Atherosclerosis is universal; everyone develops fatty atherosclerotic plaques in their arteries at some point, and to some degree. Plaques narrow blood vessels to impede blood flow, and rupture of unstable plaque causes heart attack, stroke, and embolism. It is the largest cause of human mortality, and at present the best that the medical community can do is to slow down plaque growth. Established therapies based on reducing the amount of cholesterol carried outward from the liver on low-density lipoprotein (LDL) particles produce something like a 15% mortality risk reduction at best, and do not regress plaque to any meaningful degree. Interestingly, the drivers of atherosclerosis are sufficiently complex and varied for there to be a few lucky people who exhibit 10% or more plaque regression in response to some combination of lifestyle change and medication. The flip side of that point is the majority of people who show up in a hospital in the immediate aftermath of a first heart attack or stroke do not in fact exhibit elevated LDL cholesterol, and probably benefit very little from the relentless clinical focus on LDL cholesterol.
It isn't all that easy to assess the degree of plaque present in the early stages of atherosclerosis. Imaging approaches have improved greatly over the past ten to fifteen years, but still struggle to distinguish small amounts of plaque. Little to no assessment takes place in the early stages of the condition. Many people have no idea as to whether or not they are in a high risk group until it is far too late. Simple risk factors are well understood, such as chronic inflammation, being overweight, suffering metabolic disease, and so forth. But as the discovery and continued research into the role of Lp(a) in atherosclerosis risk illustrates, there is a great deal yet to be catalogued of how exactly specific differences in metabolism yield differences in the pace at which atherosclerotic lesions emerge. It remains largely a mystery as to why any given person exhibits a given degree of atherosclerosis.
