Atrial fibrillation occurs when the upper chambers of the heart beat fast and erratically. This is the most common form of sustained abnormal heart rhythm which reduces the heart’s ability to pump blood. When atrial fibrillation first occurs, it tends to correct itself. However, in a later form known as paroxysmal, this fast and erratic beat can last for as long as seven days and then recur. The most serious form of atrial fibrillation becomes permanent without therapy. Why this erratic and fast heart beat in the atria return has not been understood, however a team of international researchers led by those at Baylor College of Medicine believe that the problem occurs at the molecular level. The new study has found that the ryanodine receptor 2 on the sarcoplasmic reticulum allows for calcium ion leakage.
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Xander Wehrens, professor of Molecular Physiology and Biophysics and director of the Cardiovascular Research Institute at BCM, and colleagues, have discovered the molecular event responsible for chronic atrial fibrillation in mice that have progressive atrial fibrillation. The molecular event involves increases in phosphorylation, which initiates ryanodine receptor 2 activity. Researchers found that if they bred a mouse with chronic atrial fibrillation with a mouse that has a mutation that blocks phosphorylation, the mutation prevents atrial remodeling and chronic atrial fibrillation.
Wehrens notes that understanding how this progression occurs answers a very important question: “Now people may wait until patients have more severe disease to do an ablation (a procedure to eradicate the malfunctioning cells in the heart) to treat the problem. If we can find a way to prevent this, people may never develop the more serious form of the disease. There is an active program to develop those kinds of drugs.” In a recent report, Wehrens and colleagues demonstrated that this kind of calcium leak occurs in early stages of atrial fibrillation.