Answer: E. Regional subendocardial nonenhancement surrounded by a ring of DHE. Microvascular obstruction is present in the most severe acute infarctions. Gadolinium is unable to penetrate the myocytes due to necrotic blood vessels, so there is subendocardial nonenhancement. The ring of DHE represents infarcted myocardium without destruction of blood vessels, thus allowing gadolinium to reach this abnormal tissue. Isolated subendocardial enhancement is typically seen with smaller infarcts, while transmural DHE may be present in more severe infarcts. Myocarditis and other infiltrative processes demonstrate DHE in the mid myocardial wall or epicardium.

Answer: C. Subendocardium. The mechanism for increased susceptability of the subendocarium to ischemia is not completely understood, however, it is likely related to decrease perfusion during systole, higher levels of wall stress, and differences in metabolism as compared to the mid myodcardium and subepicardium.

Answer: B. Stunned Myocardium. When blood flow is restored to ischemic myocardium that has not yet infarcted, there is often a period of time in which this myocardium continues to be dysfunctional. This is referred to as stunned myocardium. Over time, this myocardium regains function. Hibernating myocardium is a result of chronic ischemia. As a result, the myocardium adapts by down regulating functional, and therefore metabolic, activity to preserve viability. Microvascular obstruction is the area of infarcted myocardium that receives no blood flow due to destruction of blood vessels. Shocked myocardium is not a term used in cardiac MRI.