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Kamkin, A. N.; Bukhan’ko, N. G.; Глухов, Л. М.

doi:10.1023/a:1020603703569

Cited by 3 publications

(2 citation statements)

References 12 publications

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“…But several groups of scientists still stand out, in particular, Professor A.G. Kamkin's team, which upon special studies in 1985-2002 has made some far-reaching conclusions [1]: "The cardiomyocytes and the fibroblasts to an even greater extent efficiently convert mechanical stimulation into electrical responses, and as this takes place, the performance of the first sort of the cells (cardiomyocytes) is modulated by the second one (fibroblasts). " Unfortunately, those theoretical and experimental conceptual findings were not used, in my opinion, by a reason as follows: nobody dared or has seen any possibility of "how to apply it".…”

Section: Resultsmentioning

confidence: 99%

New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms.

Ermoshkin¹

2016

Cardiometry

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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.

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Section: Resultsmentioning

confidence: 99%

New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms.

Ermoshkin¹

2016

Cardiometry

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“…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.…”

Section: Resultsmentioning

confidence: 99%

Pathological Role of the "Invisible" Anastomoses

Ermoshkin¹

2016

J Bioengineer & Biomedical Sci

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Thesis: An attempt to analyse the mechanism of cardiovascular disease (CVD). It is now believed that most heart disease of unknown etiologic and mechanism, with the CVD mortality is very high. Why theoretical medicine for over 100 years has such limited success? What is the true reason, for example, venous plethora?Methods: Finding information in the literature, participation in medical conferences in Russia (2012Russia ( -2016, as well as in Australia, Brisbane "Arrhythmia-2016", correspondence with scientists, discussions with leading Russian cardiologists, publication of my original articles.Results: I was able to show that in modern theoretical cardiology there are significant errors. Our group with an instrument "Cardiocode" were able to confirm the presence of large arteriovenous anastomoses (AVA) in otherwise healthy people. The sudden opening of the lumen AVA causes a sharp drop in blood pressure.When closing AVA, usually a few seconds, the blood pressure increases again. Such manipulations AVA, apparently provided by nature to protect the blood vessels from the peak pressure values. It turns out that the longterm "wrong" operation AVA, especially when an unhealthy lifestyle usually leads to two major problems. First problem:The periodic disturbances of heart rhythm, sometimes with fatal outcome, due to excitation of the heart by means of a pulse of mechanical waves running through the contour of the vessels with the return of their heart. The second problem is: violation of "metabolism" of the prolonged increase in venous pressure as a systemic and local. This paper attempts to study the causes of venous plethora and diseases of the pelvic organs in humans.Conclusions: I believe that, taking into account the vast experience of the modern official medicine, taking into account the large number of clinical observations, and using in the near future, the theory proposed by me might be able to make a breakthrough in the treatment of cardiovascular disease, including in the treatment of venous plethora.

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3D numerical simulation of the pressure-driven flow in a four-electrode rectangular micro-electrochemical accelerometer

Sun¹,

Agafonov

2010

Sensors and Actuators B: Chemical

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Untitled

Cited by 3 publications

References 12 publications

New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms.

New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms.

Pathological Role of the "Invisible" Anastomoses

3D numerical simulation of the pressure-driven flow in a four-electrode rectangular micro-electrochemical accelerometer

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