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Results We have succeeded in demonstrating the fact that researchers ignore the fact that cardiomyocytes can be excited by mechanical pulses, when considering the arrhythmia mechanisms. We have conducted trials using the Cardiocode device. Under stress in a human, opened may be large and small arteriovenous anastomoses, via which blood under high pressure is ejected into veins. It leads to pressure surges in arteries and veins. The vena cava dilates, its tonus increases. In some cases, the pulse waves travel via anastomoses along the vena cava walls to the atria and the ventricles. An above-threshold concentration of tensions from mechanical pulses may excite cardiomyocytes from different points of the myocardium, disturbing the sinus rhythm. As a result, extrasystoles, tachycardia attacks, blocking of blood circulation in the peripheral segments of the venous arterial networks, edemata, thrombosis and metabolism disorders appear. Arrhythmia, tachycardia attacks and concomitant myocardial ischemia lead to progression of heart fibrosis. Such changes increase the probability of fibrillations and sudden cardiac death.

New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms.