Eur J Cardiothorac Surg 1999;15:12-19
© 1999 Elsevier Science NL
Partial left ventriculectomy – the Batista procedure 1
Randas Batista*
Hospital Angelina Caron, 83, 430-000 Campina Grand do Sul, Brazil
* Tel.: +55-41-367-6505; fax: +55-41-335-8227.
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Introduction
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Heart transplantation is a good option for heart failure, but there are not many organ donors; even in the most developed countries of the world, only 1% of those who need heart transplantation will receive it. The situation is even worse in Brazil. So I would like to discuss a procedure I developed for the 99% of patients who do not have access to heart transplantation, which is the partial left ventriculectomy (PLV). Its concept is that rather than operating on the heart, I am operating on its diameter. If you look at the heart as a bad muscle, it does not make any sense to excise a piece of it in order to make it better because the heart needs more muscle. Why then does the patient improve? It has to do with the diameter.
Nature has been shaping the heart for 100 million years, which is a great deal of experience bringing it to where it is today. The snake heart is very tiny, and if it is placed beside a human heart and a buffalo heart, it is immediately recognized as a snake heart (Fig. 1
). But if a computer image of the snake heart is enlarged to the size of the buffalo heart, you can no longer determine which is which. The ratio of mass to diameter is the same in both hearts. In fact, all hearts have the same ratio of mass to diameter, from the snake to the buffalo to the whale. Everything in nature, from strawberries to oranges to hearts, has the same ratio, regardless of its size.
Thus there is a single formula common to all hearts in nature, which is that muscle mass is 4 times the radius cubed (M=4xR3). A small snake heart is 1 cm and 5 g (Fig. 2
). A human heart is 5 times larger and has 100 times more muscle mass; an ox heart is 10 times larger and has 1000 times more muscle mass. Any heart that is not within this formula simply needs to be returned to it.
Fig. 3
shows a transplanted heart that looks like a normal ox heart from the outside, but cross-sections reveal that it is not (Fig. 4
). For this heart to be normal, either the cavity must be filled with muscle or the diameter must be decreased. Fig. 5
shows what the heart looks if its diameter is decreased. Removing a piece of the heart and decreasing its diameter returns it to its natural state, where the diameter is appropriate for the amount of muscle.
We performed experiments in sheep to determine the importance of the heart's diameter. In a normal heart we split the ventricle in two and added a patch to increase the diameter of the heart (Fig. 6
). What happened? The heart simply stopped and would no longer beat. To cause it to beat again, we excised the patch. So if I were to increase the diameter of a heart by 20%, heart function (ejection fraction) would decrease by 30%. If I were to decrease the heart by 1 cm, the effect would be the same as if I added 1 kg of muscle. That is the importance of the diameter. Fig. 7
is magnetic resonance imaging showing how thick the muscle is in one area and how thin in another. If we bring one edge to the other, decreasing the diameter of the heart, it will beat much better. A dilated heart contracts isometrically, that is, it expends a lot of energy without doing much work. If I reduce it to a size that I can hold in only one hand, the resulting curvature will strengthen the heart's ability to contract.
Two groups from Japan and the Netherlands measured pressure/volume loops both before and after PLV in approximately 120 of my patients by putting pressure and conductance catheters through the apex of the heart or the aortic valve. What did they find? Fig. 8
shows preoperative and postoperative pressure and volume. Before the procedure, the area of work was small and the area of energy consumption was large, which means the heart was doing little work and expending a lot of energy. After the procedure, with the decreased diameter, the area of work was larger and the area of energy consumption was smaller, which means the heart was working much harder and expending less energy. What does this mean? These hearts became more efficient.
What is wall stress? In the large-diameter heart, tension is very high; in the small-diameter heart, tension is very low. I demonstrate this concept by blowing up a rubber glove. The pressure inside the inflated glove, or `balloon,' is the same in both the palm and the finger. But the finger is very soft and the palm is very tense. If I stick a 19-gauge needle in a finger, nothing happens to the `balloon' because the wall tension in the fingers is low. But if I stick the needle in the palm, the `balloon' bursts, and if the heart is very tense, it cannot contract to produce the same pressure. So by making the `balloon' smaller, I decrease the diameter, and with less wall tension now in the palm, I can stick it with a needle and nothing happens. Likewise, the heart with a small diameter does not need much energy to produce the same intraluminal pressure.
A group from Germany measured wall stress in some of my patients both before and after PLV. They fixed wires on the surface of the heart and inserted needles with crystals in their tips transversely into the myocardium (Fig. 9
), so that as the myocardium contracted, the crystals would directly measure wall stress in millinewtons (Fig. 10
). In a distended heart, if the left ventricle is vented and the heart does not flatten, it has enough muscle to contract. However, if the heart does flatten when the wall empties, it does not have enough muscle to be benefited. There are basically three types of connective tissue – interconnecting microfocal, transmural and parallel to the inner surface – and the end result will depend on the type of fibrosis within the muscle (Fig. 11
). In this study, wall stress decreased 43% in the areas with less decrease in diameter, 59% in the areas with more decrease in diameter, and 64% in the areas with the largest decrease in diameter (Fig. 12
). In other words, as the diameter decreased, the associated wall stress was correspondingly reduced. The result of 70 measurements was a total mean decrease in wall stress of 44%. The smaller the diameter of the heart, the less wall stress, like the glove balloon.
Chest X-ray films were taken before and after PLV in a female patient who was very sick and massaged to the operating room. Preoperatively, her ejection fraction was 8% and heart volume 490 ml; postoperatively, her ejection fraction was 25% and heart volume 112 ml. This patient is off medication and doing very well.
Left atrial pressure was measured in a series of patients, and it usually decreased after PLV (Fig. 13
). After PLV, mean pulmonary artery pressure decreases and the stroke volume and cardiac index increase (Fig. 14
Fig. 15
Fig. 16
).
I do not think papillary muscles are very important in ventricular function; if they were, the patient whose specimen is shown in Fig. 17
would be dead. They are important when preserving the valve, but the most important aspect is the ratio of mass to diameter.
A dilated heart in a patient with angina is caused by a mismatch between the oxygen offering and oxygen demand (Fig. 18
). If the oxygen offering is increased, the angina is cured, but the patient will be in heart failure. So instead of increasing the oxygen offering, the oxygen demand should be decreased, which both cures angina and avoids heart failure.
Fig. 19
shows the left ventricle open on the operating table, with the left anterior descending, circumflex, marginal, and posterior descending arteries. All of the diagonal arteries meet the marginal artery and all of the branches from the posterior descending artery also meet the marginal artery. So if there is no coronary artery disease, the marginal artery can be completely excised between the two papillary muscles, and the patient will not only not be harmed but will actually improve (Fig. 20
).
This video demonstrates the principle of PLV. Shown is a patient in end-stage heart disease with swollen ankles, a very large dilated heart, mitral regurgitation, and an ejection fraction of approximately 12–13%. Three-dimensional echocardiography confirmed the large ventricle and the mitral regurgitation, and transesophageal echocardiography in the operating room just prior to the procedure showed a poor-functioning heart, which was also confirmed by the pressure volume loop. However, the muscle was viable, so it was difficult to explain how this patient could be in heart failure with so much muscle. We cut the apex of the heart all the way down to the annulus of the mitral valve, and as soon as we opened the ventricle, we placed suction inside it to avoid clamping the aorta. The ventricle was approximately 3–4 cm thick. How can a heart with a 3-cm-thick ventricle be in heart failure? Because what is wrong is not the muscle but the diameter. The specimen excised was 450 g, including the mitral valve and the papillary muscles, from the left anterior descending artery down to the posterior descending artery. Its width was approximately 16 cm, which means the diameter of the heart was decreased by 5 cm. While the heart was beating, we replaced the mitral valve with the CarboMedics® Prosthetic Heart Valve, with very good exposure through the open ventricle and no cardioplegia. I perform this procedure on the warm, beating heart because I can better evaluate which areas are not beating well and need to be excised. Then I simply sew over and over the ventricle; its thickness can be truly appreciated once the heart has shrunk. No inotropic agents are used, and transesophageal echocardiography performed immediately after coming off bypass showed that the heart was beating much more effectively. Preoperatively, this patient required dobutamine to maintain a pressure of 80–90 mmHg; postoperatively, the patient required Nipride to keep the pressure below 100 mmHg. Her ejection fraction increased from 12% to 63%.
Fig. 21
shows preoperative and postoperative chest X-ray films in a 35-year-old man who was very sick and on dobutamine before having PLV. Prior to the procedure, he could not work; now he is doing very well, working and living a normal life taking only minimal medication. Preoperatively the muscle was hypertrophied with little connective tissue (Fig. 22
). His preoperative ejection fraction was approximately 15%; postoperatively it increased to 40% within 1 week and 50% within 3 months, and now it is 65%.
