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Ann Thorac Surg 1997;63:104
© 1997 The Society of Thoracic Surgeons
Department of Cardiovascular Surgery Hôspital Lariboisière 2, rue Ambroise Pare 75475 Paris Cedex 10 France
This article brings a valuable contribution to our current knowledge of the effects of retrograde warm blood cardioplegia. Using a canine model of extended (3 hours) aortic cross-clamping during which myocardial protection was achieved either by intermittent cold or continuous warm retrograde blood cardioplegia, Kamlot and associates carefully describe changes in levels of high-energy phosphates and lactate occurring during arrest. The main finding is that adenosine triphosphate levels in the right ventricle are less well preserved in the warm cardioplegia group than in cold-protected dogs, whereas creatine phosphate demonstrates an opposite pattern. In addition, electron microscopic analysis showed only reversible injury in both ventricles, without any difference in the scoring system between the two methods of protection.
However, in a surgically oriented perspective, interpretation of these data should take into account several methodologic problems inherent in the experimental design. First, for anatomic reasons, the dog is not the most appropriate species for studying the effects of retrograde perfusion. Furthermore, all animals had normal coronary arteries, no induced ischemia at the time of cardioplegic arrest, and no left ventricular hypertrophy. In keeping with several well-documented clinical reports, it is therefore not unexpected that Kamlot and associates failed to show major differences between the two groups. Surgeons know that if such a difference is to occur, it can only become apparent under more challenging conditions of myocardial protection like evolving myocardial ischemia, depressed function, or left ventricular hypertrophy. Second, the conditions for true aerobic arrest were probably not met because of the (unnecessary) blood dilution with crystalloid cardioplegia according to a 1:4 ratio. Although hematocrit values were not reported, it is likely that this mode of cardioplegia delivery resulted in an insufficient oxygen supply, actually reflected by an increased tissue content of lactate at the end of arrest. Furthermore, maintenance of strict normothermia during "warm" cardioplegic perfusion is not representative of usual practice patterns, which now usually entail allowance for core temperature to drift to tepid values that have been shown to be maximally cardioprotective. Third, results have been exclusively assessed on biochemical markers and ultrastructure. These data are of limited clinical relevance in the absence of a concomitant evaluation of function, which remains the major end point for comparison of myocardial preservative strategies. Kamlot and associates' reference to one of their previous studies in which left ventricular ejection fraction was compared between cold and warm blood cardioplegia does not completely address this methodologic shortcoming. The lack of sampling during reperfusion may have further contributed to missing potentially discriminant information. I am a happy user, not a blinded zealot of retrograde continuous warm blood cardioplegia, and consequently, I completely agree with Kamlot and associates' conclusion that the overall good clinical outcomes associated with the use of this technique can be further improved. Whether this improvement may result from changes in the conduct of aerobic cardioplegia or from completely different conceptual approaches such as on-pump or off-pump beating heart operations remains to be determined. The data presented in this study provide an additional stimulus for clarifying this issue.
Related Article
Ann. Thorac. Surg. 1997 63: 98-104.
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