Biography
Biography: Vladimir Ermoshkin
Abstract
Goal.
C делана попытка нового анализа м еханизм аAn attempt to study heart failure.
Methods.
An examination of the literature, participation in conferences, and discussions with Russian leading cardiologists.
Results.
Heart failure (HF) can be chronic (CHF) or acute (AHF). This terminology was in the 12th Congress of Physicians in 1935, more than 80 years ago. Up until now, the disease has been considered incurable and with an unknown cause, or with unknown etiology.
With current clinical position, CHF is a complex disorder with specific symptoms (dyspnea, fatigue, decreased physical activity, edema, heart rhythm and palpitations al.), which are related to inadequate perfusion of organs and tissues at rest or during exercise. Another characteristic feature of chronic heart failure is fluid retention in the body. Most often, edema begins in the lower extremities, pelvic organs and gradually rise above the body up to the heart and lungs.
Currently, the primary mechanism HF is considered the deterioration of the heart's ability to fill or empty the chambers due to damage to the myocardium, including heart attacks while with concomitant imbalance neurohormonal systems. As a rule, HF ejection fraction is reduced to 30-45%, with the required fraction of 50-65%.
The treatment of heart failure is ineffective. There is a high death rate from heart failure after diagnosis. Symptomatic heart failure occurs in 1.8-2.0% of people. Among people older than 65 years, the frequency of occurrence of heart failure is 6-10%. Further, after heart failure, the five-year survival of patients with heart failure less than 50% and the risk of sudden death in CHF is 5 times higher than in the general population.
Over the past few decades thousands of articles have been written listing the following causes: myocardial infarction, cardiac ischemia, atherosclerosis, high blood pressure (BP), disease of the heart valves, inflammatory and non-inflammatory disease of the myocardium, congenital heart defects, lung disease, alcohol abuse, drug reception, addiction to tobacco.
Thus, HF is widespread, its mechanism is unknown, the treatment of symptomatic, effective treatment of heart failure has not been found, and there is a high mortality rate.
The main conclusion of the interim etiology HF: heart failure can be a major manifestation of virtually all heart disease [1].
Heart failure necessarily occurs following a heart attack, but there are instances of heart failure where no heart attack occurred.
The new theory of cardiovascular disease is based on the fact that the arterial and venous pools may periodically be linked large anastomoses (natural shunts) [2,3,4,5,6]. In normal conditions, arteriovenous anastomoses (AVA) are closed, but during periods of increased physical and psychological stress due to increased blood pressure, they can open. The most common pathological role extended AVA manifests in the liver area. This leads to a reset of the arterial blood directly into veins. Because of this, some groups of working cells are left without sufficient food. Under certain conditions, the AVA may be open too long. As a result, blood high pressure penetrates into the venous bed and gradually fills it. Usually first affecting the liver and portal vein.
Further, high blood pressure occurs not only in the right atrium area, but throughout the vena cava, and extending downwards to the small veins. Much depends on the diameter and network location of the veins, the location of the AVA (one AVA or cascade), lifestyle, and the prevailing human posture.
Of course, a substantial pressure increase in small venules and veins occurs over a long period. In the first stage, venous valves counteract the pathological process, but after some time the venous valves begin to break down. This is due to the necessary counteraction of the total pressure of 60-70 mm Hg and above. The total pressure consists of the diastolic blood pressure and the hydrostatic pressure of the liquid column located above the valve. Due to the lack of pressure difference between arterioles and venules capillary circulation slows in some organs, or even stops. Lymph also stagnates.
In my opinion, obstacles in the form of a blood clot, tumor emboli do not raise the pressure in the veins near the venules, but add additional pressure transmitted through the veins of the confluence zone of large anastomoses [6]. Over time, because of the permeability of vascular veins occur swelling of tissues, varicose veins, venous thrombosis. Cardiology has made a mistake by confusing the cause and effect. If proper prevention is not provided, the process of the disease is enhanced, and further diseases in the small pelvis, lower limbs, and others, including some types of cancer will occur.
Yes, it is, of cancer. There are studies which have shown that the average time of the first heart attack to cancer is equal to only 2.8 years [7]. Another study shows 70% increase in the risk of cancer in patients for three years after a diagnosis of heart failure [8]. Thus, the incidence of heart failure and cancer rigidly connected and this connection is probably due to the stagnation of blood in the veins due to open AVA!
Thus, according to the new theory, the majority of cardiovascular diseases occur due to malfunction of the AVA, due to venous plethora. Extras: because pulse waves running through a crowded vena cava, with mechanical and electrical excitation arrhythmic CMC [2, 9].
Thus, in my opinion, the following provisions must be corrected in cardiology.
1. "The inadequate perfusion of the organs and tissues at rest or under load" in heart failure - is the result of open-AVA, which naturally leads to stasis capillary blood flow in some organs, perfusion to the slowdown.
