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Ann Thorac Surg 1998;66:S25-S28
© 1998 The Society of Thoracic Surgeons
Doctor Edmunds, do you have an intraoperative cocktail of some sort, perhaps consisting of steroids or other agents, that you use to minimize the inflammatory effects of cardiopulmonary bypass and open heart surgery?
DR. L. HENRY EDMUNDS (Philadelphia, PA):
I really do not at this point. I am afraid of steroids, because their use is associated with an increase in the incidence of infection. Also, there are some studies that show steroids do not have very much antiinflammatory effect acutely in cardiopulmonary bypass. Of course, patients undergoing heart transplantation are all loaded with steroids.
QUESTION FROM THE AUDIENCE:
Do you not think that steroids are beneficial?
DR EDMUNDS:
The Mayo Clinic studies showed some benefit. But there is another study that showed no benefit with methylprednisone, so I think the issue is still undecided. I think steroids do reduce complement, but the role of complement probably is not as important as we formerly thought. I see the neutrophil as the major culprit; Ed Verrier sees the endothelial cell. We probably are both half right.
DR KENNETH M. TAYLOR (London, England):
I agree that the issue of steroids needs to be further examined. But I think that we will be better able to evaluate the role of steroids or other therapies as we increasingly understand the mechanisms that produce the inflammatory response. I think that perhaps we are reaching the stage at which we can define protocols to look at protease inhibition, or steroids, in terms of the leukocyte–endothelial cell interaction. We did not have that level of understanding of the underlying mechanisms when steroids first came into use, so many people used them just because it seemed a good idea at the time. But rather than just throw out the concept of steroids, our responsibility now is to investigate the effects of their use in the modern context and actually demonstrate whether they have a specific effect on the inflammatory responses we are trying to inhibit.
DR EDWARD D. VERRIER (Seattle, WA):
There shortly will be a paper presented on the use of steroids in cardiopulmonary bypass in infants and children. It makes the point that the effects are partially dependent on the timing of when they are given. These investigators have been able to show some benefit.
DR EDMUNDS:
A steroid is a very nonspecific agent. The research now under way is trying to identify very specific inhibitors of the inflammatory response. We first have to understand the main actors responsible for this response, because we want to selectively and specifically inhibit these actors. I think we are on the threshold of being able to do that. With the number of researchers now interested in this challenge, and the major companies supporting their work, this probably will come about within the next decade.
QUESTION FROM THE AUDIENCE:
Here’s a very practical question. Do you retransfuse pleural chest-tube drainage postoperatively?
DR EDMUNDS:
No.
DR JEFFREY B. RICH (Norfolk, VA):
Sometimes.
DR EDMUNDS:
I modify my response. If there is a large volume of drainage, I will take the patient back to the operating room.
DR HENDRICK B. BARNER (St. Louis, MO):
I did that once, but I have not done that for 8 years.
DR TAYLOR:
If I had chest-tube drainage, I would not retransfuse it.
DR VERRIER:
I think there are times when you have to, depending on the amount of bleeding. But analysis of that fluid shows that it contains a huge amount of cytokines, and we know that cytokines are tremendously important in activating blood components. So if you can avoid retransfusing the drainage in routine cases, you will decrease the inflammatory response to some degree.
QUESTIONS FROM THE AUDIENCE:
Is there any significant inflammatory response to external ventricular assist devices, such as left-heart assist devices or intraaortic balloon pumps? And what is the role of heparin in minimizing the response, if it exists?
DR VERRIER:
There is a great deal of information about assist devices that will be emerging in the next few months, particularly in relation to the Heartmate and the Novocor devices. The Heartmate is being analyzed because it is a membrane that activates the inflammatory response so that everything adheres to it. So you get this tremendous reaction to it initially, and then it declines. That is why you do not have to heparinize patients over the long term with the Heartmate. But another reason almost all patients on the Heartmate experience a very profound coagulopathy is that the Heartmate causes NF-ß and endothelial cell activation.
As we all know, if you put a patient on an Abiomed for 2 weeks, you end up with multisystem organ failure. Although the Heartmate will cause an inflammatory response in the early phases after insertion, that response is important to the device’s effectiveness. But one of the reasons the Aviamed is not a long-term device is that ultimately the systemic inflammatory response catches up and you end up with multisystem organ failure.
QUESTION FROM THE AUDIENCE:
Do heparin-coated circuits remove AT-III?