The largest experience with PLV outside Brazil has been from the Cleveland Clinic. Pat McCarthy presented 53 patients at the 1997 annual meeting of the American Association for Thoracic Surgery. At the same time, they reviewed 74 patients in whom PLV had been performed at several universities throughout the United States (Fig. 23
). In the Cleveland experience, of the 53 patients, 51 had dilated cardiomyopathy. Three patients were not candidates for heart transplantation. Sixty percent were in New York Heart Association (NYHA) class IV, and 44% were status I on the transplantation list. The myocardial oxygen consumption rate was 11.5±4.2, and the norepinephrine level was 855±500. At 6 months to 1 year, the end result was the same with PLV as with transplantation. There was were no hospital deaths, and only one death occurred 3 months postoperatively because of hemorrhagic stroke. In terms of cost at the Cleveland Clinic, placement of a HeartMate device between 6 months and 1 year costs 1 million dollars, heart transplantation during the same timeframe costs a half a million dollars and PLV costs $50 000.
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Fig. 23. Partial left ventriculectomies reported at the American Association for Thoracic Surgery 1997 annual meeting.
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The Texas Heart Institute has had basically the same results. Of 13 PLV patients, nine (69%) survived, 5 in NYHA class I, one in class II, and two in class III. Of ten transplantation patients, nine (90%) survived. New York University performed PLV in 33 patients between June 1996 and April 1997, with five hospital deaths and three late deaths. Postoperatively, 50% were in NYHA class I and 30% in class II. Their initial experience without proper selection of patients (some patients were massaged to the operating room) was poor; the first ten patients at 22-month follow-up had a 33% survival rate (Fig. 24
). However, after improved patient selection, the next ten patients at 13-month follow-up had a 66% survival rate (Fig. 25
), and the last ten patients had an 90% survival rate at 10 months (Fig. 26
). So patient selection plays an important role in the results with PLV.
There are also some scattered cases. Norman Shumway at Stanford operated on the child whose X-ray films are shown in Fig. 27
. This patient was taken to the operating room for a bidirectional Glenn operation, but a PLV and a mitral valvuloplasty had to be performed first, and after the left atrial pressure decreased, the bidirectional Glenn operation could be performed. The patient went home after 2 weeks in good health. Heart transplantation showed poor results in the beginning, but because of Dr Shumway's persistence and perseverance, we are seeing the results we have today. He views heart transplantation with optimism because most experiences are now showing improved results.
My personal experience with PLV in Brazil over the last 14 years is comprised of 580 patients, 75% men, ranging in age from 8 months to 95 years (mean 53 years). All patients were in NYHA class IV with end-stage heart disease and ejection fractions between 3% and 18%. Postoperatively, 10% were in class III, 20% in class II, and 60% in class I. The most common pathologies were ischemic in 30%, valvular in 20%, viral in 20%, and idiopathic in 20%; Chagas' disease was present in less than 10%. We performed some type of associated valvular surgery, either mitral, aortic, or tricuspid replacement, in 90% of patients; coronary artery bypass grafting was performed in 30% and heart autotransplantation in 10%. The most common morbidity was renal failure (20%), followed by arrhythmia (15%) and bleeding (10%). Ninety-five percent survived the procedure, 80% survived the hospital, and 60% survived for 2 years.
In the centers in Brazil that perform heart transplantation, patients on the transplantation list are dead within 2 years without transplantation, and after transplantation, the survival rate is approximately 60% at 2 years. However, if I do not do something to help my patients, they will all be dead within 6 months, and if I perform PLV, 60% will still be alive at 2 years. I think this a reasonably good result, given the kind of patient I have.
In conclusion, the improved NYHA class in all patients means that PLV can serve as a bridge to transplantation. The results are reproducible; in fact, most centers today have better results than mine. It is low cost and increases life span, which gives hope to not only the patient but also the cardiologist. In my environment, PLV helps patients tremendously, because without it they really suffer. And more important than life is the quality of life, so even if the patient dies 6 months later, his quality of life was much better.
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Appendix A
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Conference discussion
Mr S. Westaby
(Oxford, UK): This is always such an exciting presentation. I think identification of which patient to do this operation on is very important. We began to do it in patients with ischemic cardiomyopathy, because that is what is common in Britain, and had good early results, but later, as the scar in the ventricle began to stretch in the ischemic patient, we had late deaths because of ventricular fibrillation. Have you seen this with ischemic patients in Brazil?
Dr R. Batista
: We have seen arrhythmia problems in not only ischemic patients but also valvular patients. Dr Cox, who knows more about arrhythmia than I do, believes that if you cryoablate the remaining part that connects the incision to the mitral valve, it will not cause arrhythmia. He believes the arrhythmia is due to a reentry circle around the scar tissue and that ablation will eliminate the ventricular tachycardia or fibrillation. I do not have a cryo probe, or I would do it. I think it will probably be the solution in the future. But we do not see arrhythmia in only ischemic hearts, so I do not think the arrhythmia is related to the ischemic pathology. We will know more about it in the future. Some patients we operated on already had an automatic implantable cardioverter defibrillator because of arrhythmia. Most patients who had arrhythmia postoperatively had it preoperatively, too. Fortunately, patients in the United States can have implantable defibrillators, but we cannot afford to put $25 000 in these patients' chests in Brazil. So we hope to excise the arrhythmogenic areas. That is why I like to operate on the warm, beating heart, because once I open the ventricle, the scar tissue is easier to identify and excise. I try to leave what looks macroscopically like good tissue.
