• Angina pectoris symptoms

    Angina pectoris is an actual, social and medical problem of the modern day , even if it is not very pronounced, is always a formidable symptom. Usually it is impossible to diagnose only on the basis of complaints, but angina is in this respect an exception. If the complaint is true, then, despite the lack of supporting data obtained during an objective and appropriate examination, a diagnosis of angina pectoris can be made. More than a century ago, Brown wrote: "The patient always has complaints. This is the property of nature;but objective signs that can be obtained with the help of more specific and subtle methods of research - a stethoscope, a microscope, etc., can not always be established, but they complement the objective diagnosis. "Since in patients with angina pectoral objective signs are rare and can be recognized most often only by highly qualified specialists, careful collection of anamnesis is especially important."The more carefully and the more often the doctor questions patients in detail about the pains in the chest and pays attention to the special words used by them, intonation, stresses and especially their gestures, the more qualified he will become in the diagnosis and differential diagnosis of angina pectoris."How to treat this ailment with folk remedies, look here.

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    Usually, the sensation of discomfort is located in the chest, in the middle part of the sternum, but pain or discomfort can be felt in any areas from epigastrium to the lower jaw, in the upper limbs down to the brushes, and also in the interscapular space;Sometimes pain is localized in other areas;the paths of irradiation will be considered below. Read here a detailed and understandable article on the symptoms and therapy of angina pectoris at home. Learn all that is needed, about the drugs for angina pectoris, about the prevention of the first and repeated infarction. If the pain is felt only in the epigastrium or only in the lower jaw, it still has a characteristic relationship with the load or some other known provoking factor, which makes it possible to correctly recognize its cause. Strange as it may seem, pain rarely arises only in the left half of the chest, "from all the various points of its location the most rare place of localization is the region of the apex of the heart."

    Very rarely, the localization of ischemic pain is indicated by a finger or described by the patient as stitching or changing when the position of the body changes or is associated with breathing. Typical gestures of patients sometimes give an idea of ​​the intensity of discomfort, as well as the localization of these sensations. Martin( 1957) called this "the unconditional diagnosis of the pain of coronary insufficiency."He noted that some patients are poor observers, and others can not give a clear description of their feelings. Therefore, observing patients with angina pectoris, coronary insufficiency and MI, he registered all their gestures. Most often these gestures were used in infarction, especially when the patient is so weak that it is difficult for him to answer questions. However, if a patient with coronary insufficiency or angina is asked about his pain, he involuntarily uses gestures to reinforce the description. The author described how the patient puts his palm on the chest and holds it from side to side. Other patients put their hands on the lower part of the chest so that the fingers touch the sternum, and then separate them or lay them on both sides of the chest, and then reduce to the middle. Some patients grip their fingers in the grip position and move them up and down, as if tying a tie, sometimes lifting their hands up to the neck or lower jaw. Martin classified these gestures and gave them names, but their real value is not in the names, but in that it emphasizes the need to observe such gestures, especially in patients who are difficult to clearly convey their feelings.

    Discomfort usually has a small area of ​​spread and is localized mainly in the chest, but in some cases in other areas. If pain occurs in the lower abdomen or legs, it is most likely not associated with cardiac ischemia. If the patient complains of unpleasant sensations in the head, it is necessary to find out whether these feelings were before taking nitroglycerin, since it usually causes a headache. Sampson and Cheitlin( 1971), oddly enough, included the "crown, neck, eyebrows and cheeks" as places of pain localization and described a patient whose pain radiated to the left leg. They analyzed 150 cases of angina in terms of various factors, including localization and ways of radiating pain. In 90% of cases the pain was localized in the chest, of which in 34% of cases it was its only zone. In approximately one-third of patients, she irradiated into the left arm and hand, in 10% of cases - in the right arm and in 13% - in the right hand. In 22% of cases, the pain irradiated in the neck, in 9% - in the lower jaw, and in 16% - in the scapular region. Exceptional location of pain outside the chest was very rare, namely in 2 cases, the pain was localized only in the neck, in two - only in the left hand and in one - only in the epigastrium. Often the pain is felt in the chest and simultaneously either in the forearm or in the hand, but not in the area adjacent to the chest, for example, in the shoulder.

