The histologic border zone of acute myocardial infarction--islands or peninsulas?

Observation of isolated islands of apparently surviving myocardium within areas of necrotic tissue at the edge of myocardial infarctions has been interpreted by some as histologic evidence of a unique "border zone" region. Serial section reconstruction of transmural canine myocardial infarctions was performed in this study to establish whether these islands were truly isolated or were continuous peninsulas of tissue separated by the plane of section. Three-dimensional analysis of the infarcts revealed no true islands but instead demonstrated a region composed of highly complex interdigitating peninsulas. We conclude that there is an extremely irregular but sharp boundary demarcating normal and infarcted myocardium with no intermediate zone. This observation is discussed in relation to recent data, based on coronary blood flow and creatine phosphokinase analysis, which also demonstrates a sharp boundary between the normal and infarct zones.

[1]  H. Thompson,et al.  Time course and zonal variations of ischemia-induced myocardial cationic electrolyte derangements. , 1975, Circulation.

[2]  P. Libby,et al.  Reduction of Infarct Size Following Coronary Occlusion , 1974, Circulation research.

[3]  B E Sobel,et al.  Distribution of myocardial injury and its relation to epicardial ST-segment changes after coronary artery occlusion in the dog. , 1972, Cardiovascular research.

[4]  P. Libby,et al.  The effect of glucose-insulin-potassium on cardiac ultrastructure following acute experimental coronary occlusion. , 1973, The American journal of pathology.

[5]  E. Braunwald,et al.  Use of Changes in the Epicardial QRS Complex to Assess Interventions which Modify the Extent of Myocardial Necrosis following Coronary Artery Occlusion , 1976, Circulation.

[6]  P. Libby,et al.  Effects of Intraaortic Balloon Counterpulsation on the Severity of Myocardial Ischemic Injury following Acute Coronary Occlusion: Counterpulsation and Myocardial Injury , 1972, Circulation.

[7]  H A Fozzard,et al.  ST-segment potentials and mapping. Theory and experiments. , 1976, Circulation.

[8]  M. Maxwell,et al.  Studies on the mechanism of ventricular activity. VII. The origin of the coronary QR wave. , 1954, The American journal of medicine.

[9]  E. Sonnenblick,et al.  Absence of a Lateral Border Zone of Intermediate Creatine Phosphokinase Depletion Surrounding a Central Infarct 24 Hours after Acute CoronaryOcclusion in the Dog , 1977, Circulation research.

[10]  J. Kastor,et al.  Myocardial changes associated with cardiogenic shock. , 1971, The New England journal of medicine.

[11]  R. Jennings Early phase of myocardial ischemic injury and infarction. , 1969, The American journal of cardiology.

[12]  E. Sonnenblick,et al.  Redistribution of Collateral Blood Flow from Necrotic to Surviving Myocardium following Coronary Occlusion in the Dog , 1976, Circulation research.

[13]  J. Cox,et al.  The ischemic zone surrounding acute myocardial infarction. Its morphology as detected by dehydrogenase staining. , 1968, American heart journal.

[14]  E. Stokely,et al.  Pathophysiology of technetium-99m stannous pyrophosphate and thallium-201 scintigraphy of acute anterior myocardial infarcts in dogs. , 1976, The Journal of clinical investigation.

[15]  S. Epstein,et al.  Experimental Acute Myocardial Infarction: Characterization and Treatment of the Malignant Premature Ventricular Contraction , 1973, Circulation.

[16]  R. Jennings,et al.  Structural Changes in Myocardium During Acute Ischemia , 1974, Circulation research.

[17]  R. Jennings,et al.  Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. , 1960, Archives of pathology.

[18]  E. Stokely,et al.  Morphologic Correlates of Technetium‐99m Stannous Pyrophosphate Imaging of Acute Myocardial Infarcts in Dogs , 1975, Circulation.

[19]  R. Jennings,et al.  Kinetics of calcium accumulation in acute myocardial ischemic injury. , 1972, The American journal of pathology.

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

[21]  J. Edwards Correlations in coronary arterial disease. , 1957, Bulletin of the New York Academy of Medicine.

[22]  B. Sobel,et al.  Depressed Myocardial Creatine Phosphokinase Activity Following Experimental Myocardial Infarction in Rabbit , 1970, Circulation research.

[23]  R. Kerber,et al.  Three Dimensional Geometry of Acutely Ischemic Myocardium , 1975, Circulation.

[24]  P. Libby,et al.  Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction. , 1977, The New England journal of medicine.

[25]  B. Chance,et al.  Ischemic areas in perfused rat hearts: measurement by NADH fluorescence photography. , 1976, Science.