Peter Libby, MD, discusses the science behind inflammation and cardiovascular health.
Inflammation is a critical factor in cardiovascular events and going on in the future should become increasingly a part of screening processes for patients, according to two keynote presentations today, Oct. 21, at the 2010 Cardiometabolic Health Conference.
Peter Libby, MD, chief of cardiovascular medicine at Brigham and Women’s Hospital, delivered a presentation on the science behind inflammation and cardiovascular risk, to kick off the session.
Libby began his presentation by describing some of the traditional views of atherosclerosis and how the research has evolved throughout the years. Previously, the view was that the condition was similar to “rusting in a pipe.” Later on, the idea progressed to where medical researchers began to view the arteries as having living components that were crucial to its functioning. Of this understanding came the “Response to Injury” theory which posited that the condition formed as a result of what the body identified as injury. Perceived injury to artery cells released certain mediators that would promote atherosclerosis.
Today, a growing body of research demonstrates that the biological process that causes atherosclerosis is inflammation, he said. The process occurs at the endothelium level. A normal artery endolethium produces mediators that protect the layer from inflammation or oxidative stress, he said. However, during the initiation of atheroma, attachments of monocytes attack the endolethium and invade the layer. Recently, research has been focused on uncovering why these macrophages form and invade the layer, and a key finding Is that all monocytes are not created equal, he said. Specifically, a subset of pro-inflammatory monocytes exists. Not only does inflammation play a role in cardiovascular events, but obesity and diabetes as well.
An overload of fatty acids is associated with metabolic syndrome in diabetes. Adipose tissue is a source of pro-inflammatory cytokines as well, which plays a role in stimulating macrophages. Libby presented data that demonstrated the pro-inflammatory markers associated with high fat diets in animal models and the result of oxidative stress. Data from the 1940s clearly demonstrates adipose fat as being metabolically pernicious, he said.
There is also a profound metabolic differences between visceral adipose tissue and subcutaneous adipose tissue. T cells play a key role in the process, sending controlling messages to macrophages. However, there are also regulatory T cells that can mute the action of pro-inflammatory T cells, according to research. Along with regulatory T cells, mast cells, which are known agents in allergen disease also play a role in atherosclerosis, Reducing the number of mast cells has been shown to reduce the risk of obesity and diabetes in genetically altered mice.
Inflammation also plays a key role in thrombosis, he said. Inflammatory mediators are released at site of thrombosis and amplify local inflammation. A process that is profoundly influential on diabntes abd atherosclerosis, he said.