Audience
: Since visiting you in Brazil and doing the pressure/volume loops, I have performed some PLVs, but I still wonder what we can do about the right side. We always have to plicate the right side. Do I go intra- or extrapapillary?
Dr R. Batista
: In the right side, you are outside both papillary muscles. I usually go from the pulmonary valve down to the right side of the heart. In other words, the papillary muscles remain in place and I excise mostly the roof of the conal part of the right ventricle. So I do not see it as a problem for the papillary muscles because both will be far down in the right ventricle.
Mr S. Westaby
: I think the point about the right heart is important. If you improve left ventricular function, you increase the preload to the right ventricle, which frequently is suffering from the same disease in dilated cardiomyopathy. Have you had problems supporting the right ventricle when you have made the left ventricle better?
Dr R. Batista
: No. The best thing for the right ventricle is to improve the left ventricle, because once you bring the left atrial and pulmonary artery pressures down, you decrease the afterload on the right ventricle. Probably 90% to 95% of these patients have right heart failure with tricuspid regurgitation, and simply plicating the tricuspid and making it competent decreases the oxygen consumption of the right ventricle anyway. So decreasing left atrial and pulmonary artery pressures and restricting the tricuspid, making it competent, helps the right ventricle a lot. And if we decrease the diameter of the right ventricle, it improves even further. Dr Kirklin mentioned in one of his papers that mortality is higher with a transannular patch for tetralogy of Fallot; I agree, but I disagree regarding why. He thinks it is the transannular patch. I do not think that has anything to do with it. The problem is it is a large transannular patch, and when a surgeon makes a transannular patch that large, the right ventricle opens up completely and fails, like the sheep I patched. But the right ventricle is not failing because of the transannular patch, but because it is such a large transannular patch. The transannular patch should only be just large enough to relieve the right ventricle. But surgeons make it too large and the right ventricle fails.
Prof Dr F.W. Mohr
(Leipzig, Germany): How bad can the ventricle be where you can still do the procedure? In other words, what if the patient is on inotropic agents and may require mechanical assistance to further bridge him to transplantation or perhaps just the PLV? Looking at the data from the Cleveland Clinic, they lost all patients in NYHA class IV on inotropic agents, and my personal experience with PLV in emergencies is terrible. If you have a young patient with cardiomyopathy, how bad can he be? I think the right ventricle is very critical. Looking at the success rate of implantable left ventricular assist devices, if the right ventricle is too bad, you will have a problem with univentricular assistance. And if myocardial function is too bad, you may end up with a problem in the operating room. Could you comment on this?
Dr R. Batista
: The single most important thing I want to see preoperatively is chest X-ray film. If the heart is large, I am not afraid. If the heart is small and in heart failure, then you have a problem. A small heart does not have a large diameter, so you cannot make it better by decreasing diameter. So if the patient has a small heart and is in heart failure with pulmonary edema in the emergency room, he will not do well with a PLV. He should be put on a HeartMate, because the PLV will not do any good. On the other hand, if the heart is really large, you do not need to be afraid; you can go after it and be assured of good results.
Dr E. Pattakos
(Athens, Greece): I follow three patients we operated on in July with Dr Batista and they are all doing extremely well. But my colleagues in Washington had one patient who dilated months later and the heart reached the same diameter. Do you follow your patients, and do you see this recurrence? And if it is not valvular, what do you think is the reason for this recurrence in this patient?
Dr R. Batista
: I redid one case 6 months later on purpose. The heart was so big that I was afraid to resect too much, so I resected just enough to avoid diastolic problems, and 6 months later I took out another piece. But I do not have much experience with the heart regrowing in 6 months in patients in whom I resected enough. So if it did recur in that patient within 6 months, it was probably because the wall tension was still high coming off bypass 6 months earlier at the time of the operation. Patients who have very low wall tension, 20 to 30 millinewtons, which is normal, do not regrow. So the surgeon probably did not excise enough.
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Footnotes
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1 Presented at the Sulzer Carbomedics Sixth International Clinical Symposium, Copenhagen, Denmark, 27 September, 1997. 
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Introduction
Appendix A
