Potential clinical implications of abnormal myocardial perfusion patterns immediately after reperfusion in a canine model: A myocardial contrast echocardiography study

• Published in: The American heart journal 1996-08, Vol.132 (2), p.303-313
• Main Authors: Kates, Marc A., Meza, Mario F., Barbee, R.Wayne, Revall, Susan, Moreno, Carlos A., Perry, Bret, Murgo, Joseph P., Cheirif, Jorge
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cardiology. Vascular system; Cardiotonic Agents; Cell Survival; Coronary Disease - diagnostic imaging; Coronary Disease - pathology; Coronary Disease - physiopathology; Coronary heart disease; Disease Models, Animal; Dobutamine; Dogs; Echocardiography; Heart; Hemodynamics; Medical sciences; Myocardial Reperfusion; Myocardial Reperfusion Injury - diagnostic imaging; Myocardial Reperfusion Injury - pathology; Myocardium - pathology; Necrosis; Observer Variation; Predictive Value of Tests; Regional Blood Flow
• ISSN: 0002-8703; 1097-6744
• DOI: 10.1016/S0002-8703(96)90426-3

During myocardial infarction, lack of myocardial opacification after reperfusion has been associated with poor or no recovery of function. We have previously documented the presence of perfusion abnormalities after brief coronary occlusions without infarction and the absence of perfusion abnormalities after prolonged occlusions with infarction. To characterize myocardial perfusion patterns immediately after reperfusion, we studied 53 animals in two groups in a coronary occlusion-reperfusion model. Temporary occlusions (group 1, 15 minutes; group 2, 30 to 360 minutes) were performed, followed by reperfusion with and without dobutamine. Myocardial contrast echocardiography was performed with aortic root injections of sonicated 5% serum human albumin (Albunex) during each intervention. Group 1 dogs showed no evidence of myocardial infarction. In group 2, 26 to 40 dogs had infarctions. After reperfusion, no perfusion abnormalities were seen in 13 of 26 group 2 dogs with infarctions; perfusion abnormalities were identified after reperfusion in 2 of 13 group 1 and in 8 of 14 group 2 dogs without infarctions. In animals subjected to prolonged ischemia, the absence of perfusion abnormalities after reperfusion did not rule out the presence of necrosis. Similarly, in animals without infarction subjected to ischemia, the presence of a perfusion defect after reperfusion did not represent the presence of necrosis but an abnormal microvascular reserve. These results suggest that early after reperfusion, assessment of perfusion by myocardial contrast echocardiography has significant limitations in the evaluation of myocardial viability and salvage.