Theory of arrhythmia based on mechano-electric feedback between cardiac myocytes and cardiac fibroblasts

Imprint

Sergey V. Kolmakow. Theory of arrhythmia based on mechano-electric feedback between cardiac myocytes and cardiac fibroblasts. Cardiometry; Issue 8; May 2016; p.31–32; doi: 10.12710/cardiometry.2016.8.3132 Available from:

When analyzing the articles submitted to our current issue, we involved into the preparation processing some relevant papers deserving special attention. The papers reveal the mechano-electric mechanism of the feedback between cardiac myocytes and cardiac fibroblasts that is capable of directly initiating cardiac arrhythmia. In the meantime, unfortunately, direct communication with Russian researchers Kamkin A.G., Kiseleva I.S. and Yarygin V.N. was not possible, but nevertheless, we are of the opinion that it is reasonable to review their articles, which discuss this interesting and logically justified mechanism of arrhythmia.

The theory proposed by the above authors is based on a new conceptual philosophy that cardiac myocytes and cardiac fibroblasts interact with each other via mechano- sensitive ion channels, which are activated upon mechanical action on biological tissue [1-13].

Such condition may occur during the repolarization phase. As a result, a mechano- induced depolarization appears. In this case, generated is a potential of significant amplitude, which causes extra-potentials of action that leads to extrasystoles, and under the stable mechano-induced depolarization it leads to fibrillations. In a healthy heart, the mechanism of the action potential, firing upon stretch of the tissue, is within the physiological norm, and it is reversible, when the stretch is released [1-13].

It should be noted that the ion channels are employed to organize Na-ions conduction. And in case when an extraordinary flux of Na-ions through the channels is organized in diastole again, it causes the generation of an extra QRS complex similar in the shape to the normal one.

According to the conceptual philosophy of the above mentioned authors, a pronounced degree of the fibroblasts response to the mechanical action allows considering them as natural mechano-electric converters in the heart. In case of heart pathologies, the sensitivity of the fibroblasts to the mechanical action sharply increases owing to an elevation of the channel concentration. Observed is also an increase in their sensitivity to the cardiac tissue stretching with age.

The total number of fibroblasts in the heart is rather high. They are widely found in the atria and, first of all, in the sinoatrial node area, where they surround the pacemaker cells on all sides [14-21].

The authors of the said theoretical concept logically conclude that stretch of a cardiomyocyte leads to its depolarization, and stretch of a fibroblast provides for its hyperpolarization. They also note the following: “Under the normal conditions, these processes are well balanced. But in case of pathology, the reaction to stretching is extremely pronounced for both types of the cardiac cells. In such a case, the degree of their intercellular interaction and the degree of their response to the mechanical action is of importance. If the hyperpolarization of the fibroblasts is greater than the depolarization of the cardiomyocytes, the fibroblasts show their greater influence, and that will produce an effect of heart rhythm slowing-down up to possible cardiac arrest. But if the depolarization of the cardiomyocytes is greater, as compared with the hyperpolarization transmitted from the fibroblasts, arrhythmias appear”.

Unfortunately, we are missing references to literature, which may contain evidence to support practical applications of the proposed theory. But we share the opinion of the authors thereof: “This fundamentally new theory has a great value not only for theoretical substantiation of the heart performance, but also for implementation under clinical conditions, in particular in cases of slow chronic myocardi- al stretch, for example, under increased intracardiac pressure. In the above case, even postural changes of a post-myocardial infarction patient leads to the known dramatic outcome due to the change in the heart blood filling and cardiac tissue stretching” [1-6, 8-10].

In conclusion, let us present our views on this fresh approach. In our opinion, the proposed theory meets all requirements to be applied to proof in natural sciences. The conceptual approach is logical and may be widely used in practice. We hope some novel methods for correction of the described type of arrhythmias will be offered in the future. And, that is more important, the measures to prevent or avoid progression of pathological heart rhythm processes will be successfully developed.