Immune Defense Creates Holes in the Heart

SadaNews - Researchers have found that a protein produced by immune cells creates holes in heart cells after a heart attack, indicating that immune cells play a critical role in sudden death and arrhythmias.

The study was conducted by researchers from Harvard Medical School in the United States, and its results were published in the journal "Science" on September 4 of this year, as reported by the website EurekAlert.

Myocardial infarction and sudden cardiac death are among the deadliest complications of coronary artery disease.

Occlusion of one of the heart's arteries during a myocardial infarction leads to a lack of oxygen supply to heart muscle cells, weakening their ability to maintain a steady rhythm, which can cause arrhythmias (cardiac rhythm disorders) known as ventricular tachycardia and ventricular fibrillation.

In ventricular tachycardia, the heart beats very fast but in a coordinated rhythm, while in ventricular fibrillation, the rhythm is chaotic and uncoordinated.

Infiltration of Immune Cells

Both ventricular tachycardia and ventricular fibrillation are serious arrhythmias that can lead to sudden cardiac arrest and death within minutes.

Most cases of arrhythmia occur within 48 hours after a myocardial infarction, coinciding with a significant infiltration of immune cells into heart tissues.

The researchers were interested in how these immune cells exacerbate arrhythmias and found in laboratory mice that neutrophils, which come to the infarct area (the area of dead tissue resulting from a lack of oxygen supply) in large numbers, regulate the gene "Retnlg", which encodes a protein called RELMy, part of a family of pore-forming proteins that defend the host against bacteria by puncturing their membranes.

When the researchers removed this protein from the neutrophils in the mice, the burden of arrhythmia after myocardial infarction decreased by 12 times.

The researchers found a similar gene, "RETN", in heart tissues of humans affected by myocardial infarction.

Source: EurekAlert