Probably each of us knows that smoking has a detrimental effect on the heart and the blood supply system as a whole. I have always tried to mention this fact when conducting STOP-TOBACCO training, seminars and individual courses for freedom from tobacco addiction. But I saw that this fact does not make an impression on my listeners. And I often heard from my clients the words that not only smoking has a harmful effect on the heart, but in general, no matter what - everything has a bad effect on the heart - stress, alcohol, physical inactivity, unhealthy diet, etc. They gave examples - my grandmother did not smoke, did not drink, but died of a heart attack. I still decided to look into this issue - how much smoking actually affects the heart. Maybe the harm of smoking on the heart is really exaggerated, as often happens in unsuccessful anti-tobacco campaigns? What I found out shocked me. But everything is in order. The greatest danger to the heart from smoking is that it is a risk factor for the occurrence of coronary heart disease. What is coronary heart disease and what does smoking have to do with it? Coronary heart disease (the same as coronary heart disease) is a pathological condition characterized by an absolute or relative disruption of the blood supply to the myocardium due to damage to the coronary arteries of the heart. It is caused by an imbalance between coronary blood flow and the metabolic needs of the heart muscle. In other words, the myocardium needs more oxygen than is actually supplied by the blood. IHD can occur acutely (in the form of myocardial infarction (MI), as well as chronically (recurrent attacks of angina). Ischemic heart disease is a very common disease, one of the main causes of mortality, as well as temporary and permanent disability in the developed countries of the world. There is classification of coronary heart disease according to clinical forms, each of which has its own significance in view of the characteristics of these manifestations, prognosis and elements of therapeutic tactics: 1. Sudden coronary death (primary cardiac arrest) is presumably associated with electrical instability of the myocardium If resuscitation measures were not carried out or were carried out. unsuccessful, then primary cardiac arrest is classified as sudden coronary death.2. Angina pectoris is characterized by the presence in the vessels of atherosclerotic plaques with a smooth endothelial-covered surface, while with progressive angina plaques with ulceration, ruptures, and the formation of parietal thrombi are more often found.3. Myocardial infarction - occurs with the development of ischemic necrosis of the myocardium, caused by absolute or relative insufficiency of its blood supply.4. Cardiosclerosis as a complication of coronary artery disease is included in the diagnosis no earlier than 2 months from the date of myocardial infarction. The diagnosis of post-infarction cardiosclerosis is established if there are clinical and electrocardiographic signs of focal myocardial sclerosis (sustained rhythm disturbances, conduction, chronic heart failure, signs of scar changes in the myocardium on the ECG). Common to all clinical forms of coronary heart disease is the picture of atherosclerotic lesions (or thrombosis) of the arteries of the heart, usually detected in the sections of the large coronary arteries. There are many risk factors associated with cardiovascular diseases. Biological factors: older age, male gender, genetic factors, hypertension, glucose tolerance, diabetes mellitus and obesity. Anatomical, physiological and metabolic (biochemical) features: arterial hypertension, obesity and the nature of the distribution of fat in the body, diabetes mellitus. Behavioral (behavioral) factors that can lead to exacerbation of coronary heart disease: eating habits; smoking; insufficient physical activity or physical activity exceeding adaptationbody capabilities; alcohol consumption, etc. Of all the factors, smoking turns out to be the most potent factor in the occurrence of coronary heart disease. Nicotine contained in tobacco smoke causes a significant increase in heart rate and blood pressure. As a result of smoking, the heart is forced to work harder and needs more oxygen. Carbon monoxide from tobacco smoke reduces the amount of oxygen carried by the blood to the heart. Nicotine and carbon monoxide damage the walls of normal arteries, causing fat-like substances circulating in the blood to leak into these walls. As a result, the walls of the arteries become scarred and thickened, their lumen narrows and almost becomes blocked. The heart muscle remains healthy only if there is good blood flow to it through the coronary arteries. Over the years, as part of the normal aging process, these vessels gradually become narrower due to degenerative processes in their walls. For smokers, this process occurs faster than usual. Often the blood flowing through such narrowed vessels suddenly clots to form blood clots (coronary thrombosis), causing serious damage to the heart muscle. It is believed that myocardial infarction occurs as follows: an atherosclerotic plaque forms on the heart artery, it gradually grows and one day clogs artery In itself, the growth of atherosclerotic plaque does not pose any danger to human health (although it is better to prevent their appearance). People involved in the study of diseases have long known the fact that one blood vessel replaces another, dead or injured. A dead capillary is replaced by a neighboring one that is temporarily inactive (the body always has a huge army of capillaries in reserve). The dead vessel is replaced by a neighboring one, smaller, but quickly developing to the required size (the lumen in the vessel can increase 10 times compared to its original size). Substitute vessels that provide blood delivery in a roundabout way to the place where blood was previously delivered by the main vessel are called collaterals. And this replacement blood circulation occurs anywhere in our body, including in the coronary arteries of the heart. Let us assume that a person who does not eat properly gradually develops atherosclerotic plaques on the coronary arteries of the heart. But collaterals develop much faster than atherosclerosis. Collaterals (replacement vessels) develop in hours and days, and atherosclerosis takes years to impair the blood supply to the myocardium. Coronary heart disease (myocardial infarction) is a blockage of the arteries of the heart, in which the rate of blockage much exceeds the rate of growth of collaterals. We can conclude that blockage of the coronary arteries (coronary artery disease) occurs only because a small piece of tissue (embolus) has come off somewhere upstream in the bloodstream. This embolus was brought by the blood flow to the site of thrombus formation in the coronary artery, and it was in this place, where the passage was narrowed due to an atherosclerotic plaque, that the brought embolus stuck. This is how an acute attack of myocardial infarction develops. It develops completely out of the blue, against the background of apparently normal health and well-being. If the embolus, which was brought by the bloodstream and stuck on an atherosclerotic plaque, was pushed further with the help of vasodilators (validol, nitroglycerin), then everything ends well. If it is not possible to push it through, then myocardial infarction develops. Where do emboli (teared off pieces of blood clots) come from? Where can these emboli be brought into the coronary artery of the heart? If you take an anatomical atlas, you can see that there is one single place where an embolus can form, leading to the development of coronary heart disease. This place is the pulmonary blood vessels. Only they are located along the blood flow in front of the heart. Before them are.