    Usually unpleasant sensations of angina are described as a feeling of pressure, compression or heaviness, sometimes burning and even pain, it can be called pressing or compressive;often the sensation of pain is deep, not superficial. Discomfort in the arm or both arms, if any, appears to be a loss of sensation. In general, as will be shown, the time of the onset of pain gives the most important clue to the disclosure of its cause, but even in cases where the author has twice observed, when patients describe their sensations in the chest as a "tingling," a characteristic relationship with the load,that the patient actually suffers from angina pectoris. Often the patient insists that he does not feel pain, but rather unpleasant sensations, and repeatedly emphasizes this point, if the doctor pronounces the word "pain" with further questioning. Some patients, realizing that something forces them to stop walking, can not specifically assess their feelings, sometimes even indicate where they experience these feelings, and then still put their palms with a characteristic gesture on the chest. Patients often indicate that they feel an irresistible need to stop when walking. Such a sign was noted, describing the patient who said that he could not make a step even if he was forced to go under the threat of a revolver.

    When the patient is able to control the development of the pain syndrome, for example, in case of provoking his load, then to some extent he can decide for himself to what extent he can allow this pain to intensify. Often the patient slows down walking or sucking nitroglycerin( or both) at the first hint of the occurrence of angina pectoris. Usually the most severe attacks occur in cases when the patient is unable to control the situation, for example, if the pain is provoked by emotional stress or an attack of tachycardia. The pain can be very intense if the patient argues or watches boxing, wrestling or jumping on TV( especially if he is betting at the same time).At present, when the circumstances leading to the appearance of tachycardia or hypertension, or both diseases together, have become more understandable, it is easier to understand many unusual cases of angina pectoris.

    One of the most important characteristics of angina pectoris is that attacks are usually short, usually 2-3 minutes, some - less than 1 minute or more than 20 minutes. Often patients can control both the duration and intensity of angina, since rest or taking nitroglycerin or both together usually stop the attack. Not only does the increase in physical stress determine the intensity and duration of an attack caused by a load. Raab et al.(1962) showed that, with a heavy load on the cat's heart, an increase in the concentration of neurogenic and humoral catecholamines leads to a sharp local myocardial ischemia as a result of the limitation of normal compensatory vasodilation. Load is one of the stimulating factors of increased release of catecholamines in humans. Differences in this respect probably determine the different duration of angina in patients under comparable loads. If persistent tachycardia or hypertension or both are not the cause of longer seizures, then the possibility of developing MI should be considered. In some patients, tachycardia can be caused by an anxious condition. Gastrointestinal bleeding causes pain in the heart.

    If the patient complains of chest pain throughout the day, it is unlikely that this pain is associated with cardiac ischemia, unless, of course, there is an MI or arrhythmia. In a study of 1000 correlations of angiographic and clinical signs, a disproportionate number of cases with "angina pectoris" and a normal coronary arteriogram, which had previously been regarded as examples of particularly prolonged pain, were found. The authors point out that "educated patients can present an accurate anamnesis on the basis of well-known facts or acquaintance with literature".In a study of 49 patients with chest pain and coronary angioplasty confirmed, and 23 patients with episodic chest pain and normal arteriograms, rest pain was found more often( 61%) in the group of patients with normal vessels than in other groups(49%).Today, when using invasive methods of research and surgical treatment of angina, one has to doubt the mental usefulness of those who try to simulate angina or do it subconsciously. Angina pectoris is one of the most easily aggravated diseases only because the diagnosis is mainly based on complaints of patients, and clinical signs are often absent;this fact is a potential prelude to simulating coronary thrombosis in patients with Munchausen's syndrome.

