LAUSR

Many clinicians feel strongly about the value of bringing patients’ low-density lipoprotein cholesterol (LDLC) to the risk-appropriate safe zone, be it <100, 70, or 55 mg/dL, whereas others feel equally strongly about the value of using the right doses of medications proven to reduce risk of atherosclerotic cardiovascular disease (ASCVD), perhaps even death. On the surface, these views may seem at odds, but a closer examination reveals that they represent two sides of the same coin. Specifically, LDL-C goals are often reached with the use of maximum doses of evidence-based therapies and, similarly, the most effective medications mitigate atherosclerotic risk because they lower LDL-C, often to goal levels. The discrepancies arise, naturally, when the LDL-C goal is attained in the absence of optimized, guideline-directed medical therapy or, conversely, when the appropriate medications at the recommended doses fail to achieve LDL-C goals. Does a patient with coronary artery disease who achieves an LDL-C of 50 mg/ dL via veganism, supplements, and a bile-acid binding resin not enjoy the same cardioprotection as another patient who achieves an identical LDL-C with a highpotency statin? Similarly, is a coronary patient who takes rosuvastatin 40 mg and ezetimibe 10 mg daily sufficiently protected even though their LDL-C continues to hover around 90 mg/dL? These are the questions created by a false dichotomy of views; that is, providing the appropriate medication and dose versus targeting the proper LDL-C goal.