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Ann Thorac Surg 1999;67:289-290
© 1999 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, University Hospital Hamburg-Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany
To the Editor
I enjoyed the important contribution of Dean and coworkers [1] on the genesis of myocardial edema during orthograde and retrograde perfusion. In a pig heart model they demonstrated benefits of retrograde coronary perfusion in respect to the reduction of perfusion-induced myocardial edema compared with orthograde coronary perfusion. They reported lower myocardial water content, reduced ventricular stiffness, and a retrograde flow rate of 1.1 mL/s at 49 mm Hg, which was six times lower than in their orthograde perfusion group. These findings are surprising in so far as until now I considered the heart perfused via the coronary sinus to be more susceptible to myocardial edema. Consequently, in the clinical setting I anxiously avoided retrograde perfusion pressures exceeding 30 mm Hg measured within the coronary sinus, and thus kept them well below the oncotic pressure of our hydroxy ethyl starch-containing Eppendorf-cardioplegic solution, which had an oncotic pressure of about 40 mm Hg. Even at these lower retrograde perfusion pressures, the flow rates in my experience distinctly exceeded the flow rates achieved during pressure-controlled orthograde cardioplegic coronary perfusion at 40 mm Hg. These clinical impressions are backed up by experimental settings of other authors [3] reporting a flow rate of 150 mL/min at a retrograde perfusion pressure of about 25 mm Hg in a pig heart model.
In their study Dean and colleagues measured the orthograde perfusion pressure via a pressure-monitoring port directly within the aortic root. They did not mention whether the tip of the pressure probe during retrograde perfusion was located within the coronary sinus. Pressures recorded on other sites of the perfusion system would indeed be much higher and would not represent the exact perfusion pressure within the coronary venous system. In this respect I fear that the observed low flow rates are due to this or another artifact. On the other hand, it would explain the low flow rates and low water content demonstrated in this study.
Furthermore, to achieve comparable results in an experimental setting, pressures of orthograde and retrograde perfusion should not differ because they determine flow rates and filtration. Two important factors preventing perfusion-induced myocardial edema are not mentioned: the oncotic pressure or protein content as well as the erythrocyte count or hematocrit of the different perfusion solutions used here. Starling [4] has shown the protein-dependent mechanism of filtration of water into tissues. In a more recent study [2] my coworkers and I demonstrated the prevention of perfusion-induced edema by addition of erythrocytes. We postulated that erythrocytes having a large diameter than capillaries partially prevent the transmission of a high-perfusion pressure to the capillary area and thus reduce filtration into the interstitial space. We did not notice perfusion-induced edema in orthograde cardioplegic perfusion of rabbit hearts even in the absence of erythrocytes but in the presence of hydroxy ethyl starch when the perfusion pressure was kept below the oncotic pressure.
For the interpretation of the results one should determine pressure-flow relations, hematocrit, and oncotic pressure in the different subgroups of perfusates to exclude factors in the genesis of perfusion-induced edema other than the modes of myocardial perfusion.
References
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