Spread the love

Quite paradoxically, in our time, in many cases, heart disease fighting these diseases from the beginning is doomed to failure only because these diseases are mistakenly diagnosed as angina.

Myocardial infarction and angina almost exhaust the concept of coronary heart disease. The difference between these two kinds, as they say in the pathogenesis between those (and only those!), how long and totally occludes the coronary artery embolus. If the embolus is small and during the time to 20 30 minutes the body manages by itself or coronary means (validol, nitroglycerine) to push an embolus in one of the smaller vessels, we are dealing with angina. If the embolus is large enough and using nitroglycerin fails to push it through the coronary artery for 20 to 30 minutes, then we are dealing with a myocardial infarction; after 6 — 8 hours increased by a few days the body temperature, and real help can be expected, according to modern views, only fibrinolitikov, resolving embolus.

 

 

Myocardial infarction and Angina

 

 

The resulting difference between angina pectoris and myocardial infarction, is the largest damage to attack damage.

 

  • Angina are clogged with the embolus and, eventually, killed one of the smaller vessels and damage to the myocardium is insignificant.
  • Myocardial infarction sealed with embolus to the coronary artery and damage to the myocardium is so great that can have disastrous consequences for the organism.

 

Angina does not have a prolonged course. Long flowing strokes — this is myocardial infarction. Chronic angina can not be.

 

 

 

Angina is happily not an established myocardial infarction. But a warning — the next attack may be myocardial infarction.

 

Outstanding bass Evgeny Nesterenko in the newspaper “Trud” reported that the future academician I. P. Pavlov in his youth after the presentation of “Boris Godunov” by Mussorgsky said that in the death scene of Boris is given a clinically accurate picture of death from angina pectoris (angina).

 

Indeed, the picture of death is clinically precise, but not from angina, and myocardial infarction. Angina does not die.

 

The fight against coronary heart disease (embolism of the coronary arteries) is sent on release of the coronary artery from embolus in the shortest possible time. Usually strive to expand the coronary artery to dissolve the embolus, but if it fails to make quickly, then it should be a long, difficult and usually incomplete liquidation of consequences of the disease.

 

Every attack coronary heart disease can be either angina or myocardial infarction.

 

Angina does not transform and does not end with a heart attack. Although many authors write that 1/3 of cases of angina pectoris ends with myocardial infarction.

 

Ends with angina only angina pectoris, myocardial infarction — myocardial infarction.

 

 

 

Specific instruction manuals usually indicate that if the angina is delayed, prolonged oxygen starvation of the myocardium may lead to myocardial infarction. These guidelines are deeply flawed. If the attack is delayed, it was from the outset myocardial infarction, not angina.

 

In connection with angina pectoris are given conflicting advice (and explain them), in what position should the patient be in during an attack: vertical or horizontal. Often referred to junk in the horizontal position, the outflow of blood from the lower extremities and a corresponding increase in the inflow of blood to the heart, increases the load on the myocardium.

 

The most important thing during a seizure is more likely to vacate coronary artery from embolus. And this requires a vertical position of the patient or a sitting position, as in horizontal position receives the advantage of the parasympathetic division of the autonomic nervous system, which contributes to narrowing of the coronary arteries. It is necessary, first and foremost, worry about the expansion of the coronary arteries. Patients usually themselves instinctively sits up in bed, keeping my feet or even up to facilitate the attack.

 

The advantage of the parasympathetic division of the autonomic nervous system, the main representative of which is the vagus nerve (vagus), which is manifested in the narrowing of the coronary arteries at the position of a man lying down, leads to the fact that the attacks of coronary heart disease more often at night (“night — Kingdom of the vagus nerve”).

 

Quite paradoxically, in our time, in many cases, heart disease fighting these diseases from the beginning is doomed to failure only because these diseases are mistakenly diagnosed as angina.

 

Angina (angina pectoris) is characterized by pain behind the breastbone or in the region of the heart, sometimes in epigastralgia region. This is the main diagnostic feature of angina.

 

Pain angina squeezing, pressing, sometimes just a feeling of tightness, pressure, sometimes burning sensation. The pain is paroxysmal, ie, have a fairly clear beginning and end. Pain of moderate intensity. Duration of pain — minutes, rarely up to half an hour.