2. Increased venous pressure in the vena cava and some veins of smaller caliber primarily because of the open ABA. Diseases of the heart valves and the venous valves are usually secondary.
3. "Apnea" occurs due to swelling of the lung tissue. Lungs not only have vessels of the pulmonary circulation, but also arteries and veins of the systemic circulation. At night, in a horizontal position, the excess venous pressure of a great circle reaches the lungs, because all human organs in the supine position are almost equal footing in relation to the Earth's gravity [3].
4. Reducing or maintaining ventricular ejection fraction of the heart, especially at the initial stage of development of heart failure, often does nothing. The problem of hypertension leads to dilation of the heart cavities. The statements regarding the impact of ejection fractions confirmed by the data published in the British Heart Foundation online magazine [10]. «Some people with heart failure have a normal ejection fraction, so ejection fraction is used alongside other tests to help diagnose heart failure». Additionally, there is information in the American Heart Association online journal [11]: «A significant proportion of patients with heart failure happen to have a normal ventricular ejection fraction at ECG during examination».
5. The occurrence and rate of development of heart failure is also influenced by additional human factors, including lifestyle, education level, physical activity, sedentary work, proper diet, special exercises, and genetics.
6. Apparently, there is found the explanation high values pairwise correlations between most of cardiovascular disease. Cardiovascular diseases are correlated with the some types of cancer. The reason is the "wrong" working AVA, it is in the position "open" too long and, unfortunately, are deep inside the human body.
Conclusions.
In my opinion, it is necessary to correct the errors in the field of cardiology. These errors have affected the efficiency of Cardiology for 50-100 years. It is necessary to check and discuss new proposals enabling a new era in cardiology.
References:
1. Ðаучный центр Ñердечно-ÑоÑудиÑтой хирургии им. Ð.Ð. Бакулева. Интернет реÑурÑ. 2017. http://www.bakulev.ru/cyclo/detail.php?ID=39219
2. Ermoshkin VI. New theory of arrhythmia. Conceptual substantiation of arrhythmia mechanisms. Cardiometry; Issue 8; May 2016; p.6–17; doi:10.12710/cardiometry.2016.8.617. http://www.cardiometry.net/issues/no8-may-2016/new-theory-of-arrhythmia
3. Ermoshkin VI. The mechanism of bronchial asthma. Why do the most serious asthma attacks occur at night? EC Cardiology, Volume 2 Issue 4 November 2016 https://www.ecronicon.com/eccy/pdf/ECCY-02-000030.pdf
4. Ermoshkin VI. Arteriovenous anastomoses and cardiovascular diseases. 8th Cardiovascular Nursing & Nurse Practitioners Meeting. August 08-09, 2016 Las Vegas, USA, DOI: 10.4172/2155-9880.C1.045 http://www.omicsonline.org/proceedings/arteriovenous-anastomoses-and-cardiovascular-diseases-48866.html
5. Ermoshkin VI. A New Theory of Certain Cardiovascular Diseases. EC Cardiology, Volume 2 Issue 5 November 2016 https://www.ecronicon.com/eccy/pdf/ECCY-02-000034.pdf
6. Ermoshkin VI. Venous congestion due to large arteriovenous anastomoses. 566 Chiswick High Road, London,
Greater London, W4 5YA, United Kingdom, DOI: 10.15761/HCCT.1000101 https://oatext.com/Venous-congestion-due-to-large-arteriovenous-anastomoses.php
7. Jyoty Malhotra, Paolo Boffetta. Association of increased cancer risk with heart failure. Journal of American College of Cardiology. Vol. 68, No 3, 2016.
8. Clark RA , Berry NM , Chowdhury MH , McCarthy AL , Ullah S. , Versace VL , Atherton JJ , Koczwara B , & Roder, D. (2016) Ð¡ÐµÑ€Ð´ÐµÑ‡Ð½Ð°Ñ Ð½ÐµÐ´Ð¾ÑтаточноÑÑ‚ÑŒ поÑле Ð»ÐµÑ‡ÐµÐ½Ð¸Ñ Ñ€Ð°ÐºÐ°: ХарактериÑтики, выживаемоÑти и ÑмертноÑти анализа данных , ÑвÑзанного Ñо здоровьем. Roder D. (2016) Heart failure following cancer treatment: Characteristics, survival and mortality of a linked health data analysis. Внутренние болезни журнал, 46 (11), ÑÑ‚Ñ€. 1297-1306. Internal Medicine Journal , 46 (11), pp. 1297-1306. http://eprints.qut.edu.au/101771/
9. Kamkin AG, Kiseleva IS, Yarygin VN. Fibrillation, defibrillation. Priroda. 2002;4:1040. [Russian]
10. British Heart Foundation. Heart failure. Internet resource. 2017. https://www.bhf.org.uk/heart-health/conditions/heart-failure