Acute Myocardial Infarction (AMI) or heart attack is responsible for an estimated 610,000 deaths (1 in every 4 deaths) in the United States each year. Heart attack survivors will suffer with long-term consequences, since it potentially leaves part of the heart muscle damaged.
An AMI is the result of a blood clot blocking the blood flow in a coronary artery that feeds the heart. Coronary artery reperfusion therapy is the best form of treatment, because it addresses the primary issues of Segment Elevation Myocardial Infarction (STEMi).
Upon reperfusion, all of the mediators and inflammatory cells that accumulated in the circulation during the infarction process will move into the myocardium, the middle layer of the heart wall responsible for stimulating heart contractions to force blood from the ventricles and atria into the pulmonary and systemic circulatory systems, leading to more damage to the heart. Playing a major role in the damage that occurs upon reperfusion is activated neutrophils, the most abundant white blood cell in humans. The size of the infarction in the end will be the main determinant for long-term morbidity and mortality. It is of paramount importance to limit the degree of infarcted tissue, if at all possible.
Beta-blockers have been utilized to treat hypertension (high blood pressure) and arrhythmias, an irregular heartbeat for over 4 decades. A recent study reveals that early administration of metoprolol, a commonly used beta-blocker, was capable of reducing the size of infarction in heart attack patients. The mechanism by which metoprolol was protective in a heart suffering with a myocardial infarction (MI) was unclear.
The findings reveal that during a MI, metoprolol has an immediate effect on neutrophils preventing their inflammatory activity. Stunning the neutrophils will prevent them from being able to exert injury to the heart upon reperfusion, leading to a reduction in the size of the infarction.
This is the first time that beta-blockers have shown to have a strong influence on activated neutrophils. Previously, the effect of beta-blockers was thought to occur by only targeting cardiac cells. The effect of metoprolol on circulating cells opens up opportunities for new applications. The drug may also be helpful in treating other conditions in which activated neutrophils are responsible for causing more damage, such as sepsis.
The authors note that future studies are required to analyze the effect of metoprolol on other diseases that are negatively influenced by activated neutrophils.
The study was first published in the journal Nature on January 30, 2017 and published online April 18, 2017.