 

The name of the disease comes from the Greek words “stenos” narrow, cramped and “kardia” — heart.

 

From among the processes leading to coronary heart disease, we excluded spasms of the coronary arteries. But in application to of angina this issue requires further consideration. Here we are dealing with old and firmly established misconceptions widespread, misconceptions “multi-story”, i.e. including when errors are layered on one another, misconceptions, unfortunately, often associated with a reputable name.

 

In specific guidelines, as a rule, it is said that when angina occurs a reflex (involuntary, automatic) effects on spastic coronary arteries in the skin and lung in the cold, have stomach when diseases (gastrocardiac syndrome), the gallbladder (cholecysto coronary syndrome Botkin).

 

It is reported that the viscero-coronary angina be 30.7% of the total incidence of angina.

 

Indicate clear dependence of stenokardicheskie pain in the heart from acute foci of irritatie (irritation) on the part of the gastrointestinal tract (often with cholecystitis) in 1/3 of patients with angina, etc., etc.

 

Moreover, all such arguments are erroneous in the sense that the spasm of coronary arteries in General and is not characteristic of angina is not fundamentally can be based on natural “spastic effect”, but only in spasms, caused by the artificial introduction into the body of chemicals.

 

These provisions are proved in the present work for the first time, the authors of special works of these provisions was not known and admitted their errors can be considered as quite natural.

 

But in all specific guidelines they say it is a reflex spastic effect on the coronary arteries, based on the irritation of going to the heart branches of the vagus nerve due to irritation of branches of the vagus nerve in the other visceral (internal) organ.

 

Fortunately for the people, nature has taken care that this very common idea is not true.

 

Hard to imagine what would happen to humanity if any disease of the stomach, liver or intestines automatically (reflex) caused disease all other (or at least part of) the internal organs, including the heart.

 

Suffice it to recall that the vast majority of patients with cholecystitis and other visceral diseases never had any episodes that resemble stenokardicheskie. The reflex effects on visceral organs can exist only selectively among individuals, the reflex path all the same.

 

The spread of this “double-Decker” error contributed to the actual observation similar to angina effects on the heart cold, cold wind, inflammation of the gallbladder.

 

In rare (aortic aneurysm, diaphragmatic herniation) or funny (overflow of the stomach with food, flatulence intestines) cases, we can speak of mechanical compression of the heart and its vessels from the outside, but not on angina, but the pain stenokardicheskie type.

 

In most cases, is administered to a invalid drug of chemicals or mixing with angina pain, reminiscent of stenokardicheskie but relapses caused by acquired heart diseases and other heart diseases.

 

Thus, the influence of the cold, cold wind on your heart when you got defects due to the direct influence of cold on the blood vessels of the lung (small) circle of blood Circulation and strengthening of hypertension in these vessels due to their cooling and contraction. Pain in this case is very similar to stenokardicheskie.

 

With acquired valvular heart disease any increase of load on it, including the inevitable increased burden in diseases of the internal organs (according to the teachings of H. Selye), is not accompanied by adequate increase of blood circulation heart that causes pain similar to stenokardicheskie.

 

To distinguish pain similar to stenokardicheskie, in acquired heart defects from genuine angina is usually is not difficult. This helps us shown above, the idea of angina as a short-term option of embolism of the coronary arteries.

 

Pain in acquired heart defects typically are reduced by merely reducing the load (stop when driving, etc.).

 

In true angina there is no reduction of the load to the relief of an attack does not, because the blood supply to the heart at inadequate and alone (an embolus in the coronary artery!).

 

The termination of angina is associated only with the displacement of the embolus of the coronary artery in one of the smaller vessels of the heart, and not with reducing load.

 

It’s a shame that a special manual is incorrectly oriented doctors, indicating the possibility of relief of angina attacks by reducing the stress.

 

All specific guidelines given as the following symptoms: during an attack there is often a radiating (spreading) of pain in the left arm, left shoulder blade, left shoulder, left hand fingers, rarely in the neck or lower jaw on the left. This is a consequence of compression of the enlarged left atrium left subclavian artery in Association with a stagnant overflow of the left atrium.

