Physicians' Academy for Cardiovascular Education
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.
Prof. Ray explains how he decides on the amount of LDL-c lowering that is needed in a given patient, and why he chooses this approach.
The ICONIC study provides support for the hypothesis that higher-density calcified plaques are more stable, as patients who had ACS had lower high-density plaque volume than those without an event.
The new ESC/EAS Dyslipidaemia Guidelines focus on high-risk patients, and prof. Laufs shares evidence for the treatment recommendations. Test your knowledge
Prof. Landmesser shows data that form the rationale behind new guideline recommendations, among which the lower LDL-c target for patients at very high risk.
Prof. Lüscher paints a picture of how atherosclerosis has been a fact of human life throughout time, and the evolution of insights on how to lower LDL-c and its associated CV risk.
Presence of calcified plaques have been found in the mummified remains of three of four studied young Inuit individuals who lived 500 years ago.
AHA 2019 The 9-months data of the EVAPORATE study show slowing of several markers of plaque progression, although the primary endpoint of low attenuation plaque was not met.