    Another important characteristic of angina pectoris is its seizure. The frequency of seizures in a number of cases depends on how often the circumstances that provoke pain recur. Since the threshold of pain is different for each patient, a greater frequency of seizures is observed in patients with more severe coronary artery disease, especially if 3 arteries are involved in the process. In such cases, there is a tendency to combine an increase in intensity, frequency of seizures and less effective action of nitroglycerin. A variety of aggravating, as well as favorable factors, which will be considered below, naturally, change the frequency of seizures. In this respect, the patient's way of life and his reaction to his illness are also important determinants. The favorable social conditions make it possible to avoid attacks of angina pectoris.

    It is noted that angina usually occurs during walking, after eating and in winter. Walking uphill against the wind has long been recognized as one of the possible causes. The increase in the appearance of unpleasant sensations causes most patients to stop. For the first time attacks can occur under the circumstances, for example, in a person who, after breakfast, has to walk uphill to a bus stop. Nowadays, many people hardly remember when they had to go uphill for the last time against the wind. In the patient, angina appeared after the breakdown of the dishwasher, as an episodic and probably annoying washing of dishes was almost the only physical activity. With a certain oxygen consumption, the hand load is the more likely cause of angina pectoris than the load performed with the feet. Pain is especially easily provoked when the hands work above the head level and even when brushing the teeth. It is shown that the load on the legs with a load in the hand, as when carrying gravity, raises blood pressure more than just the load on the legs, i.e., the threshold for the occurrence of angina pectoris can be reduced. Gravity elevation and defecation are other commonly recognized aggravating factors of angina pectoris.

    Sometimes the load can be hidden, as in the case of the housewife, whose pain appears every time she flexes, but she did not feel it necessary to mention that she had to work in this position. Pain, which appears regularly after a load or "after a hard day," is almost never associated with cardiac ischemia.

    One of the causes of angina pectoris can be public speaking. Doctors speaking at conferences, there is a significant increase in cardiac activity, in some cases accompanied by multiple extrasystoles. Often there are deviations in the ECG of the ST segment and, in particular, the T wave, even in young and healthy individuals. There is also an increase in the concentration of circulating norepinephrine, free fatty acids and triglycerides. Although tachycardia is probably less pronounced in older lecturers who are of the "coronary age group," for whom lecturing is not a stressful situation, Osier nevertheless described the case when angina occurred with his colleague at the time of the performance.

    You can include emotional phone conversations to especially likely causes of angina pectoris. The questioning of the doctor in itself can also be the cause of the attack: "There is something in me that causes angina in the patient."Every medical student knows how John Hunter described his life;that it was "in the hands of any swindler who, if he wanted, could annoy and pester me."Yet in those less nervous times, anger was a relatively rare cause of angina pectoris;indeed, strange as it may seem. In England, angina is rarely seen with food, but this variant of angina appears to be more common in the United States, at least in Boston. Perhaps in this case it is due to the habit of smoking and drinking ice water during meals. According to the data, the stenocardia arising in the process of smoking was first mentioned as a "tobacco toad".This is a rare form of the disease. There are reports that smoking increases the number of heartbeats, systolic and diastolic pressure, cardiac output and diastolic pressure in the left ventricle, so it's surprising that this form of angina is not very common. In some patients, smoking also increases the release of catecholamines. Everyday stressful situations at home, at work are defined by the sick as the causes of angina attacks. It was shown that in healthy autodrivers when moving in the flow of transport, the number of heartbeats can be more than 150, and with lesion of the coronary arteries it can reach 180 per minute. In two patients who had observed them, a stroke of angina appeared behind the wheel, and one patient, whose heart rate reached 150 per minute, developed pulmonary edema. In another case, the number of heartbeats in the driver doubled after he "barely collided".The threshold for the development of angina decreases after a plentiful meal. Some patients note that alcohol has the same effect. Most of the circumstances, both pleasant and unpleasant, can increase the release of catecholamines and, thus, change the threshold for the onset of angina pectoris.

    One of the patients of the author, who found out about her husband's death on the phone, had pain in the heart with the subsequent development of MI.

