Practice Update: Cardiology

CONFERENCE COVERAGE 16

ESC 2017: The Interleukin-1 β Inhibitor Canakinumab Cuts Cardiovascular Disease and Lung Cancer Risk by Reducing Inflammation – CANTOS Trial

persistent, elevated levels of high-sensitivity C-reactive protein, a marker of inflammation. All patients received aggressive stand- ard care, which included high doses of cholesterol-lowering statins. In addition, par- ticipants were randomized to 50, 150, or 300 mg of canakinumab, or placebo, adminis- tered subcutaneously once every 3 months. Patients were followed for up to 4 years. The primary endpoint was the first occur- rence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. The secondary endpoint was the first occurrence of any of the above, or of hos- pitalization for unstable angina requiring urgent revascularization. Canakinumab at doses of 150 or 300 mg reduced the risk of a cardiovascular event (the primary endpoint) by 15% and 14%, respectively. Hazard ratios for the pri- mary endpoint in the 50, 150, and 300 mg groups were 0.93 (95% confidence interval 0.80–1.07; P = .30), 0.85 (95% confidence interval 0.74–0.98; P = .021); and 0.86 (95% confidence interval 0.75–0.99; P = .031), respectively.

The interleukin-1β inhibitor canakinumab lowered risk of cardiovascular disease and lung cancer risk by reducing inflammation. This conclusion, based on results of the Canakinumab ANti-inflammatory Thrombosis Outcomes Study (CANTOS) trial, conducted in 39 countries, was presented at the 2017 European Society of Cardiology (ESC) Congress, from August 26–30. P aul M. Ridker, MD, of the Center for Cardiovascular Disease Prevention at Brigham and Women’s Hospital, Bos-

The CANTOS trial aimed to determine whether reducing inflammation in patients who had a prior heart attack can lower risk of another cardiovascular event. The eval- uated drug was canakinumab, a human monoclonal antibody that neutralizes inter- leukin-1β signaling, thereby suppressing inflammation. It is used to treat rare inherited conditions associated with overproduction of interleukin-1β. Interleukin-β is known to play “multiple roles in the development of atherothrombotic plaque,” the investigators noted. These roles include inducing procoagulant activity, pro- moting monocyte and leukocyte adhesion to vascular endothelial cells, and promoting the growth of vascular smooth-muscle cells. The study included 10,061 patients who had previously suffered a heart attack and had

ton, Massachusetts, said, “These findings represent the end game of more than two decades of research, stemming from a crit- ical observation that half of heart attacks occur in people who do not have high cholesterol.” He continued, “For the first time, we’ve been able to definitively show that lower- ing inflammation independent of cholesterol reduces cardiovascular risk. This has far-reaching implications. By leveraging an entirely newway to treat patients – targeting inflammation – we may be able to improve outcomes significantly for certain very high risk populations.”

© ESC Congress 2017 – European Society of Cardiology

PRACTICEUPDATE CARDIOLOGY