How blood vessels cause arrhythmias


The heart contracts thanks to a system of special muscle fibers that are not similar to those that make up the bulk of the heart, and which themselves generate a contractile impulse, spreading it to the entire heart muscle. The parts of the heart must work in a certain order and in a single rhythm. If the rhythm is upset, arrhythmia develops.

Arrhythmia has several types and several causes. One of the reasons is the activity of the heart tissue outside the heart. It sounds strange, but in fact, in the vena cava and pulmonary veins connected to the heart, there are so-called myocardial sleeves – sections of the myocardium that extend from the heart to the vessels. The myocardium of the vessels differs from the myocardium of the heart, moreover, it is capable of its own electrical activity. Electrical impulses, which are spontaneously generated in the myocardium of the vessels, enter the heart and prevent the atria from contracting in the correct rhythm. Most often, interfering impulses come from the myocardium of the pulmonary veins, in 15–20% of cases these impulses come from the vena cava, which bring venous blood from the upper and lower parts of the body into the right atrium.

Employees of Moscow State University, along with colleagues from the Institute of Bioorganic Chemistry of the Russian Academy of Sciences and the University of Manchester, describe in Acta Physiologica a mechanism that causes the myocardium of the vena cava to generate unnecessary impulses. The electrical activity of cells is provided by the work of special proteins – ion channels, which let different ions into and out of the cell and thereby change the charge on both sides of the cell membrane.

The researchers studied the channel proteins Kir2.1, Kir2.2 and Kir2.3, which provide the flow of potassium ions from the cells of the heart muscle to the outside. The flow of potassium through the membrane is necessary in order for a stable negative electrical potential to remain in the cell – the so-called resting potential. There are many such potassium channels in the working cells of the atria and ventricles, so their resting potential is stable, and they are not able to spontaneously generate electrical activity. These cells are excited only when a wave of excitation comes to them from the pacemaker of the heart, that is, from those very special muscle fibers that we mentioned at the beginning. At the same time, these special muscle fibers that set the rhythm themselves are practically devoid of the Kir2.1, Kir2.2 and Kir2.3 channels.

In other words, potassium channels do not allow spontaneous independent electrical activity, but allow activity “dictated” from the outside. Therefore, they are not in the pacemaker cells, but they are in ordinary cells that perform contractile work.

However, in the myocardial cells of the vena cava channels, Kir2.2 is synthesized less than, for example, in the cells of the atrial myocardium. Moreover, if the adrenergic receptors α1, then the potassium current through the channel decreases. As a result, the resting electric potential changes so that it becomes easier for the cell to show spontaneous activity. The same receptors are also present in the atrium, but if they are activated in the atrium, muscle cells do not show spontaneous activity – probably because they have more potassium channels and the resting potential is not so easy to knock down.

Α adrenergic receptors1that react to adrenaline and norepinephrine are activated under stress, which means that under stress, the vascular myocardium is more prone to spontaneous electrical activity, which can cause arrhythmias. Perhaps, if you purposefully act on the receptors of the myocardium of the vena cava, you can reduce the likelihood of some types of arrhythmias.

Based on materials from the press service of Moscow State University.


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