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J Thorac Cardiovasc Surg 2000;120:544-551
© 2000 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
From the Institute for Biodiagnostics, National Research Council of Canada,a and the Department of Cardiovascular Surgery, Faculty of Medicine, University of Manitoba,b Winnipeg, Manitoba, Canada.
This work was supported by the Medical Research Council of Canada (9609OP-34-8-BME-CDAA-26321), the Heart and Stroke Foundation of Canada (381-3143-06), and the National Research Council.
Address for reprints: Ganghong Tian, MD, PhD, 435 Ellice Ave, Winnipeg, Manitoba, Canada R3B 1Y6 (E-mail: tian{at}ibd.nrc.ca ).
Objective: The present work was designed to study the myocardial perfusion and energy metabolism during retrograde cardioplegia performed with different methods, including deep coronary sinus cardioplegia, coronary sinus orifice cardioplegia, and right atrial cardioplegia.
Methods: Isolated pig hearts were subjected to antegrade cardioplegia, right atrial cardioplegia, deep coronary sinus cardioplegia, and coronary sinus orifice cardioplegia in a random order. Cardioplegic distribution was assessed by T1-weighted magnetic resonance imaging in 1 group of hearts (n = 8). The flow dynamics of cardioplegia were assessed by T2*-weighted imaging in a second group of hearts (n = 8).
Results: T1-weighted images revealed an apparent perfusion defect in the posterior wall of the left ventricle, the posterior portion of the interventricular septum, and the right ventricular free wall during deep coronary sinus cardioplegia. The perfusion defect observed in the first 2 regions with deep coronary sinus cardioplegia resolved with coronary sinus orifice cardioplegia. Right atrial cardioplegia provided the most homogeneous perfusion to all regions of the myocardium relative to the other 2 retrograde cardioplegia modalities. T2*-weighted images showed that the 3 retrograde cardioplegia modalities provided similar cardioplegic flow velocities. Localized phosphorus 31 spectroscopy showed that the levels of adenosine triphosphate and phosphocreatine were significantly lower in the posterior wall (adenosine triphosphate, 42.86% ± 5.91% of its initial value; phosphocreatine, 11.43% ± 11.3%) than the anterior wall (adenosine triphosphate, 89.19% ± 8.83%; phosphocreatine, 59.54% ± 12.58%) of the left ventricle during 70 minutes of normothermic deep coronary sinus cardioplegia.
Conclusions: Deep coronary sinus cardioplegia results in myocardial ischemia in the posterior wall of the left ventricle and the posterior portion of the interventricular septum, as well as in the right ventricular free wall. Coronary sinus orifice cardioplegia improves cardioplegic distribution in these regions. Relative to deep coronary sinus cardioplegia and coronary sinus orifice cardioplegia, right atrial cardioplegia provides the most homogeneous perfusion.
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