One important contribution to the buildup of atherosclerotic plaques and eventually atheromas is the damaged lipids generated by age-related damage to your mitochondria. Here, researchers look at what happens further down the line when the plaques become dangerous: "some 2 percent of all plaques [will] eventually lead to the development of an acute blood clot and to heart attack, sudden death, or stroke. ... The billion dollar question is why 98 percent cause no problem, and 2 percent do. ... Their report adds support to the notion that so-called endoplasmic reticulum (ER) stress together with the body's natural way of coping with that stress is one answer. ... In the case of atherosclerosis, ER stress within plaques could lead to the massive death of cells - and of macrophages in particular - leading to the generation of a structure called the 'necrotic core.' Those necrotic cores are known to be a defining feature of plaques that are vulnerable to rupture and blood clot formation." The researchers show that mice lacking the cell death response to ER stress suffer half the number of blood clots. As always, however, a much better solution would be to regularly clear the plaques rather than tinker with fundamental cell mechanisms to try and make the plaques less dangerous.