The formation of cholesterol crystals and embolization during myocardial infarction

Abstract

Cholesterol crystals (CCs) released into the coronary circulation during plaque rupture have multiple adverse impacts on both the arterial conduit as well as the myocardium. CCs form within the atheromatous plaque by the saturation of free cholesterol deposition via facilitated LDL-c entry because of a dysfunctional endothelium. Once formed, CCs are viewed as a foreign body and activate inflammation via the innate immune system. Eventually, an inflamed atheromatous plaque ruptures by virtue of the growth and expansion of CCs that begin to occupy a greater volume than the liquid phase cholesterol. In some instances, the sharp edges of CCs can puncture and tear the plaque's fibrous cap causing rupture leading to thrombosis and myocardial infarction. In these circumstances, CCs are released from the ruptured plaque and travel down the coronary artery where they can scrape the endothelial lining which enhances vasospastic activity, further worsening ischemia. Moreover, when CCs lodge in the distal arteriolar and capillary beds, they not only obstruct blood flow to further aggravate ischemia but also activate an inflammatory response in the myocardium that leads to further tissue injury. Treatment of CCs has thus far been limited but studies using statins, aspirin and colchicine have demonstrated them to be effective in dissolving CCs that may provide additional benefits for both prevention and potentially for acute cardiovascular events.