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Ann Thorac Surg 1996;62:681-682
© 1996 The Society of Thoracic Surgeons
DR ROLAND HETZER (Berlin, Germany): I am most grateful to have the opportunity to comment on this very important contribution of Dr Frazier and associates which, in my opinion, marks the opening of a promising new era in the treatment of patients with chronic myocardial failure. Our own experience strongly supports the expectation of recovery to normal function in the hearts of many patients who as of now we had considered transplant candidates as the only option. Up to now we have explanted left ventricular assist devices in 4 patients after complete or near complete cardiac recovery after prolonged support of between 160 and 347 days. All 4 are men, ranging in age from 38 to 58 years. All had the clinical findings of dilated cardiomyopathy that had developed years after viral myocarditis in 3 and chronic alcohol intake in 1. At the time of assist implantation, all were on maximum intravenous inotropic support and death was expected to occur within days. Three received a Novacor system and 1 a pneumatic TCI HeartMate system.
At time of assist implantation, cardiac index was less than 1.8 L • min-1 • m-2 in all, left ventricular diastolic diameter was between 69 and 72 mm, left ventricular ejection fraction was estimated at less than 0.15. During the following months and on repeat pump-off studies, left ventricular diastolic diameter decreased to normal sizes, between 52 and 55 mm, and left ventricular ejection fraction increased to between 0.48 and 0.55.
These parameters have not shown relapse of failure since assist explantation between 4.5 and 11 months ago. On the contrary, there has been a slight further improvement during follow-up. The pumps were explanted leaving both inflow and outflow cannula in place.
Beta-1-receptor autoantibodies were found at high levels at the time of assist implantation. They decreased and finally disappeared in the same time course as ventricular function recovered and have not reappeared since. Apart from their assumed role in the pathogenesis of cardiomyopathy, we consider monitoring these antibodies important for the judgment of the state and the potential of the myocardium to recover.
All 4 patients are fully rehabilitated. The younger 2 men are back to work. The others enjoy active retirement. Their sole medication consists of angiotensin-converting enzyme inhibitors. Among the 10 patients presently on assist devices for up to 600 days in our institution and at home, 4 more have displayed promising cardiac recovery and are considered candidates for pump removal.
Of course, there is a multitude of questions to be answered, in particular relative to the long-term durability of the success. I would like to ask Dr Frazier three questions:
The most important, obviously, is are there any biochemical or functional markers that will predict the potential of myocardial recovery before assist implantation? In such a case, assist application would be justified at an earlier stage of the disease.
Second, can the speed and the degree of recovery on assist be related to the size of the hearts and the type of disease?
And third, do you have any thoughts about technical modifications of the pumps and the cannula that would facilitate pump removal without jeopardizing the hearts and the patients?
DR FRAZIER: Thank you, Dr Hetzer. It is important for researchers in the United States to know the clinical results of our European colleagues. I believe a prospective study of preimplantation markers that may predict recovery is needed. As Dr Hetzer's and my group have shown, there are patients who will recover some ventricular function after receiving a temporary ventricular assist device. I believe that using norepinephrine levels as a marker of recovery may be simpler than monitoring the beta-1-receptor autoantibodies, as is done in Germany, but this remains to be shown. As we continue our research, we hope to study the potential of the various markers of heart failure and their clinical applicability.
We have been better able to analyze tissue from patients with idiopathic rather than ischemic cardiomyopathy. The plug in patients with ischemic cardiomyopathy is generally scar tissue, and analysis of such samples has not been very revealing. Our impression thus far is that heart size and idiopathic disease are the factors most likely to benefit from prolonged ventricular unloading.
I also think Dr Hetzer has raised a good point about the technical modifications necessary to make the device easily removable. This subject was not considered during the late 1970s and early 1980s, when work on these assist devices began. Technical improvements may have to be made to make explantation easier, and in particular, to allow us to remove the cannula altogether from the ventricle. With the cannula removed, the need for anticoagulation for the device would be minimized.
Again, I appreciate the important work Dr Hetzer has done and his willingness to share his results with us.