    Angina often provokes the process of undressing in a cold bedroom. Angina in the bed can arise as a result of several known causes, but in many cases it remains unexplained. Probably the most common reason is sexual intercourse, a combination of stress with excitement easily provokes pain in the heart as part of the examination during 24 hours of daily life. 7 young people registered blood pressure and the number of heartbeats during sexual intercourse. At the student of 20 years arterial pressure during an orgasm reached 214/135 mm Hg.p.the average number of heartbeats during orgasm in 3 other men under the age of 30 was 150 per minute, and the average diastolic pressure was more than 120 mm Hg. Art. The diastolic pressure increased significantly more than in any other form of activity for 24 hours. Usually, blood pressure quickly dropped to the baseline within 30 seconds after orgasm. When examined on a doctor and his wife, automatically registering systolic blood pressure, found that during orgasm, her husband's pressure rose to 157 mm, and his wife - to 200 mm Hg. Art. It would be incorrect to transfer the results of these observations to patients of "coronary age".Hellerstein and Friedman( 1970) recorded an ECG for 24 hours in patients who underwent MI, and had the opportunity to record various indicators during intercourse - the so-called sex check test. They found that during orgasm the average maximum heart rate in men was 117 per minute, and concluded: "The cardiovascular costs of marital sexual activity of partners( 26 years of marriage) were relatively low."One of these patients had a greater number of heartbeats during a conversation with the family over dinner. The authors reported that with extra-sexual intercourse cardiovascular costs are higher. About deaths in similar circumstances from time to time reported in the press, but such situations in marital relations are rarely made public.

    In some patients, angina occurred during intercourse, and men usually reported this fact if they were asked about it. It is advisable to clarify such facts, since it worries both patients and their spouses, and discussion, explanation and gaining confidence often benefits. A good effect in these cases is given by β-blockers. In one study, systolic blood pressure in a man during an orgasm was 175 mm Hg.and the number of heartbeats is 140 per minute. The same indices in the same conditions in 1/2 hours after taking 120 mg of propranolol( obzidana) were equal to respectively 140 and 84. His wife's systolic pressure was 130 instead of 200 mm Hg.and the number of heartbeats decreased( figures are not given).As noted, the sexual act did not become less satisfying after the action of propranolol. This is probably the most acceptable form of therapy for angina pectoris arising during sexual intercourse, but the preventive intake of nitroglycerin can also be useful. Less effective sedatives, because they can reduce the potency.

    In some cases, pain occurs in the supine position - the so-called decubital angina. In one of the patients observed by the author, angina appeared constantly in this position for 2-3 min, and the decrease of the ST segment on the ECG preceded for a few seconds the sensation of pain. When the patient sat down, the pain immediately disappeared.

    Painful sensations can wake sleepers. From 80 to 85% of healthy people, awakened during sleep, accompanied by rapid movement of eyeballs, reported that at this time they had dreams. At the same time, the REM-period is only 20% of the duration of sleep, and of those who woke up at another time, only 10-15% noted dreams. Of the 39 cases of nocturnal heart pain accompanied by changes in the ECG, 32 of them developed in the REM sleep period. As might be expected, dreams, whose elements were fear and load, were most often combined with angina. In these cases, p-blockers can have a paradoxical effect, since nightmares are their unfavorable side effect. It has been suggested that in a number of these cases, angina is the result of reduced perfusion of the coronary vessels, since the blood pressure drops during sleep. Some patients develop a variant of Prinzmetal angina pectoris, in others it can also be periodically combined with hyperlipidemia. In some cases, nocturnal seizures are accompanied by symptoms of left ventricular failure;the patient's sitting position and nitroglycerin intake usually not only reduce pain, but also stop shortness of breath, since nitroglycerin is a powerful dilator of systemic veins, and the increase in the volume of the venous system of a large circulation reduces the volume of blood in the lungs. Digitalization of such patients reduces the likelihood of seizures. Paroxysmal tachycardia can also be the cause of angina in some patients prone to this disease. Often the patient knows that following a tachycardia, even if it is barely felt, a painful attack follows - such a sign facilitates the diagnosis. Sometimes, if the patient does not even suspect of tachycardia, the key to solving the problem may be polyuria, often accompanying prolonged attacks of paroxysmal tachycardia. The cause of unstable angina may be paroxysmal tachycardia. Most often, such seemingly inexplicable bouts of pain are caused by sinus tachycardia, the trigger mechanism of which are emotions, but the doctor, and sometimes the patient himself, hardly recognize this cause. Emotions sometimes cause paroxysmal arrhythmia: in one case, paroxysms of atrial fibrillation appeared in the patient at the time when she was passing by the bus past the house in which her husband's mistress lived.