DR EDMUNDS:
No. Jim Anderson actually measured this in a study we did jointly. Heparin-coated circuits increase the binding of AT-III on the surface fivefold. In the normal reaction when a circuit is not heparin-coated, heparin is released from the combination of thrombin and AT-III, so the heparin can catalyze another reaction. But when you have AT-III on the surface and it combines with thrombin, that is the end of it, because the heparin cannot get loose. The preponderance of evidence now is that the heparin-coated circuit does not reduce the circulating thrombin.
And I do not think that you can use heparin-coated circuits to avoid heparinization. Bypass produces thrombin, and the longer the time on bypass, the more thrombin produced. And once the pump clots, you have lost a patient. So go ahead and give heparin. It is not ideal, but we can deal with it. I disagree with those who are using half-dose heparin with heparin-coated circuits. Although the Boston University group shows some reduction in the inflammatory response, that is only one study, and the remaining studies are less convincing. And I think that the downside is just too dangerous.
QUESTION FROM THE AUDIENCE:
With more minimally invasive surgery being used, there has been some return to using smaller venous cannulas, with suction now applied to the venous reservoir. Will this increase blood damage, and thereby increase the inflammatory response?
DR TAYLOR:
I suppose that theoretically it is possible, but my guess is that in the context of all the other mechanisms activating the inflammatory response, the contribution of shifting from conventional venous cannulas to the smaller ones used with pump assistance is unlikely to make very much quantitative difference.
QUESTION FROM THE AUDIENCE:
Suppose you had a patient in the coronary care unit with unstable angina who now is going to have an urgent bypass. The patient’s platelet count is 80,000, on heparin. How do you manage a patient who you suspect has heparin-induced thrombocytopenia?
DR VERRIER:
That is a difficult problem right now. Ancrod and other alternative drugs are very difficult to come by. There are a few experimental drugs currently under investigation. I think it is particularly important to determine whether or not a patient has the antibody, if you have the luxury of being able to do so. If the patient has the antibody, then you have to use something other than heparin, for with heparin the patient will not stop bleeding. If the patient does not have the antibody, there are those of us who believe that you can give the patient heparin and follow that with lots of platelets. But it is a very difficult problem if the patient truly has the antibody.
QUESTION FROM THE AUDIENCE:
Do you use preoperative testing to decide whether to use aprotinin or another protease inhibitor, such as Amicar (
-aminocaproic acid) or tranexamic acid?
DR RICH:
I do not use either aprotinin or Amicar for routine cases. But the more coagulopathic I consider the patient to be and the more I want to stop bleeding, the more likely I am to choose aprotinin.
DR TAYLOR:
Amicar and tranexamic acid have not really become much of a part of UK practice. And I still remain somewhat skeptical with regard to the studies that demonstrate effectiveness for these agents. I am not fully convinced that their effectiveness has been assessed on a comparative basis in serious cases, such as those involving septic endocarditis or major redos.
QUESTION FROM THE AUDIENCE:
Doctor Barner, what method do you use when you do a preoperative Allen test? Do you use pulse oximetry or have your test result confirmed in the vascular laboratory? And how bad does the result have to be for you not to use a radial artery?
DR BARNER:
I do the test when I see the patient the night before the operation. I occlude both arteries at the wrist, and have the patient vigorously open and close his hand 20 times. Then I release the ulnar artery, and count the seconds to capillary refilling of the skin of the palm and digits. If it is 10 seconds or less, we harvest the radial artery; if it is greater than 10 seconds, we do not. We do not do any other testing.
In our series of more than 600 patients, we found 4.4% with a bilaterally positive test requiring that we not use a radial artery. We usually harvest the nondominant radial artery, but with patients who have unilateral positivity we will harvest the dominant radial artery, and we have not seen any problems with that. We have harvested the dominant radial artery in about 65 patients.
DR VERRIER:
We do not feel quite as comfortable with just doing the Allen test. So, for a while we used the vascular laboratory, but that proved too costly. Now we still do the Allen test but we also fairly routinely use a small Doppler unit in the operating room to determine whether the palmar arch is patent before starting to harvest a radial artery. Actually, there are a variety of techniques that can be used to determine patency. Some people use a portable plethysmograph.
QUESTION FROM THE AUDIENCE:
Doctor Rich, in the data that you reported from your IMAGE study, was there any information on stroke rates?
