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Archive - Apr 18, 2017

Mechanism of Action Determined for Long-Time Heart Attack Drug--Metoprolol Reduces Damage from Myocardial Infarction by Inhibiting Inflammatory Action of Neutrophils

Scientists at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) in Madrid, Spain, together with collaborators, have discovered a new mechanism of action of metoprolol, a drug that can reduce the damage produced during a heart attack if administered early. The team led by Dr. Borja Ibáñez, Clinical Research Director at the CNIC and cardiologist at the Fundación Jiménez Díaz University Hospital Health Research Institute (IIS-FJD), has identified the mechanism that explains why this drug is so beneficial: rapid administration of metoprolol during a heart attack directly inhibits the inflammatory action of neutrophils, a type of blood cell. The reduced inflammation translates into a smaller area of damaged tissue in the post-infarcted heart. The finding, published on April 18, 2017 in Nature Communications, opens the way to new applications for this cheap, safe, and simple drug. The article is titled “Neutrophil Stunning by Metoprolol Reduces Infarct Size.” Acute myocardial infarction is a serious disease that affects more than 50 000 people a year in Spain. Treatment has advanced a great deal in recent years, especially in the extensive use of coronary angioplasty, in which a catheter is used to re-establish blood flow through the blocked coronary artery. Nevertheless, many heart attack survivors have seriously impaired heart function that limits their long-term health and generates major costs to the health system. The search for treatments to limit the irreversible damage caused by a heart attack is an extremely important research area in terms of both patient care and health policy. Neutrophils are white blood cells that target and fight infections.

FEATURE: CEO of Chronic Fatigue Syndrome Advocacy Group Is Paradoxical Ball of Productive Energy

On first meeting Carol Head (photo) ( there are many things that you would not likely guess right away. You would not guess, for instance that she was VP of the Organizing Committee for the 1984 Summer Olympics in Los Angeles. You would also likely not guess that she had spent eight years in a variety of executive positions at the LA Times. And most of all, you would never guess that she suffers from the debilitating energy-sapping disease commonly known as chronic fatigue syndrome (CFS). (Patients prefer to call the disease M.E. for myalgic encephalomyelitis and, as a result, the disease has recently been re-named to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).) [For more information on this disease, please go to this web site (]. But Carol does have this debilitating disease and, for the last three years, this paradoxically dynamic woman has served as CEO and President of the increasingly effective Solve ME/CFS Initiative (SMCI) (, the primary research and advocacy organization for ME/CFS patients in the United States and an international leader in biomedical research for the disease. For the work she is doing with SMCI, Carol was recently recognized as one of fourteen Health Heroes for 2017 in Oprah Winfrey’s O Magazine ( In 2015, Francis Collins (, M.D. Ph.D., Director of the National Institutes of Health (NIH) and former Director of the National Human Genome Research Institute (NHGRI), and leader of the Human Genome Project said, “Of the many mysterious illnesses that science has yet to unravel, ME/CFS has proven to be one of the most challenging.”