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Ann Thorac Surg 2000;69:769-773
© 2000 The Society of Thoracic Surgeons

Original Articles

Autopsy findings in early and late postoperative death after partial left ventriculectomy

Patricia M. Cury, MD, PhDa, Maria de Lourdes Higuchi, MD, PhDa, Paulo S. Gutierrez, MD, PhDa, Luiz Felipe P. Moreira, MD, PhDa, Edimar A. Bocchi, MD, PhDa, Noedir A.G. Stolf, MD, PhDa, Adib D. Jatene, MD, PhDa

a Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil

Address reprint requests to Dr Cury, Heart Institute (InCor), Av Dr Eneas Carvalho de Aguiar, 44, CEP 05403-000 São Paulo, SP, Brazil
e-mail: pmcury{at}hotmail.com


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Partial left ventriculectomy (PLV) is an alternative to heart transplantation for patients with severe heart failure. However, this procedure is accompanied by high morbidity and mortality. Therefore, we studied the hearts of 12 patients who underwent this procedure to increase our understanding of the causes of bad outcome.

Methods. We analyzed the autopsy hearts of 11 of 16 patients who died after PLV, and one heart from a patient who underwent heart transplantation.

Results. Six patients died less than 30 days postoperatively, 4 of cardiogenic shock, 1 of arrhythmia, and 1 of coagulopathy. Five patients died from 36 to 120 days after the procedure, 4 of cardiogenic shock and 1 of arrhythmia. The patient who underwent heart transplantation had a cardiogenic shock 230 days after PLV. Ten hearts weighed more than 500 g and nine had myocardial infarction that extended to the papillary muscles. Four patients had infarction of both papillary muscles and 3 of them had episodes of arrhythmia, suggesting some relation between these events.

Conclusions. We found several important morphologic clues for bad outcome: infarction of both papillary muscles, which may be associated with the development of arrhythmia, and myocardial infarction and pericardial hemorrhage, which may contribute to the outcome of heart failure.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Partial left ventriculectomy (PLV) is a new surgical procedure that has been proposed for the treatment of severe heart failure in dilated hearts [1]. It consists of a resection of a large portion of the free left ventricular (LV) wall to decrease the chamber volume/mass relation and consequently reduce LV wall tension. The aim is the restoration of myocardial contractility, delaying the progression of the underlying disease. This is an interesting surgical alternative to heart transplantation for patients with idiopathic dilated cardiomyopathy (IDC) because it improves LV function and reverses congestive heart failure [2–5]. However, morbidity and mortality mainly because of heart failure progression and arrhythmia [6–11] have been considered too high in most serial cases of this procedure. Although there are many groups studying this procedure, there are no detailed autopsy data from the patients who died as a result of it.

With the aim of contributing to the understanding of the high level of failure of this surgical procedure, we describe the autopsy findings of 11 patients who died after PLV, and one heart from a patient who underwent heart transplantation after PLV surgery.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Between April 1995 and August 1997, 37 patients (30 men and 7 women) underwent PLV at our institution. Sixteen patients were in New York Heart Association (NYHA) class III heart failure, and 21 were in persistent class IV heart failure at the moment surgery was indicated. The age of the patients ranged from 28 to 72 years (mean age, 46.1 years). No patient had significant coronary artery disease. PLV was performed according to the technique of Batista and associates [1]. A slice as large as possible of the ventricular myocardium was resected between the papillary muscles, from the apex of the heart up to 2 or 3 cm from the mitral annulus. The resected myocardial specimen measured 10.9 ± 2 cm in length and 5 ± 0.8 cm in width, and it usually carried the obtuse marginal branches of the circumflex artery. The left ventricle was repaired with a double 3-0 polypropylene suture anchored in bovine pericardial strips. Mitral valve annuloplasty was performed if any degree of mitral regurgitation occurred, which happened in 27 patients. Two patients had mitral valve replacement, and 8 patients had only PLV. The patients were followed for a mean of 26.8 ± 9.2 months. Sixteen of these patients died, 7 in the early postoperative period. Actuarial survival was 56.7% ± 8.1% at 6 and at 36 months of follow-up.

