The underlying mechanism of<unk>  is centered around the damage caused by microvascular obstruction (MVO). There have been two proposed underlying causes of<unk> : # Structural<unk>  is present in the microvasculature of regions of necrotic myocardium. Prolonged ischemia impairs perfusion to the endothelial cells that line the walls of the microvasculature. Impaired perfusion leads to decreased ATP production within the endothelial cells, which ultimately leads to cellular swelling and irreversible damage of the endothelial cells. This cell damage contributes to the formation of fibrin thrombi within the microvasculature, occluding the vasculature lumen, and resulting in MVO. Additionally, swelling within necrotic tissue surrounding the microvasculature can further compress the vessel lumen, resulting in loss of capillary integrity, and further contributing to MVO. Structural no<unk>  is largely irreversible. An example would be seen in an area of myocardium post-myocardial infarction that was not reperfused quickly enough. # Functional<unk>  occurs when the microvasculature is anatomically intact, but has been temporarily compromised due to spasm, microembolization, or reperfusion injury, ultimately leading to MVO. Functional<unk>  is largely reversible due to the fact that the microvasculature is still intact. ## Micromembolization can occur during primary percutaneous coronary intervention (pPCI) to revascularize an occluded epicardial vessel due to disruption of thromboembolic material, such as plaques within the coronary arteries. ## Reperfusion following ischemia causes acute inflammation within the microvasculature, leading to neutrophilic proliferation. Neutrophils further contribute to endothelial cell damage by releasing free radicals via oxygen-dependent mechanisms, as well as pro-inflammatory mediators. Pro-inflammatory mediators contribute to MVO by causing extravasation of red blood cells, platelets, and leukocytes, into the vessel lumen. ## Neutrophils and platelets within the microvasculature cause alpha-adrenergic activation of the neurohumoral system. This leads to prolonged vasospasm of the microvasculature, further contributing to MVO. In both types of<unk> , the extent of damage to the microvasculature is directly proportional to the length of time the tissue is ischemic, with longer periods of ischemia related to greater damage to the arterial microvasculature.
No reflow phenomenon
Mayer waves
Isotropic bands
Apex beat
Fogging phenomenon
Double bubble 
Venous translucence
Non-lifting sign