    It has been known for a long time that angina may occur for no apparent reason in a critical review of cases of spontaneous anginal attacks that have established a lot of reports on this topic. In most cases, systolic pressure was raised by 10-80%, as well as diastolic pressure. However, Prinzmetal et al.(1959) isolated a variant form of angina in which pain episodes arise at rest, are rarely provoked by a load and are combined with a transient rise in the ST segment. Since then, the picture of the syndrome, supplemented by new facts and is presented in the following form:

    These symptoms can be added frequent attacks during the night or early morning and the possibility of a dangerous arrhythmia and sudden death. The term "variant form of angina" may be controversial, but this definition is acceptable, since it refers to one of several variants of angina pectoris. A thorough interview with the patient is the main key to diagnosis and that in many cases it can be diagnosed before the ECG was registered. Later Prinzmetal et al.(1960) also stressed that one should not expect in all cases the presence of all signs.

    Most, if not all, of the listed factors occur in other forms of angina pectoris. Regret is expressed about the lack of blood pressure indicators in most of the described cases of angina attacks of the Prinzmetal variant and believe that many patients did not recognize hypertension. Usually coronary angiograms of such patients are changed.

    Some patients showed a decrease in cardiac output and blood pressure, an elongation of isometric voltage and an average isometric pressure increase rate, a decrease in the average systolic ejection rate during a pain episode, and concomitant changes in the ECG.All this indicates a decrease in the function of the left ventricle without any increase in the work of the heart at the time of the appearance of disturbances on the ECG.Similar changes were to be expected if the angina itself was the result of an increase in local coronary resistance, which was assumed. This assumption was expressed earlier. With the help of radioisotope methods, the deterioration of blood flow in the area of ​​the altered ST segment was confirmed. During such seizures at rest angiographically marked localized reversible coronary arterial block. These authors also reported that on 7 of the 750 coronary angiograms there were signs of coronary spasm;it is possible that in 3 cases it was caused by a trauma with the tip of the catheter, but in 2 cases a spasm appeared at some distance from it. Three patients felt pain, but in each case the spasm was stopped by the ingestion of nitroglycerin;a patient had cardiac arrest, and another developed myocardial infarction. Especially convincing examples of spasm in the right coronary artery at a distance from the tip of the catheter in a patient with attacks of angina pectoris, despite the fact that coronary film arteriograms poorly reproduce these data. The spasm was stopped by the ingestion of nitroglycerin. Spasm is probably aggravated by a relatively small atheroma. After the operation, the attacks of this patient disappeared. A case of variant angina with normal coronary arterograms is described, with pain often accompanied by fainting. Nitroglycerin reduced pain and thus could prevent fainting. Various results were obtained in the surgical treatment of variant angina pectoris. The results of surgical shunting using v.saphena in 7 patients: 5 patients received a single, and 2 - a double shunting. At 6 of 7 operated patients, angina pectoris resumed within 4 weeks. The intake of nitroglycerin is often ineffective. The same authors reported that propranolol( obzidan) not only prevents and stops seizures, but also improves the function of the heart, but did not explain the mechanism of this action. The majority of patients with time comes spontaneous improvement, some people have stenocardia instead of rest angina, the third disease is asymptomatic in the future.

    Periodicity is a common symptom characterizing the pain associated with migraine or peptic ulcer. To a lesser degree, it is characteristic of angina, except that the course of it can worsen in winter compared with the summer period. The frequency of seizures is also observed in people working with nitroglycerin in military plants. Eight women and a man were observed whose pains in the heart appeared 12-48 months after the beginning of contact with a 37% nitroglycerin-cellulose mixture at the rocket plant.

