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Ann Thorac Surg 1996;61:134
© 1996 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery The Boston University Medical Center Hospital Suite B404 88 E Newton St Boston, MA 02118
The introduction of continuous warm blood cardioplegia was heralded as a significant advance in myocardial protection. However, it soon became apparent that the continuous infusion of blood cardioplegia resulted in inadequate visualization of the operative field, necessitating interruption of flow during the construction of distal anastomoses. Our own experimental studies showed that interrupting antegrade warm blood cardioplegia during the revascularization of acutely ischemic myocardium was detrimental to left ventricular function and increased cellular necrosis.
With these concerns in mind, Christakis and his co-workers undertook this prospective, randomized clinical trial to determine whether intermittent antegrade warm blood cardioplegia was detrimental to postoperative right ventricular hemodynamics. They conclude that interruption of normothermic antegrade blood cardioplegia results in no deleterious effects on postoperative right ventricular (RV) function and may even be beneficial compared with intermittent antegrade cold blood cardioplegia. I, however, have major concerns regarding the interpretation and omission of data from this study. The only indices of RV function found to be significantly improved in the warm cardioplegia group were RV ejection fraction, RV end-diastolic volume index, and RV end-systolic volume index as derived from a thermodilution REF-1 catheter. These measurements are affected by changes in RV afterload, and their significant improvement at 6 and 8 hours after bypass most likely reflect the decreased pulmonary vascular resistance and warmer temperatures in the warm blood group. This may be a beneficial effect of normothermic cardiopulmonary bypass and not warm blood cardioplegia. Furthermore, at 6 and 8 hours, nearly one third to one quarter of the patients in both groups were excluded because they required either inotropes or afterload-reducing agents, or were shivering and had a tachycardia.
Several important pieces of data are omitted. We are not told whether topical hypothermia, an important technique in RV preservation during cold blood cardioplegia, was used in the cold group, nor were RV temperatures measured. The distribution (proximal versus distal) of right coronary artery stenoses and the order in which the lesions were grafted are also not mentioned, nor are we told how many patients were acutely ischemic from their right coronary lesions. These factors may have had a significant influence on RV function and ultimately the conclusions from this study. Finally, the incidence of infarcts and need for inotropic support in both cardioplegia groups are not mentioned.
This study does not allay my concerns regarding the potential detrimental effects of interrupting antegrade warm blood cardioplegia during coronary revascularization, especially for patients with acutely ischemic myocardium. I sense that Christakis and his fellow surgeons had these same concerns when they noted in their discussion that ischemic times were longer in the cold group ``...because all surgeons felt more confident with the luxury of hypothermia ...'' and that ``...surgeons were, therefore, more expeditious when constructing anastomoses in the warm group.'' Their data actually show that the increased ischemic time necessary to perform the distal anastomoses in the cold group had no detrimental effects on RV or left ventricular function. In our current practice of coronary artery bypass grafting, when distal vessels are smaller with more diffuse disease, the surgeon must rely on cardioplegic techniques that give an unobscured field to construct a perfect technical anastomosis as well as afford excellent myocardial protection for acutely ischemic hearts with lower ejection fractions. In my opinion, intermittent, antegrade warm blood cardioplegia is less likely to safely achieve both these goals.
Related Article
Ann. Thorac. Surg. 1996 61: 128-134.
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