Clinical trials in recent years have proven that inflammation contributes to atherosclerotic cardiovascular disease. Peter Libby, MD, FACC, a leader in the study of inflammation, will track its metamorphosis since the 1980s from theory to scientific fact when he presents today's Eugene Braunwald Keynote.

"When I started out, the concept of inflammation in cardiology was quite foreign," says Libby, Mallinckrodt professor of medicine at Harvard Medical School and president of the International Atherosclerosis Society. "It wasn't until the 1990s, with the advent of the application of clinical biomarkers of inflammation, that clinical practitioners began to take seriously inflammation in atherosclerosis. Now it is really a quite widespread view and the basic concept is well accepted that inflammation contributes importantly to many cardiovascular diseases … almost all of them."

Libby says he initially had to fight the perception that inflammation supplanted other established risk factors for atherosclerosis and cardiovascular disease, including cholesterol, hypertension, high blood pressure, smoking and aging.

"There is no competition between traditional risk factors and inflammation," he says. "Inflammation involves a series of biological pathways that can link the traditional risk factors to the altered biology of the blood vessels and the heart that give rise to disease."

In his Keynote, Libby will review the basic bench research that led to small-scale clinical investigations and biomarker studies and explain how that science has been translated into clinical practice. A key in convincing skeptics that inflammation contributes to cardiovascular disease was a reduction in clinical events when researchers blocked some of those pathways.

"As a proponent of the inflammation hypothesis, I have viewed inflammation as a set of biological pathways that provide a transducer of those established risk factors to change behavior of the cells of the artery wall and also recruit inflammatory cells," he says. "Functions that ordinarily help us fight pathogens, repair injury and staunch bleeding in our host defense responses can actually turn against us when we encounter chronic inappropriate stimuli, such as classical risk factors, and promote rather than protect against disease."

Libby will also explain recent research about clonal hematopoiesis and the role of bone marrow stem cells that develop mutations that accumulate with age and comprise a newly discovered driver of cardiovascular diseases, completely independent of traditional risk factors.

"Today, we have anti-inflammatory drugs that we can deploy in cardiovascular practice. I will talk about some ongoing studies with medications that we believe can confer cardiovascular benefits," he says. "We increasingly appreciate how chronic emotional or societal stress, sleep disturbance and dietary factors may influence heart disease risk by modulating inflammation. I planted my flag in this arena in the early 1980s. It was very lonely back then when our early basic science work pointed to inflammation as a key component of vascular disease. But a lot of what I hypothesized back then has turned out to be right."

Providing an update on his inflammation research during the Eugene Braunwald Keynote is particularly gratifying for Libby, who met Braunwald, his career-long mentor, on the first day of medical school and has worked with him for many years.

"Dr. Braunwald's career and those of many of the people he trained and inspired, including myself, exemplify the clinician-investigator. Now, more than ever, it is important that we have clinically trained, clinically active physicians who engage in research, both fundamental and clinical," Libby says.