Treating high-risk patients with cardiovascular (CV) disease to LDL-cholesterol (LDL-C) goals of ≤70 mg/dL may not be feasible despite an influx of new LDL-C lowering drugs, according to Dr Jennifer Robinson of the University of Iowa College of Public Health in Iowa City, Iowa, US. [Robinson JG, AHA 2017, abstract CM.SMP.2505]

“Certainly the apolipoprotein Bs are causal. We have definite proof that lowering them reduces CV events,” Robinson said. “[But] in these trials, we have patients with advanced, extensive burden of plaque. The event rate will never go to zero… [It also] doesn’t make economic sense.”

Even in the FOURIER trial, in which evolocumab plus statin therapy significantly lowered LDL-C and reduced CV events in patients with stable atherosclerotic CV disease, patients who achieved very low LDL-C levels of about 20 mg/dL still had an 8 percent event rate. [N Engl J Med 2017;376:1713-1722]

“Proprotein convertase subtilisin–kexin type 9 [PCSK9] inhibitors can approach cost-effectiveness in very high risk patients with LDL-C levels above 130 mg/dL, and should be reserved for these patients,” said Robinson, emphasizing statin therapy as the primary treatment pathway for bringing cholesterol under control otherwise.

“Use a little bit more nuanced approach where you think about what is the magnitude of benefit from adding a drug,” she said. “I think you’d prefer not to jeopardize adherence to other evidence-based therapies to squeeze out additional LDL-C reduction.”