Contraction bands are intensely eosinophilic intracellular "stripes" that are perpendicular to the long access of the myofibers. These bands represent hypercontracted myofibrils. They likely occur by two mechanisms:

1) In the absence of ATP, actin and myosin remain tightly bound, producing hypercontracted bands that resist the pull from other myofibrils with remaining ATP. This is the microscopic equivalent of "rigor mortis."

2) In the instance where the contractile machinery is hyperactivated by the influx of calcium into the damaged myocardium (either at the periphery of the infarct, or because of reperfusion.

Here are five microscopic images of myocardial infarctions at different stages.

They are in a random order. Click the icons on the left bar into view the associated images.

Where do you see necrosis?

What type of necrosis is it?

What type of inflammation do you see in each?

Of the 5 images, which is most likely to match your case and why?

The first signs of a myocardial infarct are subtle and only visible histologically after a few hours. MIs are undetectable prior to this time, making the diagnosis of death due to acute infarct difficult. By 2-4 hrs, the myofibers will appear "wavy" and exhibit contraction band necrosis.

By 12-24 hours, infarcts can be grossly identified by a reddish-blue area of discoloration caused by stagnated, trapped blood. Coagulative necrosis predominates.

Within a day, neutrophils begin to marginate in the vessels around the infarct and transmigrate into the tissue. As is the case here, they frequently must migrate in from the edges of the infarct because the blood supply to the infarcted area has been (obviously) cut off.

By 2-8 days, you can see extensive migration of neutrophils into the periphery of the infarct. This is the time that tamponade frequently occurs.

By 1 to 2 weeks, the infarct is rimmed by a hyperemic zone of highly vascularized granulation tissue. At this time the neutrophils have digested the necrotic tumor and macrophages are removing the debris.

After 2 weeks, there is increased deposition of collagen and gradual decreasing cellularity.

By 2 months, the infarct appears as a dense collagenous scar.