Physicians' Academy for Cardiovascular Education
"Lowering LDL-c is the first, second and third thing we have to do to lower atherosclerotic event rates, but what can we do beyond LDL-c-lowering", asks Prof. Ridker. He talks about targeting inflammation in patients with residual CV risk.
In a REDUCE-IT substudy, icosapent ethyl had little to no effect on biomarkers associated with atherosclerotic disease, such as IL-1β, IL-6, oxidized LDL-c, and Lp(a). However, mineral oil increased these levels.
What are potential mechanisms that may explain the benefits observed with icosapent ethyl? Prof. Bäck discusses three mechanisms: TG lowering, anti-thrombotic effects, and resolution of inflammation.
Using data from the CANTOS trial, the investigators assessed the relative contributions of hyperlipidemia and inflammation to CV clinical outcomes in atherosclerosis patients on statin therapy, stratified by eGFR.
EASD 2022 In patients with new onset T2DM in the DD2 cohort, high CRP was a better marker of all-cause mortality than future CV events, whereas high C-peptide was a better marker of increased CV risk.
"There are 3 patients with residual inflammatory risk for every patient with residual cholesterol risk," says prof. Ridker. Learn how perspectives on inflammation in atherosclerosis have changed from the1970s up until now and how (novel) anti-inflammatory therapies may reduce CVD risk.
EAS 2022 We need a better understanding of the mechanisms leading to ischemic heart disease (IHD) to improve treatment, says prof. Crea. He explains 4 mechanisms that can lead to thrombus formation and IHD.
Elevated plasma sLOX-1 levels –observed during acute coronary syndromes (ACS) – predict fatal events beyond both established CV risk factors and the updated GRACE score, in the multicenter SPUM-ACS study.
On the topic of inflammation in CVD, prof. Libby and Ridker discuss the journey from theory to testing the hypothesis to reality. "Ultimately, the inflammation hypothesis is going to yield great dividends for our patients", concluded prof. Libby.
"There are 3 patients with residual inflammatory risk for every 1 patients with residual cholesterol risk," says prof. Ridker. What are current and future therapies to lower inflammation in these patients with residual inflammatory risk?
What is the role of inflammation in the occlusion of coronary arteries? Prof. Lüscher presents findings from studies on this topic and discusses outcomes of trials with anti-inflammatory therapies.
Prof. Crea discusses three challenges when considering anti-inflammatory therapies for patients with residual CV risk.