DR RICH:
There was no difference in stroke rates between aprotinin and placebo.
QUESTION FROM THE AUDIENCE:
Doctor Verrier, what has been your experience with systemic inflammatory response as related to the use of leukocyte filters? If you have not used them, what do you think of them?
DR VERRIER:
There has been some benefit shown with their use, both experimentally and in some clinical studies in both children and adults. We have found a substantial reduction in neutrophil count when we have used leukocyte filters in the laboratory, but not to the same extent as when using something like monoclonal antibody (MoAb) 60.3, which is an antibody that completely blocks the CD-11/CD-18 complex on the neutrophil so that it cannot adhere. I think the concept is a good one, but the problem is that the available clinical studies have not been very scientifically rigorous, with most trials not blinded and with questionable end points. We actually are now engaged in a blinded trial.
QUESTION FROM THE AUDIENCE:
What are your current thoughts on the use of aprotinin in patients undergoing deep hypothermic circulatory arrest with respect to its effects on cerebrovascular accident incidence or organ hypoperfusion?
DR RICH:
I do not use aprotinin for patients undergoing deep hypothermic circulatory arrest.
DR TAYLOR:
We do use aprotinin in the small number of cases in which we use deep hypothermic circulatory arrest. I think caution was justified after Dr Kouchoukos and the St. Louis group first raised concerns about its use in this circumstance. But other studies since then have been reassuring, such as the positive experience reported in a large series by Craig Smith of New York. But I do think that because deep hypothermia involves potential modifications to the conventional hematologic changes that occur, the issue should be looked at in more detail than perhaps it has. So I would not argue strongly with those of you who still feel uneasy just now about using aprotinin in deep hypothermic circulatory arrest.
QUESTION FROM THE AUDIENCE:
Doctor Barner, is the right coronary artery an important enough vessel to warrant a third arterial conduit harvest, assuming that you have used two arterial conduits to revascularize the left side?
DR BARNER:
I do not think anyone knows the answer to that. Obviously, this is a patient variable. In some patients, the coronary artery is the second most important vessel, and the second arterial conduit should go to the right coronary artery rather than to the circumflex system. But I think that how you manage that third coronary artery depends on your philosophy about the use of arterial conduits. With the T-reconstruction that Dr Tector and I use, we can revascularize the entire heart with two conduits. But although that is the way we approach that situation, I am not in a position to say that is the way it ought to be done.
QUESTION FROM THE AUDIENCE:
Professor Taylor, have magnetic resonance imaging images been done on patients after major noncardiopulmonary bypass procedures, such as carotid artery operation or abdominal aortic aneurysm repair?
DR TAYLOR:
We used controls in our early studies, but not patients having carotid operation because the issue of interruption of the cerebral circulation might compromise the study. But in our major abdominal vascular procedures and major general surgical procedures, patients do not show acute brain swelling.
QUESTION FROM THE AUDIENCE:
Is pulsatility relevant to the maintenance of effective cerebral blood flow?
DR TAYLOR:
That was the first area of cardiopulmonary bypass pathophysiology that we investigated about 20 years ago. We certainly convinced ourselves that pulsatile flow offers superior blood flow delivery, and the argument for it is hemodynamically sound, so we have used it routinely ever since in our clinical practice.
QUESTION FROM THE AUDIENCE:
Doctor Rich, have you ever had a case of late tamponade from retained, unlysed clot after the use of aprotinin?
DR RICH:
No.
DR ANDREW S. WECHSLER (Philadelphia, PA):
I think that when using aprotinin as a late strategy for treating postoperative bleeding when it has not been used earlier in the case, you do have to be very aware of the potential for rapid clot formation at a time when the patient may still be bleeding. You do have to be alert to the possibility of tamponade then.
QUESTION FROM THE AUDIENCE:
Doctor Barner, should the radial artery not preferably be anastomosed to the aorta rather than, for example, to the side of the internal mammary artery? And what would be the rationale for doing it one way or the other?
DR BARNER:
There are a number of reasons for doing it either way, and I initially did it both ways. The argument for doing the anastomosis to the mammary artery is that you then do not have to deal with the aorta; you do not have to clamp the aorta except for working on the heart. As I indicated, there is some loss of patency for other free arterial circuits when relocated to the aorta. Calafiore’s data and then Tector’s experience were instrumental in leading me to pursue this approach.
