Mechanism of vascular calcification

In the early 1900s, cholesterol deposition in atherosclerosis was considered a passive, degenerative, inevitable and end-stage process of ageing. After decades of research, it is now recognized as an active, regulated, treatable and preventable disorder related to deposition and oxidation of lipoprotein components. Similarly, in the past few decades, vascular calcification also has been considered a passive, degenerative, inevitable, and endstage process of ageing. But, after recent clinical and laboratory findings, there is increasing recognition that vascular calcification is an active, regulated process related to oxidized lipids that may be treatable and preventable. The fact that complete bone tissue forms within the atherosclerotic artery wall has been known since at least the 1800s. In 1863, Virchow observed that vascular calcium deposits were not mere calcification, but ossification.1 In 1908, investigators reported red marrow elements in bone tissue within atherosclerotic plaque.2,3 Experimental models of atherosclerosis also have cartilage and marrow within plaque.4 As an overview, vascular calcification in general, and coronary calcification in particular, increase with ageing, are present in almost all subjects over age 65, are more frequent in diabetics, less common in African-Americans, and extremely common in end-stage renal disease. Current studies of coronary calcification utilize electron beam computed tomographic scanning (EBCT). This method has been described as an ‘inaccurate’ predictor of stenosis severity. While this is not incorrect, it may leave the wrong impression since EBCT is accurate when used to predict the presence of significant coronary artery disease, and the degree of plaque burden.5