"There are 3 patients with residual inflammatory risk for every 1 patients with residual cholesterol risk," says prof. Ridker. Learn how perspectives on inflammation in atherosclerosis have changed from 1970s up until now and how (novel) anti-inflammatory therapies may reduce CVD risk.

EAS 2022 Prof. Kausik Ray, the president of the EAS, reflects on the EAS congress, now that participants are onsite again after 2 years.

ACC 2022 ACS patients frequently harbor vulnerable plaques in non-infarct related coronary arteries. The PACMAN AMI study investigated to which degree vulnerable plaques can regress and stabilize in patients receiving alirocumab on top of high-intensity statin.

Prof. Crea discusses three challenges when considering anti-inflammatory therapies for patients with residual CV risk.

Prof. Libby introduces a series of presentations on immunity and inflammation in atherosclerosis. He discusses perspectives on atherosclerosis from 1976 up until now.

This study investigated the predictive value of a targeted plasma proteomics approach, analyzed with machine learning techniques in a secondary prevention setting.

A study shows that elevated Lp(a) is independently associated with accelerated progression of low-attenuation plaque in patients with advanced multivessel CAD on guideline-directed preventive therapies.

Peter Libby, John Deanfield and Charalambos Antoniades talk about the relevance of coronary inflammation in clinical practice and discuss how inflammation in the coronary circulation can be measured.

Charalambos Antoniades explains why coronary inflammation needs to be diagnosed and treated and shows how perivascular fat analysis from routine CTCA can provide a quantitative assessment of coronary inflammation.

Prof. Peter Libby brings us up to date on some novel aspects of inflammation in atherosclerosis.

ESC 2021 The Nature-PCSK9 trial, a naturally randomized target trial, showed a stepwise increase in the proportional reduction in lifetime risk of CV events with each earlier decade that LDL-c lowering was started by inhibiting PCSK9 with one-yearly dose of siRNA.

Higher ratio of LDL-c/ApoB was associated with MACE and with all-cause mortality and total CV events in patients with established atherosclerosis in a prospective cohort study.