Our study suggests that statin therapy—whether or not recipients have coronary artery disease—does not decrease the proportion of small, dense LDL among total LDL particles, but in fact increases it, while predictably reducing total LDL cholesterol, absolute amounts of small, dense LDL, and absolute amounts of large, buoyant LDL. If and when our observation proves to be reproducible in subsequent large-scale studies, it should provide new insights into small, dense LDL and its actual role in atherogenesis or the progression of atherosclerosis.
So you've treated your CAD patient “to goal” with statin therapy. If the patient had small dense LDL (AKA LDL pattern B) to begin with, he or she still will if all you did was use a statin. What this and many other studies have shown is that statin therapy alone will not change your patient from pattern B to the much less risky pattern A. Most of the pattern B folks have the metabolic syndrome but a significant number do not. Once you've titrated the statin to goal many patients will carry residual risk, which is why relative risk reduction for events attributable to statin therapy is on the order of 30%, not 100%.