The present study analyzes the pathologic findings from the autopsy hearts of 11 of the 16 patients who died: 9 men and 2 women, ages varying from 28 to 58 years (mean age, 41 ± 8.2 years), and one heart from a 46-year-old woman who underwent heart transplantation 230 days after PLV, because of cardiogenic shock (patient 12). Nine of the patients also had mitral annuloplasty; 1 had mitral valve replacement with a biologic prosthesis during the PLV and 1 patient had a second surgical procedure for mitral valve replacement 6 days after the PVL, due to valvar insufficiency. Transversal sections from the apex to the base of the hearts were performed. All hearts had areas of myocardial infarction (MI) adjacent to the LV incision. The MI size was measured based on the area of thickness of the midportion of a transversal heart section. The distance of the valve was based on a longitudinal section of the mitral valve region. The wall hypertrophy and dilation of the right ventricle were classified in a semiquantitative manner where 0 = absence of alteration, + = mild, ++ = moderate, and +++ = very important alteration, the same classification used for the macroscopic fibrosis of the endocardium, myocardium, and pericardium. These fibrotic foci were irregular, distinctive from a healed infarction. The LV diameter was the average of two perpendicular diameters of the midportion in a transversal heart section. The LV thickness was based on the average of the measurements of the septum and anterior and posterior walls, in the same midportion. The percentage of LV infarcted area was calculated with the aid of a digital analyzer system (Quantimet 500, Leica, Cambridge, England). Three transversal sections of the heart were analyzed. The total area of the left ventricle (TA) and the infarction area (IA) were measured in the three sections, and the IA/TA ratio was calculated. The average of the three sections was calculated in terms of percentage. In four hearts it was not possible to make the measurements because of the difficulty in obtaining three transversal sections. The same digital analyzer system was used to measure the myocardial fiber diameter in the endocardial area of the free LV wall. The method used was the same as our previous work [12], in which 50 fibers were counted in each case, using a x20 objective lens.

Microscopic analyses of the myocardial hypertrophy, fibrosis, and myocytolysis were also performed in the free LV wall, and the results were classified as 0 (absence of alteration), + (mild or scarce), ++ (moderate or multifocal), or +++ (severe or diffuse).


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
The findings are summarized in Tables 1 and 2. Six patients died less than 30 days after the surgery, 4 because of cardiogenic shock, 1 because of recurrent sustained ventricular tachycardia, and 1 because of coagulopathy. In 5 patients who died in the late postoperative period (from 36 to 120 days), the cause of death was recurrent sustained ventricular tachycardia documented by Holter monitoring in 1 patient and cardiogenic shock in 4 patients. The patient who underwent heart transplantation had a cardiogenic shock 230 days after PLV. The heart’s weight ranged from 390 to 2,600 g, and the LV thickness ranged from 0.80 to 1.8 cm.


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  		Table 1. Autopsy Findings of the Patients Submitted to Partial Left Ventriculectomy

 

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  		Table 2. Percentage of Left Ventricular Infarction Area

 
All the hearts had an area of MI adjacent to the surgical incision measuring from 2.2 to 6.0 cm, usually extending to the papillary muscles (Fig 1). The percentage of LV infarction area, surrounding the surgical procedure, ranged from 11% to 35%, with the average of 22% (Table 2). The myocardial fiber diameter of each case is also shown in Table 2. Three patients did not have papillary muscle infarctions. Four patients had infarction only at the anterior papillary muscle, 1 patient at the posterior, and 4 patients in both papillary muscles. These findings occurred in 7 patients who also underwent mitral valve correction or replacement and in the 2 patients submitted to isolated PLV. Of the 4 patients who had infarctions in both papillary muscles, 2 (patients 2 and 4) died because of arrhythmia, and another patient (patient 12) died because of cardiogenic shock and also had several episodes of sustained ventricular tachycardia immediately after the operation. A small viable zone of myocardium was usually observed adjacent to the mitral annulus, ranging from zero to 3.5 cm. Severe diffuse pericardial hemorrhage was found in 1 patient who died because of arrhythmia (patient 4) in the early postoperative period. In 2 patients who died late due to cardiogenic shock, the autopsy finding revealed large pericardial hematoma juxtaposed to the surgical incision; the adjacent myocardial wall was fibrotic and thin probably because of squeezing, resulting in ischemic lesions (patients 5 and 6). The mean LV cavity diameter ranged from 3.2 to 5.7 cm, and the mean thickness from 0.8 to 1.8 cm. The RV thickness ranged from 0.3 to 0.7 cm, and nine hearts showed moderate to severe dilatation. Seven hearts had macroscopic endocardial fibrosis, and five had myocardial and nine pericardial fibrosis, but only two hearts (patients 5 and 7) had all of these findings. In the histologic analysis, moderate to severe hypertrophy, mild to moderate interstitial fibrosis, and mild myocytolysis were detected, but none of these correlated with the cause of death.



