AHA 2020 Prevalence of CAD in a Swedish population was 4 out of 10, using CCTA data from the SCAPIS cohort. A prediction model was developed to identify those with widespread atherosclerosis.

Three experts discuss the findings of the EVAPORATE study in detail and how to interpret these. The EVAPORATE trial examined the effect of icosapent ethyl on plaque formation and was a mechanistic study for the REDUCE-IT trial.

This study evaluated the independent and joint associations of elevated Lp(a) and family history of CHD with incident ASCVD and CHD events among asymptomatic subjects.

ASCVD event rate in PAD patients is similar as that in CHD patients, yet statin therapy was lower in PAD patients.

Prof. Klaus Parhofer discusses the role of hypertriglyceridemia in the setting of residual risk.

Among asymptomatic phenotypic FH patients, patients with a genetically confirmed FH diagnosis had a higher frequency and severity of coronary atherosclerotic plaques, compared to those without a FH-causing mutation.

Presence of coronary artery calcium and risk of incident ASCVD events increased with increasing SBP levels in individuals with a SBP between 90 and 129 mmHg and no other traditional ASCVD risk factors.

This post-hoc analysis demonstrated similar BP reductions after renal denervation (RDN) across high-risk subgroups and ASCVD risk scores. Reductions were sustained up to 3 years after RDN.

P2Y12i monotherapy reduces risk of MI, but not of stroke, all cause death, vascular death and bleeding, compared to aspirin monotherapy, in patients with established atherosclerosis.

Relationships between inflammation, LDL-c and CV risk have not much changed compared to findings from two decades ago. Those with highest levels of IL-6 or hsCRP and highest levels of LDL-c have highest risk of MACE.

Lp(a) meeting Jeffrey Kroon presents his study on inflammatory mechanisms driving CV risk in patients with high Lp(a) levels and a potential new strategy to reduce atherogenesis in these patients.

The Consensus Panel of the European Atherosclerosis Society has published a statement on key biological mechanisms that underlie the central role of LDL-c in the pathophysiology of ASCVD.