Myocardial infarction

This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction. The center of the infarct contains necrotic muscle that appears yellow-tan. Surrounding this is a zone of red hyperemia. Remaining viable myocardium is reddish- brown. This cross section through the heart shows the larger left ventricular chamber and the small right ventricle. Extending from the anterior portion and into the septum is a large recent pale myocardial infarction. The center is tan with surrounding hyperemia. This infarction is "transmural" because it extends through the full thickness of the ventricular wall. The earliest change histologically seen with acute myocardial infarction in the first day is contraction band necrosis. The myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here. Note the many irregular darker pink wavy contraction bands extending across the fibers. This high power microscopic view of the myocardium demonstrates an infarction of about 1 to 2 days in duration. The myocardial fibers have dark red contraction bands extending across them. The myocardial cell nuclei have almost all disappeared. There is beginning acute inflammation. Clinically, such an acute myocardial infarction is marked by changes in the electrocardiogram and by a rise in the MB fraction of creatine kinase. In this microscopic view of a recent myocardial infarction, there is extensive hemorrhage along with myocardial fiber necrosis with contraction bands and loss of nuclei. This myocardial infarction is about 3 to 4 days old. There is an extensive acute inflammatory cell infiltrate, and many neutrophils are undergoing karyorrhexis. The myocardial fibers are undergoing necrosis so that the outlines of them are not well defined. Few cross striations remain, and cell nuclei are no longer visible. The serum troponin would be elevated. This is an intermediate myocardial infarction of 1 to 2 weeks in age. Note that there are remaining normal myocardial fibers at the top. Below these fibers are many macrophages along with numerous capillaries and little collagenization. At 3 to 4 weeks of age the intermediate myocardial infarction shown involving a papillary muscle at low power above and medium power below have decreasing cellularity along with more prominence of collagen. Note that there are remaining normal red myocardial fibers. Cardiac biomarkers are not positive at this stage and myocardial rupture is unlikely. The degree of cardiac failure depends upon the extent of myocardial loss

The myocardium shown demonstrates pale fibrosis with collagenization following healing of a myocardial infarction. There is minimal cellularity; a few remaining viable red myocardial fibers are present. This stage is reached about 2 months following the initial ischemic event. This collagenous scar is nonfunctional for contraction and will diminish the ejection fraction. Such a scar will not rupture. The heart is opened to reveal the left ventricular free wall on the right and the septum in the center. There has been a remote myocardial infarction that extensively involved the anterior left ventricular free wall and septum. The white appearance of the endocardial surface indicates the extensive scarring. One One complication of a transmural myocardial infarction is rupture of the myocardium. This is most likely to occur in the first week between 3 to 5 days following the initial event, when the myocardium is the softest. The white arrow marks the point of rupture in this anterior-inferior myocardial infarction of the left ventricular free wall and septum. Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade. In cross section, the point of rupture of the myocardium is shown with the arrow. In this case, there was a previous myocardial infarction 3 weeks before, and another myocardial infarction occurred, rupturing through the already thin ventricular wall 3 days later. There has been a previous extensive transmural myocardial infarction involving the free wall of the left ventricle. Note that the thickness of the myocardial wall is normal superiorly, but inferiorly is only a thin fibrous wall. The infarction was so extensive that, after healing, the ventricular wall was replaced by a thin band of collagen, forming an aneurysm. Such an aneurysm represents non-contractile tissue that reduces stroke volume and strains the remaining myocardium. The stasis of blood in the aneurysm predisposes to mural thrombosis. . A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow. Note how the aneurysm bulges out. The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm. The epicardial surface of the heart shows a shaggy fibrinous exudate. This is another example of fibrinous pericarditis. This appearance has often been called a "bread and butter" pericarditis, but you would have to drop your buttered bread on the carpet to really get this effect. The fibrin often results in the the finding on physical examination of a "friction rub" as the strands of fibrin on epicardium and pericardium rub against each other. Microscopically, the pericardial surface here shows strands of pink fibrin extending outward. There is underlying inflammation. Eventually, the fibrin can be organized and cleared, though sometimes adhesions may remain.