That is not an issue in late reoperations, as then the anastomosis lies in the left chest parallel to and really over the phrenic nerves so that it is totally out of the field. And the anastomosis is done before you go on bypass, at the start of the operation. The real reason for doing the anastomosis to the internal mammary artery is that it adds about 10 cm to the length of the radial artery, or in Tector’s operation, to the right mammary artery. This allows you to graft it to the circumflex system as well as to the right coronary artery system, because you have a 30-cm conduit that will reach around the left side and back of the heart. So the principal reason for doing the anastomosis this way is that it allows you to achieve complete revascularization with two conduits.
QUESTION FROM THE AUDIENCE:
Doctor Barner, do you routinely use a calcium-channel blocker? How do you administer it?
DR BARNER:
I do not use calcium-channel blockers, and I am probably the only one in the world who does not. Taking a page from Ed Verrier’s book, I believe that if you perfectly preserve the endothelium in arterial conduits, the intrinsic mechanisms by which nitric oxide is released at a basal level and released at an elevated level as flow is restored because of shear stress stimulation of the endothelial cells will maintain a vasodilated conduit. There is one caveat, which is that all conduits undergo spasm when you harvest them. I call this harvest spasm, and it occurs routinely to a variable degree. The radial artery develops more resistant spasm than other arterial conduits. So I treat all conduits with intraluminal papaverine, at a dose of 2 mg/mL of heparinized blood. Treated this way, the conduit will dilate when exposed to arterial pressure. It generally takes the radial artery about 10 minutes to dilate; the mammary artery will dilate more quickly.
DR VERRIER:
There is an emerging literature about vasomotor responses in all the conduits that we use, including the inferior epigastric, radial, and mammary arteries. Each is different teleologically, because the blood supply going to the gut differs from the supply going to the chest wall and both differ from that going to the arm. So each conduit has a different biology. And you find different responses for each type of conduit when you test for a variety of different endothelial-dependent and -independent responses. There are variable responses to all of the vasodilators, and even between one calcium-channel blocker and another. The literature now contains reports of this type of test data, indicating which vasodilators are best for which type of conduit. We stopped using papaverine some time ago because our testing of endothelial-dependent and -independent responses showed that it is not a very good vasodilator. Although all vasodilators will vasodilate, we now have an evolving science that provides data enabling us to optimally choose the best vasodilators for specific conduits.
QUESTION FROM THE AUDIENCE:
Professor Taylor, do you think spasm of the large cerebral vessels has a role in postoperative central nervous system injury? Also, what is the time course of resolution of the central nervous system edema that you demonstrated using magnetic resonance imaging?
DR TAYLOR:
We have not looked at the possible role of spasm of the large cerebral arteries, and I am not aware that anyone else has done so. As for resolution of the postoperative cerebral edema, we have not found any edema on 24-hour postoperative magnetic resonance imaging images. Edema is apparent only when magnetic resonance imaging image is taken very shortly after the operation.
QUESTION FROM THE AUDIENCE:
Doctor Barner, is non–insulin-dependent diabetes a contraindication to bilateral thoracic artery grafting?
DR BARNER:
I do not know the answer to that. I used to liberally harvest bilateral mammaries in diabetic patients, but now that I am using the radial artery, I no longer harvest both mammary arteries in diabetic patients because I have an alternative. Clearly, the incidence of mediastinal infection is greater, even in patients with non–insulin-dependent diabetes, and I do not know what is acceptable in terms of that complication.
QUESTION FROM THE AUDIENCE:
Doctor Rich, what is the current recommendation for monitoring heparinization when using aprotinin?
DR RICH:
We monitor heparinization by measuring activated clotting times with kaolin. This probably is the current recommendation. The celite activated clotting time is notoriously unreliable, because aprotinin interferes with the reagents involved in the monitoring. You also can monitor heparinization using the Hep-Con, which measures both heparin concentration and activated clotting time. There are data that suggest that measurement of either is acceptable. If available, measurement with the Hep-Con is preferable to use of the kaolin activated clotting time because it is more accurate, lending a higher level of comfort.
QUESTION FROM THE AUDIENCE:
Is there a relationship between the duration of cardiopulmonary bypass and the extent of neurologic injury?
DR TAYLOR:
There certainly are some studies showing such a relationship. If you think about the mechanisms involved in neurologic injury, particularly in relation to gaseous and particulate microembolism, then clearly the longer the patient is on the pump the greater the potential load for the cerebral circulation.
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