Heart

Beginning with stable chronic plaque, responsible for typical angina, and leading to the various acute coronary syndromes.
Sequential progression of coronary artery lesion

This cross section reveals a large myocardial infarction involving the anterior left ventricular wall and septum. The color of the infarct is whitish-yellow. This is an example of pale (anemic) infarction.
MI involving LV anterior free wall and septum


There is yellowish discoloration of the myocardium. Note the anterior scar (arrowhead), indicative of old infarct. The myocardial hemorrhage at the Lt. ventricular lateral wall (asterisk) is due to ventricular rupture and was the acute cause of death in this patient (specimen is oriented with the posterior wall at the top).
Acute myocardial infarct of the posterolateral left ventricle

Complete rupture of a necrotic papillary muscle.

MI papillary muscle rupture

Transmural myocardial infarction with rupture and hemopericardium

This is most likely to occur in the first week between 4 to 5 days following the initial event, when the myocardium is the softest. The arrow marks the point of rupture in this anterior myocardial infarction of the left ventricular free wall. Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade.

The pericardial sac is opened to display hemo pericardium. Such a massive amount of hemorrhage can lead to cardiac tamponade. This may result from rupture of the heart as a complication of myocardial infarction or an aortic dissection, when blood dissects through the media proximally.
Hemopericardium


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.
LV aneurysm complicating MI


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.
Lt ventricular aneurysm complicating healed MI

This infarct is limited to the inner third to one half of the LV wall. The red-blue cyanotic discoloration is totally encircling the Lt V inner wall.
Subendocardial myocardial infarction

Acute MI: Coagulative necrosis of myocardial cell

This myocardial infarction is about 3 to 4 days old. There is an extensive acute inflammatory cell infiltrate and the myocardial fibers are so necrotic that the outlines of them are only barely visible.The cytoplasm is rather homogeneous, deeply eosinophilic, devoid of cross striation and there are no nuclei.


Nnecrotic muscle fibres of the infarct at higher magnification. The nuclei having disappeared by karyolysis. The fibres are more deeply eosinophilic than normal fibres. The striations are still detectable focally. In the interstitial tissue there are some nuclear fragments, macrophages which have migrated into the dead muscle.
Myocardial Infarction: Coagulative Necrosis

Necrosis

Normal
Line of demarcation
Myocardial infarction-line of demarcation
By 10 to 14 days from the onset the infarct is rimmed by a hyperemic zone of highly vascularized granulation tissue (line of demarcation)


This is a 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 fibroblasts with deposition of collagen.
Myocardial Infarction: Coagulative Necrosis