It has been a long developing concept that inflammatory infiltration by white blood cells from the blood plasma is an important part of the atherosclerotic process. However, we have thought of this as a secondary phenomenon resulting from the causative insults of high concentrations of apolipoprotein B (apoB)-containing lipoproteins, toxins such as those from cigarette smoke, high blood pressure, and high blood glucose. Much research has provided evidence as to how the invading cells interact with the basic components of the arterial structure to produce the damage observed throughout the vessel wall. We have focused our preventive efforts on the clinical risk factors with significant but partial success in patients with active disease. It is a relatively new concept that suppressing the inflammation itself, as an adjunct to risk factor modification, could help reduce the clinical manifestations of atherosclerosis. This concept is now being tested in randomized clinical trials. Our discussants in this Roundtable are Dr Alan Remaley, a Senior Investigator in the Lipoprotein Metabolism Section of the National Heart Lung and Blood Institute and Dr Paul Ridker, a cardiologist at the Brigham and Women's Hospital and a Professor at the Harvard Medical School. Both have made very significant contributions to our understanding of the signaling process that drives this inflammatory aspect of the disease.
Keywords: ASCVD; Apolipoprotein B; Atherosclerosis; Inflammation; Prevention.
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