Ultrastructural Evidence of Microvascular Damage and Myocardial Cell Injury After Coronary Artery Occlusion: Which Comes First?

Both microvascular damage and myocardial cell injury occur after coronary occlusion, but the relationship of these two events is unclear; specifically, it is unknown whether microvascular damage causes myocardial cell injury. Dogs were subjected to coronary occlusion for 20, 40, 60, 90 or 180 minutes, after which subendocardial and subepicardial biopsies were obtained for electron and light microscopy of 1-, u sections. Of 312 biopsies of ischemic myocardium, 181 showed myocardial cell injury with no microvascular damage; 131 showed myocardial cell injury and microvascular damage; but none showed microvascular damage without myocardial cell injury. Although ultrastructural evidence of myocardial cell damage was present in the subendocardium after 20-40 minutes of ischemia, ultrastructural evidence of microvascular damage was not prominent until 60-90 minutes after coronary artery occlusion. Morphologic ultrastructural evidence of microvascular damage lagged behind myocardial cell injury, suggesting that ultrastructural microvascular damage is not a primary cause of ultrastructural myocardial cell injury.

[1]  R. Kloner,et al.  The no-reflow phenomenon: Not a time-limiting factor for reperfusion following coronary occlusion , 1980 .

[2]  H. Mcintosh,et al.  Emergency coronary artery revascularization of patients with acute myocardial infarction: you can ... but should you? , 1979, Circulation.

[3]  S. Phillips,et al.  Emergency Coronary Artery Revascularization: A Possible Therapy for Acute Myocardial Infarction , 1979, Circulation.

[4]  R. Kloner,et al.  Early ischemic ultrastructural and histochemical alterations in the myocardium of the rat following coronary artery occlusion. , 1979, Experimental and molecular pathology.

[5]  R. Jennings,et al.  The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. , 1979, Laboratory investigation; a journal of technical methods and pathology.

[6]  J. Lowe,et al.  The Wavefront Phenomenon of Ischemic Cell Death: 1. Myocardial Infarct Size vs Duration of Coronary Occlusion in Dogs , 1977, Circulation.

[7]  E. Braunwald,et al.  Effect of hyaluronidase during the early phase of acute myocardial ischemia: an ultrastructural and morphometric analysis. , 1977, The American journal of cardiology.

[8]  A. Carpentier,et al.  The effect of coronary artery reperfusion on the extent of myocardial infarction. , 1977, American heart journal.

[9]  R. Berg,et al.  Acute myocardial infarction: a surgical emergency. , 1975, The Journal of thoracic and cardiovascular surgery.

[10]  J. Willerson,et al.  Reduced Myocardial Reflow and Increased Coronary Vascular Resistance following Prolonged Myocardial Ischemia in the Dog , 1975, Circulation research.

[11]  J. Gavin,et al.  Changes in the microvasculature of ischemic and infarcted myocardium. , 1975, Laboratory investigation; a journal of technical methods and pathology.

[12]  R. Kloner,et al.  The "no-reflow" phenomenon after temporary coronary occlusion in the dog. , 1974, The Journal of clinical investigation.

[13]  G. Korb,et al.  Blood Supply of the Myocardium after Temporary Coronary Occlusion , 1966, Circulation research.