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Ann Thorac Surg 1992;54:1120-1125
© 1992 The Society of Thoracic Surgeons
Cardiovascular Surgical Research Laboratory, Department of Cardiovascular Surgery, Toronto Western Division, Toronto Hospital Corporation, Toronto, Ontario, Canada
Accepted for publication March 23, 1992.
* Address reprint requests to Dr Feindel, Department of Cardiovascular Surgery, Rm 14-222, Eaton Wing, The Toronto General Hospital, 200 Elizabeth St, Toronto, Ont, Canada M5G 2C4.
Retroperfusion of arterial blood through the coronary sinus reduces infarct size if therapy starts immediately after coronary artery occlusion. To determine if a new system of non-electrocardiogram-synchronized retroperfusion is able to reduce infarct size after delays consistent with clinical use, anesthetized pigs were subjected to 4 hours of left anterior descending coronary artery occlusion followed by 1 hour of reperfusion. Retroperfusion of arterial blood commenced immediately after occlusion of the left anterior descending coronary artery in the no-delay group (n = 10) and after a 1-hour (n = 10) and a 2-hour (n = 8) delay in two other groups. In the control group (n = 10), no therapy was used. In all groups, retroperfusion of arterial blood was terminated after 4 hours of occlusion of the left anterior descending coronary artery. Infarct size, expressed as a percentage of the in vivo area at risk (± the standard deviation), was smaller in the no-delay group (44.1 ± 12.9) and marginally smaller in the 1-hour delay group (71.0 ± 9.8) compared with controls (86.3 ± 7.5) (p < 0.05). Infarct size in the 2-hour delay group (75.0 ± 10.7) was not significantly different from controls. Mean coronary sinus pressure (± the standard deviation) was 56 ± 25 mm Hg, 39 ± 9 mm Hg, and 47 ± 9 mm Hg in the no-delay, 1-hour delay and 2-hour delay groups respectively. Thus, this new retroperfusion system limits infarct size by 50% if it is started immediately after coronary occlusion. However, if institution of retroperfusion is delayed, only marginal benefit is achieved in a model of minimal intercoronary collateralization.
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