A 30-year-old drug helps prevent heart-attack damage

2017-04-19 08:00:00 | | source: Source: CNIS

Time immediately after a heart attack provides a critical window in which damage to the body can be minimized

Much like in the case of strokes, the time immediately after a heart attack provides a critical window in which damage to the body can be minimized. Researchers in Madrid have just figured out how a drug that's been around for decades helps doctors use that time to best advantage.

The drug is known as metoprolol and it is an inexpensive beta-blocker, a class of drugs that lower blood pressure by suppressing the hormone epinephrine, also known as adrenaline.

In 2013, a team from the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) in Madrid conducted clinical trials with metoprolol and found that it could reduce the amount of injury sustained by the heart during an acute myocardial infarction (heart attack), a blockage in a coronary artery that cuts off the heart's blood supply. New research, published in the journal Nature Communications unravels why it works: www.nature.com/articles/ncomms14780

The key lies with neutrophils, white blood cells that fight infections in the body. When a patient is having a heart attack, the goal of doctors is to unblock the coronary artery as quickly as possible to save his or her life. However, once the blockage is removed and blood floods back into the heart, the neutrophils cause a runaway inflammatory process that causes permanent damage to the heart tissue. "When neutrophils enter the infarcted heart tissue after the restoration of blood flow, they act disproportionately, inducing the death of cells that, while weakened, have survived the infarction," says first author Jaime García-Prieto. The damaging sequence is initiated when neutrophils interact with platelets in the blood. "The neutrophils scan for platelets to initiate tissue infiltration," co-author Borja Ibáñez told New Atlas. Metoprolol blocks this interaction and stops them from inflicting their damage. "Metoprolol stuns the blood neutrophils, altering their behavior and limiting their injurious inflammatory action on cardiac muscle," explained García-Prieto in a statement. Particularly, the drug impairs the structural and functional rearrangements needed for the neutrophils to recruit the platelets.

The finding provides a different view of the drug's actions in the body. Previously it was believed that metoprolol worked directly on cardiac muscle cells known as cardiomyocytes. "We knew that platelets were an important factor in the clotting that causes an infarct, but until now we could not be certain that they also act together with neutrophils to magnify injury after blood flow restoration," said Dr. Antonio Fernández-Ortiz in a statement, study co-author and a cardiologist at the Hospital Clínico San Carlos. As Metoprolol is inexpensive and widely available, its use in helping heart attack patients survive their condition in the best way possible is evident. Now, the way in which it does that is as well. "The priority after a heart attack remains the restoration of blood flow as soon as possible, but we need to prepare the heart for this by administering metoprolol," concluded Ibáñez in a CNIS report about the finding.