(Credit for banner image: Bentzon, J. F., Otsuka, F., Virmani, R., & Falk, E. (2014). Mechanisms of plaque formation and rupture. Circulation Research, 114(12), 1852–1866. https://doi.org/10.1161/circresaha.114.302721)
Thrombus is recognized as a filling defect. It differs in appearance from atherosclerotic stenosis because the center of the vessel (where the thrombus is) fails to opacify, whereas the outer portion (in between the thrombus and the vessel wall) fills with contrast. This is common in the setting of plaque rupture, but can also occur as an embolic phenomenon. The images below show relatively normal vessels with an apical LAD thrombus which occurred after cardioversion for atrial fibrillation and thus is most likely a thromboembolus.
RAO cranial view showing LAD thrombus
RAO cranial view showing LAD thrombus
AP cranial showing apical LAD thrombus
AP cranial showing apical LAD thrombus
Prior stents are usually visible on angiography, although sometimes it is hard to tell them apart from dense calcification. They are easiest to visualize prior to contrast injection.
RAO cranial showing a stented area extending from the left main into the mid LAD, then a stent-free segment of artery following by another distal LAD stent. Bonus: RCA stents are also present in the lower left portion of the screen.
See if you can pick out the stents on this RAO cranial clip.
Coronary artery disease often results in progressive narrowing of epicardial vessels. Eventually, a vessel may become completely occluded over time. This is called “chronic total occlusion,” abbreviated CTO. This is in contrast to acute coronary occlusion which results in OMI. Sometimes it can be challenging to discern chronicity angiographically. The presence of collaterals does not rule out acute occlusion. We rely on clues like calcification, total atherosclerotic burden, and abruptness of flow termination.
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Collateral flow refers to the development of channels which provide a bridge from one coronary territory to another in response to ischemia (acute or chronic). They can develop acutely, seen in almost 50% of OMI patients under 50 years of age. Most collaterals are formed by capillaries and can be easy to overlook, although some collaterals are formed by larger epicardial arterioles.
In this AP cranial angiogram, the PDA can be seen filling late. Since the PDA in this patient is from the RCA, this provides indirect evidence that the RCA is occluded and fills via collaterals from the left circulation. These are called “left to right” collaterals.
Collateral anatomy can include:
AP cranial angiogram shows delayed retrograde filling of the PDA from left to right collaterals.
AP cranial angiogram shows delayed retrograde filling of the PDA from left to right collaterals.
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Collaterals are often abbreviated using just L and R to signify the vessel of origin and the target vessel. For example, if an OM is filling via right to left collaterals from the RCA, the report might just say “OM fills via R-L collaterals.”
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In some cases, antegrade flow in a coronary artery may be sluggish in the absence of obstructive epicardial disease. This may be due to microvascular dysfunction, which can be acute or chronic.
RAO cranial showing severe stenosis with acute plaque rupture in mid LAD
RAO cranial showing severe stenosis with acute plaque rupture in mid LAD
Before PCI, TIMI 2 lesion seen in mid LAD in the setting of anterior OMI.