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Ann Thorac Surg 2001;72:S2243-S2244
© 2001 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Beth Israel-Deaconess Medical Center, 110 Francis Street, Suite 2A, Boston, MA 02215, USA
e-mail: slevitsk{at}caregroup.harvard.edu
I really want to compliment Dr Khuri, who has worked so hard over the years, beginning first with the mass spectrometer and now finally providing a functional probe with which one can really investigate myocardial acidosis. The probe allows us to look at a surrogate of anaerobic metabolism. Normally, myocardial metabolism is aerobic and myocardial pH remains within a normal range except, perhaps, in areas that are severely ischemic in association with coronary artery disease. We know from early physiologic studies conducted in the 1960s that, when we clamp the aorta, myocardial metabolism reverts from the aerobic to anaerobic state within 6 seconds, as high-energy phosphate moieties and glycogen stores are depleted and intracellular acidosis ensues. The advent of cardioplegia has provided buffering agents to prevent or partially ameliorate intracellular acidosis, hypothermia presumably to extend safely the time of surgically induced ischemia, and potassium to effect very rapid diastolic arrest. It is important to achieve an arrest within the first 1 or 2 minutes of aortic clamping to slow down the depletion of metabolic substrates and to delay the onset of acidosis.
Let me first answer the questions I’ve been asked. First, is hypothermia useful or injurious to the myocardium? Even though I still use hypothermia in the clinical setting, there is a real question as to whether putting cold water or ice slush on the surface of the heart is injurious to the myocardium. Is myocardial temperature measurement useful? I have not found it to be so, and have stopped using it. Is there any role for topographic thermography? I have not used this technology, but if temperature measurement has not been found to be important, why would one want to use a costly technology that adds to the complexity of temperature measurement?
This review demonstrated that temperature monitoring was not important. Second—and this is the meat of this study—it showed no correlation between temperature and the volume of cardioplegia and myocardial pH. In the absence of these correlations, and since myocardial pH is an important surrogate for anaerobic metabolism, why should we spend a lot of time worrying about myocardial temperature or developing arcane equations to determine the volume of cardioplegia to be delivered?
It shows, in the nonworking heart model, that myocardial oxygen consumption becomes infinitesimal once very low myocardial temperatures are achieved. Although, in the clinical arena, I have been using cold cardioplegia, I really do not think it is necessary. Tepid cardioplegia without topical cooling is probably just as effective. I have not yet mustered the courage to use it, though.
Our laboratory has previously shown the results of the comparative measurement of high energy phosphate moieties in three types of myocardial protection techniques during 60 minutes of ischemia followed by 30 minutes of reperfusion: (1) the so-called Houston technique, which was very common in the early 1970s, and which involved warm ischemic arrest induced by aortic clamping with no subsequent myocadial protection; (2) intermittent aortic cross-clamping, in which the aorta would be clamped intermittently for 15 minute periods followed by 3 minutes of reperfusion when the aorta would be unclamped; (3) Shumway’s technique of regional hypothermia, which was an advance over these other techniques; and finally (4) multidose potassium cardioplegia. There was no difference in the preservation of high-energy phosphate moieties (HEP) in the normothermic heart with either continuous or intermittent ischemia over the same time period. Regional hypothermia resulted in mild preservation of HEP, and multidose potassium cardioplegia resulted in significant preservation of HEP.
A great deal of work in this field has come out of Toronto, and Dr Richard Weisel should be recognized as a major contributor to this work. The Toronto group examined the question of the optimal cardioplegic temperature. In a randomized study, they compared antegrade and retrograde cardioplegia, and cold (8°C), tepid (room temperature) and warm (37°C) cardioplegia. Their results varied widely. When left ventricular stroke work was used as a measure of validity of a method of cardioplegia, antegrade warm resulted in the greatest decrease in left ventricular function, and tepid antegrade cardioplegia resulted in the best protection. Warm antegrade and retrograde cardioplegia, however, were interrupted 26% to 29% of the total ischemic period to provide adequate visualization during construction of the distal coronary anastomosis. Therefore, in reality, the heart was subjected to unprotected warm ischemia during this period of time. Such were the problems associated with the warm continuous cardioplegia technique that was popular in the early 1990s.
Another study by Dr Richard Engelman and associates examined the optimal cardioplegia perfusion temperature. Cold, tepid, and warm cardioplegia were compared, again using both antegrade and retrograde delivery systems. This was a clinical study that showed tepid cardioplegia to be associated with decreased stroke rate and decreased use of blood products. Warm cardioplegia was associated with a decrease in extubation time but an increase in fibrinolysis. Cold cardioplegia was associated with an increase in extubation time and an increase in length of stay.
In my critique of Dr Dearani’s study, I have several questions. First, what is a definition of adequate myocardial protection? If a patient goes to the operating room with a heart beating and not in cardiogenic shock or requiring inotropic agents and we perform a technically adequate operation, the patient should leave the operating room in as good or better condition and certainly without the need for inotropic or mechanical assist device support. If he does not, then we have made a mistake, either in technique or in myocardial protection. Since technical mistakes are probably infrequent these days, the major culprit is inadequate myocardial protection. So how do we measure the adequacy of myocardial protection in the operating room? Clinically, I believe that if you have to defibrillate the heart during reperfusion you have probably injured the heart, although this has not been proved yet. It is a subjective feeling based on the observation that the heart usually defibrillates spontaneously when the surgeon is secure about the adequacy of myocardial protection during the course of the operation. The use of inotropic drugs is another way with which one can assess the adequacy of myocardial protection. If patients come to the operating room without inotropic support, why should they be on these agents when they leave the operating room? The use of inotropic support, I believe, is a marker of the failure of cardiac surgery, whether the failure is technical or whether it is a failure of myocardial protection. Inotropic drugs should not routinely be used postoperatively because they increase myocardial oxygen consumption. This can lead to adverse outcomes in patients with incomplete revascularization, since these patients are left with ischemic segments that are vulnerable to increased myocardial demand. The use of inotropic drugs may aggravate the ischemic insult in these segments. The need for postoperative use of intraortic balloon counterpulsation is also reflective of inadequate myocardial protection.
My second question is, what do you do when the myocardial pH decreases? I believe the pH probe is a very good measure of intracellular acidosis. But the authors have just told us that it doesn’t make any difference if you throw a little more cold water on the heart, or if you give more cardioplegia; the final pH is not altered. So, how useful is this information?
In the study, the authors used only antegrade cardioplegia. I would have been happier if they had used retrograde cardioplegia. I think that in a patient undergoing a combination of valve replacement and coronary artery revascularization, antegrade administration is less likely to get the cardioplegic solution into myocardial segments subtended by stenosed coronary arteries. I am also uncertain why blood cardioplegia resulted in lower myocardial temperatures, or how knowledge of pH helped to determine the volume and the frequency of cardioplegic administration. So, while the pH probe is a very useful method of measuring intracellular pH, the next question is what are you going to do with that information?1
Footnotes
1 Editor’s note: This question was answered by Dr Khuri in his discussion of the paper by Khabbaz and colleagues elsewhere in this volume (Ann Thorac Surg 2001;72:S2234–5). 
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