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  		Fig 1. (Patient 2) Transversal section of the heart. Myocardial infarction adjacent to the surgically resected area (arrows) at the lateral left ventricular wall. Both papillary muscles are also infarcted (arrowheads). Note the smaller left ventricular cavity compared with the right one.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
PLV has been proposed as an alternative for the treatment of severe heart failure, mainly in IDC. Although heart transplantation is the main choice for these patients, problems such as lack of donors, social problems, and infections because of immunosuppression therapy have limited the use and the success of this procedure.

However, because the morbidity and mortality caused by PLV are too high, it is very important to better understand the mechanisms and changes that this procedure brings about in the patient. In previous studies, we compared patients with good and bad outcome, studying clinical and pathologic factors; the unique factor related to the outcome was the myocardial fiber diameter [12, 13]. For this reason, we decided to study in more depth the pathologic findings, which are only completely available in the autopsy specimens. Therefore, in this study we analyzed 12 hearts from patients who had undergone PLV, 11 hearts obtained from autopsy and one from heart transplantation in a patient who had severe heart failure after PLV, seeking to identify elements involved in the poor outcome.

The cause of death in most of the patients was cardiogenic shock. This is also the main cause of death in IDC patients who do not undergo this procedure, following the natural history of the disease. Three hearts exhibited severe pericardial hemorrhage (patients 4, 5, and 6); in none of them was this complication the main cause of death, but it may have contributed to the bad outcome. These hemorrhages contributed to the very high weight found in these patients, especially patients 4 and 5, and it was impossible to separate the blood from the heart and determine the real weight of these hearts. However, the other cases did not have this problem. In patient 5, the pericardial hemorrhage compressed the myocardial wall, which had chronic ischemic lesions. Patient 7 died because of coagulopathy, characterized by thoracic hemorrhage. No morphologic signs of infection were seen in the autopsy of any of the hearts, which indicates that PLV has no more risks than other cardiac procedures.

The mean LV diameter ranged from 3.2 to 5.7 cm. We did not find a correlation between the remaining LV diameter and cause of death. An area of MI was found surrounding the surgical incision in all hearts. These lesions could be related to either heart failure or arrhythmia present in patients who underwent PLV. Concerning heart failure, it is noteworthy that the average percentage of MI in the left ventricle was 22%. This level of percentage area of MI usually does not represent a size large enough to cause death, but in the present patients, considering the association between dilated cardiomyopathy and postsurgical status, such a complication may represent an important factor that could have contributed to the heart failure. To avoid a great infarcted area, special attention to the coronary artery anatomic distribution needs to be observed during the surgical procedure. In this regard, the identification of the marginal branches and their previous ligation to the myocardial resection for area delimitation may contribute to limit the residual infarction.

The presence of a small area of viable myocardium between the infarction and the mitral valve could explain the frequent ventricular arrhythmia experienced by these patients, as the preserved myocardium in this region could be an area of reentrance of the electric stimuli [8]. However, we did not find any difference in such regions between patients who died with or without arrhythmia. On the other hand, an interesting finding in our study was that of the 4 patients who had infarction of both papillary muscles, 3 had episodes of severe ventricular arrhythmia. Additionally, in all patients who died because of arrhythmia, the autopsy revealed infarction of both papillary muscles. These data suggest that there is some relation between arrhythmia and infarction of both papillary muscles. This infarction is probably associated with the performance of a myocardial resection as large as possible between the papillary muscles, leading to the interruption of supplying coronary branches. The augmentation of the myocardial resection in the LV apex, associated with a less important resection at the level of papillary muscle implantation, could prevent this complication. In this regard, it is also important to note that the low incidence of postoperative arrhythmia seems to occur in patients who underwent PLV associated with papillary muscle reimplantation [5].