 

And again we have to talk about common cardiac mistake. These pains are not characteristic of angina, which is not accompanied by left atrial enlargement. Angina is of short duration and left atrial enlargement — long-flowing process of compensation of acquired heart defects.

 

The combination of chronic pain in heart and left arm, left shoulder, etc. helps you immediately diagnose acquired malformation of the left heart left atrial enlargement, but not angina. And acquired heart diseases are mainly rheumatic in nature and require completely different treatment.

 

Moreover, it is inappropriate to speak about pain in left arm, left shoulder blade, etc. after the stroke, because after the stroke work of the heart is indistinguishable from that which was observed before the attack.

 

The literature describes “atypical” and rare myocardial infarction, the cause of which is not a violation of the blood supply to the myocardium due to blockage of a coronary artery, and the change, according to the cardiology, metabolic processes in the myocardium. Professor A. L. Myasnikov called necrotic foci this type of myocardial infarction “nekoronarogennye”, ie, its origin is not associated with blockage of the coronary arteries.

 

If “normal” myocardial infarction is characterized by sharp pain behind the breastbone or in the region of the heart, not addressed by validol and nitroglycerin, “atypical” myocardial infarction is characterized painless for and severe shortness of breath. In this case we are dealing with a cardiac error.

 

In fact, if the necrotic lesion was not formed from the sudden blockage of a coronary artery, the cause is not in the vessels of the myocardium, not in their defects. Such a violation of the blood supply to the heart muscle, leading to necrosis, can only give acquired heart disease.

 

It is very important that these “atypical”, “noncoronary” heart attacks are not heart attacks. Myocardial ischemia, accompanied by small focal necrosis in severe forms of acquired heart diseases, and myocardial ischemia with a focus of necrosis in myocardial infarction is not the same disease. The first — a disease of the heart, the second — a disease of its arteries.

 

Myocardial infarction, in principle, only coronarienne, i.e. necessarily associated with blockage of the coronary arteries.

 

We must give up wandering from one special of the manual in other language, explaining the sharp pain in myocardial infarction nedookislennye accumulation of substances in the myocardium and the corresponding reaction of nerve endings. Usually add that a pain response warns about possible necrosis of the myocardium. This wording is far from the truth.

 

Even the necrosis of the myocardium does not give a pain response without the blockage of coronary arteries. Pain response in myocardial infarction gives tension blood pressure clogged coronary artery embolus.

 

The author allows himself to declare that painless myocardial infarction, in principle, does not happen.

 

This conclusion the author has made on the basis of accumulated medicine facts about the vegetative mechanisms of pain and pain of the visceral organs, the study which gave a lot of time and effort Professor G. N. Kassil.

 

In severe acquired heart defects the loss of fibers in the myocardium (necrosis) begins a few hours after the onset of tangible ischemia (severe dyspnea). In such cases, often the diagnosis: a severe form of angina pectoris, turning into a small focal myocardial infarction.

 

Such examples have been described in the literature. This diagnosis is not a word of truth. It’s not angina is not a heart attack, and can’t go to angina, myocardial infarction, and myocardial infarction to be small.

 

Among the authentic, coronarogenic myocardial infarction include myocardial infarction with localized pain in the epigastric region. Here we are dealing with blockage of the coronary artery in the distal her Department, or simultaneous embolism of one of the arteries of the celiac trunk and the coronary arteries with a predominance of painful effects in the arteries of the celiac trunk.

 

In conclusion, the diagnosis of angina is based on patient complaints, as objective examination does not detect any discernible pathology. After the attack changes characteristic of myocardial ischemia on the electrocardiogram is not recorded. Angina is not accompanied by the development of necrotic lesions in the muscle of the heart body temperature after an attack is not increased, leukocytosis in the peripheral blood is missing.

 

If to speak absolutely precisely, on angina should say: ischemia minor, there are no recorded necrotic foci.

 

Dear reader, we have considered a large number of cardiac failures associated with myocardial infarction and angina. However, a perspicacious reader would understand that “supply” these errors have not been exhausted. A lot of mistakes accumulated cardiology for many years.

 

The author sees the only future is to continue the investigation.published econet.ru.

Chapter from the book M. ja. Zholondz “heart attack and angina begins… in the lungs!”

LEAVE A REPLY

Please enter your comment!
Please enter your name here