DR PATRICK M. McCARTHY (Cleveland, OH): Once again Dr Frazier is to be congratulated for his pioneering efforts in the implantable left ventricular assist device field. The concept of left ventricular assist device weaning is one that he has talked about and thought of for several years. In our experience we have also reviewed histologic findings and found many of the same things that Dr Frazier is reporting with the resolution of myocytolysis. We were, however, concerned to find that there was increasing fibrosis, and many of the acute changes seem to turn to scar with time. It may be the difference in the patient population in that 75% of our patient population have ischemic cardiomyopathy. I have three questions for Dr Frazier:
First, do you think that there will be a difference in weaning the ischemic cardiomyopathy patients versus those with myocarditis, alcoholic cardiomyopathy, or dilated cardiomyopathy?
The second question is the most important: can we predict before left ventricular assist device removal if the resolution of the acute process will be sustained?
Third, how can we decide what is the best way to wean the pump?
DR FRAZIER: The data we have indicate, as I have said, that patients with idiopathic cardiomyopathy seem to benefit the most from ventricular unloading. In patients with ischemic cardiomyopathy, functional myocardium is present, but scattered. In selected patients with ischemia, however, particularly those with more localized fibrotic changes in the ventricle, we may see enough improvement in the remaining heart muscle to allow us to remove the device. The ability to predict recovery is a problem that we need to analyze. The predictive studies done by Dr Hetzer in Berlin have been impressive. I think that norepinephrine levels provide a simpler method of determining the systemic response to heart failure, but they have not been used as yet to predict device removal.
As far as weaning the patient, we propose a procedure similar to that used by Dr Hetzer's group, which is to measure the varying effects and the varying parameters of heart failure as weaning progresses. Flow rate can be controlled by both of the devices in clinical use today. Assessing native ventricular recovery during gradually decreasing device support will help us determine which patients can have the device safely removed.
Many of the clinical questions that I have considered have been addressed by Dr Hetzer, who has a patient alive 1 year after left ventricular assist device removal. Patients in Japan have also been treated successfully. How long should this support be sustained? Only further research and experience can provide the answer. However, it would clearly be beneficial to avoid transplantation whenever possible, particularly among young patients. As all of us are aware, the patient survival rate 1 year after transplantation is excellent, at 5 years the rate is good, and at 10 years, the survival rate is about 50% to 60%. Such a prognosis is not very appealing for a 30-year-old. I think it would be a much better situation for young patients to keep their own hearts, even if they remain in New York Heart Association functional class II and require on-going medical treatment.
DR MEHMET OZ (New York, NY): I echo Dr McCarthy's comments about the major force Dr Frazier has played in guiding us in this field. We have had 2 patients in whom we have explanted devices. The first was an 18-year-old idiopathic cardiomyopathy patient who had an ejection fraction of 0.40 to 0.45 at the time of device explantation; about 5 months later he was dead as his heart progressively dilated. And he had low norepinephrine levels at the time of device explantation. The second patient had ischemic cardiomyopathy. He came for his device insertion 1 week after coronary artery bypass grafting with an ejection fraction of 0.15. We were forced, due to infection of the device, to remove it; he did not receive a transplant. His ejection fraction about 8 months after explantation is 0.55 and he is completely symptom free.
I mention these two anecdotes to ask your advice on two issues. First, are there additional operative interventions you would embark upon at the time of left ventricular assist device implantation, such as coronary bypass grafting into an area that you are not sure is viable or suspect is not viable, or valve repair or the like?
And the second question is, very specifically, at this moment would you explant a device electively from a patient and, if so, what would guide you in that?
DR FRAZIER: Of course, 2 patients is a small number. I believe a prospective, multicenter trial is warranted to recruit the number of patients necessary for statistically significant data. The first patient I know about, who was at Columbia, was not weaned. However, I think a weaning period is important. Then, after the device is removed, patients will probably require treatment for heart failure. Rest is an important factor in the recovery of ventricular function. Clearly, in patients with acute ischemia or in patients who have had an acute ischemic event and could benefit from unloading, a potential for recovery exists. These patients may be suited for a clinical trial. Reparative cardiac operation should be undertaken when the device is implanted.
Measuring norepinephrine levels may be the easiest way to assess recovery, although antibody analysis has been predictive in Dr Hetzer's patients. I must add that our patients have been supported much longer than his 4 patients. The duration of support in patients of the Cleveland group has also been much shorter than those presented here. As I have discussed, Dr Burch found that the duration of rest affected patients' recovery potential, as well as their degree of ventricular dilatation and duration of symptoms.
Related Article
Ann. Thorac. Surg. 1996 62: 675-681.
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