The presence of mitral valve replacement or repair was of no influence in the survival or in the extension of the infarcted area. There was also no correlation between papillary muscle infarction and valve replacement, as 5 patients with infarction of one or both papillary muscles had only valve repair, and 1 patient with valve replacement had no infarction. Another important finding was that 10 of 12 hearts weighed more than 500 g, reinforcing our previous data that myocardial hypertrophy is one of the most important aspects related to a bad outcome in this type of surgical procedure [12, 13].

By analyzing the morphologic findings in hearts of patients who died or were submitted to heart transplantation after PLV, we showed that MI at the borders of surgical resection, present in all cases, either associated or not to pericardial hemorrhage and severe myocardial hypertrophy, could at least be responsible for such bad outcome. These lesions are possibly related to the resection of coronary branches during surgery. Arrhythmias were a major feature in the cases in which the infarction affected both papillary muscles.


   Acknowledgments
 
We thank FAPESP for financial support (96/01075-7).


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Batista R.J.V., Santos J.L.V., Takeshita N., et al. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Card Surg 1996;11:96-97.[Medline]
  2. Bombonato R., Bestetti R.B., Sgarbieri R., et al. Initial experience with partial left ventriculectomy in the treatment of terminal cardiac insufficiency. Arq Bras Cardiol 1996;66:189-192.[Medline]
  3. Batista R.J.V., Santos J.L.V., Nery P., et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634-638.[Abstract/Free Full Text]
  4. Dreifus G., Al Ayle W., Leroy G., et al. Left ventricular reduction (Batista). Arch Mal Coeur 1997;90:1521-1525.
  5. McCarthy P.M., Starling R.C., Young J.B., et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997;114:755-765.[Abstract/Free Full Text]
  6. Angelini G.D., Pryn S., Mehta D., et al. Left ventricular volume reduction for end-stage heart failure. Lancet 1997;350:489.[Medline]
  7. Bocchi E.A., Bellotti G., Moraes A.V., et al. Clinical outcome after left ventricular surgical remodeling in patients with idiopathic dilated cardiomyopathy referred for heart transplantation. Circulation 1997;96(Suppl II):165-172.
  8. Katsumata T., Westaby S. Left ventricular reduction operation in ischemic cardiomyopathy. Ann Thorac Surg 1997;64:1154-1156.[Abstract/Free Full Text]
  9. Moreira L.F., Stolf N.A.G., Bocchi E.A., et al. Partial left ventriculectomy with mitral valve preservation in the treatment of patients with dilated cardiomyopathy. J Thorac Cardiovasc Surg 1998;115:800-807.[Abstract/Free Full Text]
  10. McCarthy J.F., McCarthy P.M., Starling R.C., et al. Partial left ventriculectomy and mitral valve repair for end-stage congestive heart failure. Eur J Cardiothorac Surg 1998;13:337-343.[Abstract/Free Full Text]
  11. Suma H., Isomua T., Horii T., et al. Two-year experience of the Batista operation for non-ischemic cardiomyopathy. J Cardiol 1998;32:269-276.[Medline]
  12. Higuchi M.L., Moreira L.F., Silvestre S.M., et al. Myocardial fiber diameter as a prognostic index of outcome of patients submitted to partial left ventriculectomy [Abstract]. J Am Coll Cardiol 1998;31(Suppl C):383.[Abstract/Free Full Text]
  13. Stolf N.A.G., Moreira L.F., Bocchi E.A., et al. Determinants of midterm outcome of partial left ventriculectomy in dilated cardiomyopathy. Ann Thorac Surg 1998;66:1585-1591.[Abstract/Free Full Text]
Accepted for publication August 17, 1999.


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