    The pains did not occur at the time of contact with this mixture, but on Sundays and on mornings on Monday. These pains disappeared when returning to work or after taking nitroglycerin. In 2 patients, MI developed, and one developed a severe coronary insufficiency;in all these cases the disease began on Sunday or Monday morning. Such a rare variant of angina pectoris should be taken into account for those patients who are treated with large doses of nitroglycerin for therapeutic purposes.

    The factors determining the "weather" of angina pectoris have already been considered in the section "Time of occurrence".This section focuses more on the factors that determine its "climate".If the circumstances predispose to the development of angina pectoris, mainly as a result of the appearance of severe coronary disease, it is possible to predict the occurrence of pain. However, there are several known factors that can reduce the threshold of angina pectoris. In most cases when the threshold for the onset of angina suddenly falls in patients or the causes of seizures become diverse, for example, when pain suddenly appears at night, there is probably further blockage of the coronary arteries;the latter arises either in connection with atheroma, platelet sedimentation, thrombosis, subintimal hemorrhages, or as a result of a combination of these processes. The combination of coronary occlusion with the expansion of collateral vessels is the main factor in the appearance of tides and ebbs in the intensity of angina pectoris, but it should be borne in mind, as noted earlier, that the symptoms usually do not appear until significant changes occur in at least twomain vessels. In everyday life obesity is an important aggravating factor, and its treatment can lead to the disappearance of angina and allow the patient to engage in his usual activities.

    High temperature, as well as hyperthyroidism, provoking stenocardia, can reveal IHD.However, angina occurs both with hyper- and hypothyroidism. It has long been known that the treatment of hypothyroidism with thyroid medications can provoke angina or aggravate it. Given that the need for urgent treatment of myxedema is rare, it is advisable to treat it, especially in the elderly, with very small doses of thyroxin: fractional low-dose devices at long intervals with the simultaneous administration of P-blockers in order to reduce this risk. Even in non-angina patients, treatment with thyroxine can lead to the onset of MI.The defeat of aortic valves, especially aortic stenosis, and obstructive cardiomyopathy can be the causes of angina without concomitant coronary heart disease, but both contribute to the course of angina pectoris.

    Hypertension is one of the most important, potentially corrective, aggravating factors, both in connection with the possibility of accelerating the atheromatous process, and because of the increase in the work of the heart it causes. Angina can occur with transient hypertension, especially in connection with emotional stress, as well as with pheochromocytoma. Severe transient hypertension, combined with painful urination in patients with paraplegia, can also cause angina pectoris. The author observed the patient with paraplegia, which constantly had malaise( but not angina) after urination, accompanied by an increase in pressure to 240/140 mm Hg. However, the symptoms quickly disappeared after taking nitroglycerin. Later the patient used the drug prophylactically with good effect. It is also necessary to bear in mind other factors that increase the burden on the heart. An elderly patient got rid of angina pectoris after surgery on the botanic duct, which was not previously suspected( unpublished data).

    A change in blood composition may also have a negative effect. The most frequent change is anemia, so every patient needs to monitor hemoglobin concentration, because successful treatment of anemia can help normalize his condition. Wood( 1962) observed 2 patients about 20 years old, in whom anemia was the only visible cause of angina, the treatment of anemia led to the disappearance of angina pectoris. In addition, hypoxia can be an aggravating factor, regardless of whether it is associated with a rarefied air at altitude or with emphysema. Williams et al.(1957) found an increase in erythrocyte aggregation in conjunctival vessels after fatty food intake and believed that the increase in blood viscosity that arose in this connection could lead to angina attacks. In some patients, angina attacks occurred after such small amounts of fatty foods that could not cause significant hemodynamic disorders, while the plasma had a creamy appearance. In the patient with hyperlipidemia, the pains, accompanied by changes in the ECG, characteristic of ischemia, appeared constantly 3 hours after eating, when his blood quickly acquired a creamy appearance. The authors suggested that this can explain some cases of decubital angina. Reduction of coronary blood flow at rest by 20% without changing the performance of the ventricles of the heart, which they attributed to hyperlipidemia. This condition turned out to be reversible after correction of hyperlipidemia by lipolysis with heparin. Apparently, it is appropriate to emphasize here that many patients suffering from bouts of night pain know it well and avoid eating at night. There are also reports that the blood of patients who have recently undergone MI or arterial thrombosis has increased viscosity. There are patients who under pain of nitroglycerin pain are aggravated;as an explanation for this effect of coronary dilatation drugs, a mechanism of coronary "theft" was proposed as a result of redistribution of blood to less damaged and dilatable vessels to the detriment of ischemia sites. If this is true, then it is surprising why this paradoxical effect of nitroglycerin is extremely rare.

