Contribution of Bart van de Sluis to statement of EAS Consensus Panel on the role of LDL in atherosclerotic cardiovascular disease

Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel

Atherosclerotic cardiovascular disease (ASCVD) starts early, even in childhood. Non-invasive imaging in the PESA (Progression of Early Subclinical Atherosclerosis) study revealed that 71% and 43% of middle-aged men and women, respectively, have evidence of subclinical atherosclerosis. Extensive evidence from epidemiologic, genetic, and clinical intervention studies has indisputably shown that low-density lipoprotein (LDL) is causal in this process, as summarized in the first Consensus Statement on this topic. What are the key biological mechanisms, however, that underlie the central role of LDL in the complex pathophysiology of ASCVD, a chronic and multifaceted lifelong disease process, ultimately culminating in an atherothrombotic event?

This second Consensus Statement on LDL causality discusses the established and newly emerging biology of ASCVD at the molecular, cellular, and tissue levels, with emphasis on integration of the central pathophysiological mechanisms. Key components of this integrative approach include consideration of factors that modulate the atherogenicity of LDL at the arterial wall and downstream effects exerted by LDL particles on the atherogenic process within arterial tissue.

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