It goes without saying that calcium is one of the biggest enemies of percutaneous coronary intervention (PCI). Apart from resistance to delivering wires, balloons, and stents down the artery, calcified plaques are also responsible for suboptimal results after balloon angioplasty and stenting, with extensive dissections (sometimes ending in ruptures), underexpansion of stents, malapposition of stent struts, overexpansion of the adjacent non-calcified vessel wall segments, non-circular lumen, less acute gain, and suboptimal minimal lumen areas. All of these factors undeniably influence procedural outcomes in a negative way in the short and long term. There are two types of coronary artery calcification: atherosclerotic and medial artery calcification. Atherosclerotic calcification mainly occurs in the intima and is a result of inflammation, lipid infiltration and differentiation of smooth muscle cells into an osteogenic cell type. Medial artery calcification is more associated with older age, diabetes mellitus, and chronic renal insufficiency and results in stiffer arteries. Although the distribution of the calcium is different between both types of coronary artery calcification, they are equally related to increased risk for cardiovascular events.
Cardiovascular Revascularization Medicine, 2019-02-01, Volume 20, Issue 2, Pages 91-92, Copyright © 2019
Read the original article on Science Direct: Cracking the Calcified Plaque