New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms.

Abstract

AimsA new attempt is made to substantiate the concept of the mechanism of arrhythmia and sudden cardiac death. MethodsThe paper is based on a theoretical analysis of special literature, personal experience of participation in conferences and discussions with leading Russian cardiologists. ResultsWe 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. ConclusionsUnhealthy lifestyle, the presence of opening and not properly closing anastomoses may provoke a number of diseases. To avoid the cardiac arrhythmia attacks and prevent SCD, it is necessary to suppress travel of the mechanical waves within the following circuitry: aorta -artery -anastomosis -vein -vena cava -atria -ventricles. The travel of the mechanical waves within the same vessel circuitry explains the fact that the fixed couplings under extrasystoles are observed, and the beat-to-beat RR intervals under tachycardia remain constant. Obviously, we may consider that the reentry mechanism is rather of biomechanical, but not of bioelectrical nature, as it is generally accepted.

Pathological Role of the "Invisible" Anastomoses

“…These vessels even with venous valves are not capable of withstanding high pressure, so the liquid sooner or later runs into the extracellular space, and even occupies the free space between the bodies. There are cardiac arrhythmia due to run the pulse wave on the vena cava, and a mechanical pulse effects on the myocardium, except you experience swelling, stagnation, weight gain, "heart failure", varices, ascites [5][6][7]. On the other hand, due to the reduced at the open AVA gradient pressure between arterioles and venules occurs deceleration capillary circulation, cells do not receive power, stagnant blood becomes thicker lymph movement also slows critical drop strength immunity in stagnant fluid activated viruses and parasites.…”

“…A role in the development of pelvic congestion has a hormonal influence, raising the level of estrogen, which in turn contribute to the expansion of the diameter of the pelvic veins. Now, with the new knowledge about the causes of venous plethora of causes arrhythmia, a pathological role anastomoses AVA, apparently, in the near future we can expect a breakthrough in the understanding of the etiology of many cardiovascular diseases, among the many problems associated with the increased venous pressure [11][12][13].…”

The new theory of cancer complements ancient Chinese Qigong therapy

“…Earlier work has shown some fundamental role arteriovenous anastomoses (AVA) in the mechanism of occurrence of cardiac arrhythmias and other diseases [10][11][12][13][14][15]. It has been shown that the de fitness of the organism during periods of increased physical and nervous stress, due to the short-term or persistent high blood pressure (BP) in humans can be opened AVA.…”

Numerous Studies Show: Not an Excess of Cholesterol, but First of all a Systemic Inflammation is The Real Reason of Many Cardiovascular Diseases and of Sudden Death

“…Let us emphasize that this breakthrough, achieved at least for the last 30 years, was achieved by official medicine, not by a theory, not analytically, but by trial and error with the testing of the effect of various drugs (chemicals) on large groups of patients. But on the other hand, this important message is an additional argument in favor of the New Theory of CVD [4][5][6][7][8][9][10][11][12][13][14][15][16][17], which I have been promoting since 2011. Discovery of scientists from Harvard is an additional argument in understanding the mechanism of tissue perfusion reduction and blood stasis, which, apparently, in itself leads to many CVD.…”