cross-sectional area, on the other hand, showed no significant change after VAD support.


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  		Table 3. . Cross-Sectional Area of Myocyte and Nucleus
 


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  		Fig 3. . Correlation between body weight and (A) cross-sectional area of myocyte and (B) nucleus before support with ventricular assist device. Both cross-sectional areas show significant linear correlation with body weight.

 
Electron Microscopic Studies
An electron micrograph of a sample obtained after 30 days of support is shown in Figure 4Go. Some increases in nonorganelles were observed. The shapes of the mitochondria appeared normal, but the arrangement of mitochondria and myofibrils was disordered.



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  		Fig 4. . Electron micrograph of myocyte in sample taken after a month of ventricular assist device support. Nonorganelles were increasing in the cytoplasm. The placement of mitochondria and myofibrils was disordered, but the shape of mitochondria looked normal.

 
The results of the electron microscopic studies are summarized in Table 4Go. The volume densities of myofibrils showed a significant decrease (p < 0.05), whereas the volume densities of mitochondria did not change significantly after VAD support.


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  		Table 4. . Myofibrillar and Mitochondrial Volume Densities
 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
With a VAD, the left ventricle was mechanically unloaded under beating conditions, and the left ventricular output was approximately 20% to 40% of the total output throughout the experiment. In general, though not with every beat, left ventricular pressure was lower than aortic pressure. Previously our group [8] confirmed that the total mechanical work of the left ventricle during VAD assistance was 42% to 55% of that observed before assistance. Wei and associates [9] also found a decrease of approximately 70% of left ventricular oxygen consumption when a normal heart was assisted with a 75% bypass ratio. Therefore, the model used in the present study is suitable to provide prolonged unloading conditions to the left ventricle.

In this study, the left ventricular myocardium showed a significant decrease in size in terms of myocyte cross-sectional area after 1 month of support. This finding indicates the development of atrophy of the myocyte under the condition of prolonged unloading with VAD assistance. The decrease in the Vm to Vn ratio without a significant change in nuclear cross-sectional area suggests atrophy if it is assumed that the nuclear volume was constant. This myocyte change was accompanied with a similar change in interstitial tissue. The volume density of myofibrils showed a decrease, whereas that of mitochondria did not change significantly.

In the setting of mechanical unloading of the myocardium without a VAD, Thompson and co-workers [10] reported the development of myocardial atrophy in the right ventricular papillary muscle when the chordae tendineae were cut. In their study, the decrease in myocyte cross-sectional area was approximately 40% after 2 weeks of unloading, but each tissue element did not change in terms of volume density in the myocardium. This suggests that the absolute volume of each element decreases after mechanical unloading, a result similar to ours. Even though these authors showed a significant decrease in myofibrillar and mitochondrial volume densities in a myocyte, they also pointed out that the response of mitochondria lags behind that of myofibrils. This may explain why the mitochondrial volume density in our study did not decrease, although the myofibrils showed a decrease of 2.1% to 20.7% of volume density in cytoplasm.

Using different experimental models, several studies have evaluated the pathologic changes in the myocardium after VAD support. Harasaki [11], Takano [12], and their associates reported myocardial atrophy in a fibrillated ventricle that had VAD assist for up to 3 months. Nakatani [13] also found a decrease in ventricular wall thickness proportional to the duration of VAD assist in a heart injured by global ischemia. Previously, however, it has not been clear whether the ventricular assistance causes myocardial atrophy in intact myocardium. When ventricular fibrillation or ischemia is added, the pathologic changes may be dependent largely on their own effects, not those of the VAD. Our study using intact myocardium as an experimental model has proved progression of atrophy under VAD assistance.

We observed myocardial atrophy in the intact ventricle after long-standing unloading. However, this may not directly indicate that atrophy also occurs in remaining viable myocardium in a clinical setting of a damaged heart assisted with a VAD, because regional and global mechanical factors in a damaged heart are more complex than in the present study. Recently several groups have reported myocardial histologic changes in patients with end-stage cardiomyopathy supported with a VAD for up to 4 months. Though Scheinin and colleagues [14] and McCarthy and co-workers [15] observed an increase in the amount of myocardial fibrosis and a decrease in ventricular wall thickness when the heart was explanted for transplantation after ventricular assistance, the size of myocytes showed an increase rather than a decrease. On the other hand, Jacquet and associates [16] observed a decrease in myocyte size, but the trend was not progressive and the final size of the myocyte was still larger than normal. There continues to be some work load for the remaining viable myocardium even under VAD assistance; as shown in this study, there is still afterload, and the balance between the amount of viable myocardium and the remaining work load under VAD assistance may be an important determinant of pathologic change in the viable myocardium.

Even though myocardial atrophy has not been proved clinically, on the basis of this study, we speculate that the compensatory hypertrophic response may not progress sufficiently if full unloading is continued. This may mean less chance of functional recovery. When a VAD is used temporarily after cardiotomy in a patient in whom recovery of the damaged heart is expected, compensatory hypertrophy is a much more important issue than in a patient with end-stage cardiomyopathy in whom the VAD is placed as a bridging device. When full functional recovery is anticipated, it may be necessary to reload the ventricle by decreasing the assistance as soon as possible after salvaging the injured myocardium. These practical issues need further investigation.


   Acknowledgments
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
We thank Dr Hiroshi Mori, 2nd Department of Pathology, Osaka Medical College, Osaka, Japan, for advice on morphometric methods.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Address reprint requests to Dr Takano, Department of Artificial Organs, National Cardiovascular Center, Research Institute, 5-7-1 Fujishiro-dai, Suita, Osaka 565, Japan.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Dennis C, Hall DP, Moreno JR, Senning A. Reduction of the oxygen utilization of the heart by left heart bypass. Circ Res 1962;10:298–305.[Abstract/Free Full Text]
  2. Pennock JL, Pae WE, Pierce WS, Waldhausen JA. Reduction of myocardial infarct size: comparison between left atrial and left ventricular bypass. Circulation 1979;59:275–9.[Abstract/Free Full Text]
  3. Morgan HE, Chua BHL, Siehl D, Kochel PJ, Kira Y. Factors controlling the efficiency of protein synthesis in the heart. In: Alpert NR, ed. Myocardial hypertrophy and failure. New York: Raven, 1983:425–31.
  4. Hjalmarson AC, Rannel DE, Kao R, Morgan HE. Effects of hypophysectomy, growth hormone, and thyroxine on protein turnover in heart. J Biol Chem 1975;250:4556–61.[Abstract/Free Full Text]
  5. Crie JS, Sanford CF, Wildenthal K. Influence of starvation and refeeding on cardiac protein degeneration. J Nutr 1980;110:22–7.[Abstract/Free Full Text]
  6. Takano H, Taenaka Y, Noda H, et al. Multi-institutional studies of the National Cardiovascular Center ventricular assist system: use in 92 patients. Trans Am Soc Artif Intern Organs 1989;35:541–4.
  7. Weibel ER, Bolender RP. Stereological techniques for electron microscopic morphometry. In: Hayat MA, ed. Principles and techniques: biological applications. New York: Van Nostrand Reinhold, 1973:237–96.
  8. Nakamura T, Hayashi K, Seki J, et al. Bulk and regional mechanical work of ischemic heart during left ventricular assistance. In: Nose Y, Kjellstrand C, Ivanovich P, eds. Progress in Artificial Organs—1985. Cleveland, OH: ISAO Press, 1985:447–51.
  9. Wei CM, Yada I, Kusagawa M. The effect of left ventricular assistance on the area of infarcted myocardium. Trans Am Soc Artif Intern Organs 1986;32:217–20.
  10. Thompson EW, Marino TA, Uboh CE, Kent RL, Cooper G. Atrophy reversal and cardiocyte redifferentiation in reloaded cat myocardium. Circ Res 1984;54:367–77.[Abstract/Free Full Text]
  11. Harasaki H, Zheng Z, Morimoto T, McMahon J, Golding L, Nose Y. Morphometric studies of chronic fibrillating heart. Trans Am Soc Artif Intern Organs 1985;31:73–8.[Medline]
  12. Takano H, Taenaka Y, Nakatani T, Akutsu T, Kawashima Y, Manabe H. Long-term circulatory maintenance with a left-sided single artificial heart. J Thorac Cardiovasc Surg 1992;103:496–503.[Abstract]
  13. Nakatani T. Therapeutic effect of assisted circulation using ventricular assist device on profound biventricular failure with induced severe myocardial injury. Osaka Med J 1990;42:177–88.
  14. Scheinin SA, Capek P, Radovancevic B, Duncan JM, McAllister HA, Frazier OH. The effect of prolonged left ventricular support on myocardial histopathology in patients with end-stage cardiomyopathy. ASAIO J 1992;38:M271–4.[Medline]
  15. McCarthy PM, Nakatani S, Vargo R, et al. Structural and left ventricular histologic changes after implantable LVAD insertion. Ann Thorac Surg 1995;59:609–13.[Abstract/Free Full Text]
  16. Jacquet L, Zerbe T, Stein KL, Kormos RL, Griffith BP. Evolution of human cardiac myocyte dimension during prolonged mechanical support. J Thorac Cardiovasc Surg 1991;101:256–9.[Abstract]

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