    Many intercurrent diseases, apparently, can increase predisposition to angina pectoris, especially if they are combined with tachycardia, for example, gallbladder disease;increased angina during an attack of mechanical jaundice. It is established that gallbladder involvement is 2 times more common in coronary disease. When comparing age and sex, there was no significant difference in the incidence of coronary artery disease among gallbladder during life. There is evidence in the literature that the dilatation of the bile duct causes changes. Angina pectoris with food does not have a special connection with gallbladder diseases.

    The attack, which was associated with the load, usually quickly disappears at rest, usually within 5 minutes. Often, patients tell how burdened their need to stay in a public place and how happy they are to a suitable occasion to stand up, for example, as if looking at the shop window. The use of nitroglycerin under these circumstances is relatively ineffective. However, it can be extremely effective in attacks "provoked by emotional factors, and is so effective that in clinical practice it is one of the few rather reliable therapeutic tests. In patients with coronary disease, confirmed ethnographically, with a delayed reaction to nitroglycerin or lack thereof, there was a high incidence of multiple arterial obstructions and more pronounced violations of hemodynamics and the phase structure of the heart. Pain sensations in the heart area usually disappear at a time when a small headache appears after taking nitroglycerin, which is noted by many patients. If the patient says that 10 minutes or more passes before nitroglycerin begins to work, that drug should be considered ineffective. It is best to use nitroglycerin before exercise, if it can cause pain.

    It has long been known that pressure on the carotid sinus removes anginal attacks. Lown and Levine described in detail the use of pressure on the carotid sinus as a test for angina. With a painful attack, they recommended squeezing the carotid artery and at the same time asking the patient a question: "Does the pain get stronger?" If the heart's work is being cut, the patient with angina behaves quite characteristically: after a pause, accompanied by an uncertain and surprised look, the answer is: "No, doctor, the pain has passed "or" lets go. "Although the activity of the heart can immediately accelerate again, the pain does not resume. In patients with unpleasant sensations in the chest of a functional nature, stimulation of the carotid sinus often worsens the well-being, since the doctor fixes attention to this. You can teach the patient to use this manipulation, as is done in cases of paroxysmal tachycardia;this can be useful if the patient does not have nitroglycerin at his fingertips or has become ineffective. There is an implant device that is sensitive to the radiator of the radio waves, which the patient turns on at the moment of the onset of pain;the effect is the same. Care should be taken when pressing on the carotid sinus. Lown and Levine are recommended to perform manipulation in the half-lying or lying position of the patient due to the danger of fainting. Depressor vasomotor effect occurs in approximately 60% of patients, with arterial pressure dropping by an average of 10 mm Hg. Art. In patients with hypertension and atherosclerosis, especially the elderly, a significant drop in pressure is possible. At the same time, serious ventricular arrhythmias are almost not observed;the only serious threat can be a violation of cerebral circulation, up to hemiplegia. If noise is heard over the carotid artery, then such manipulation is impossible. Do not squeeze the carotid sinus for more than 5 seconds.

    Sometimes relief comes when breathing is delayed. The pain disappeared during the period of tension, while the arterial pressure dropped, except for patients with heart failure, who had a BP response of the so-called "square wave" type. The pain did not resume, even if the patient "overdid it".The authors suggested using this method for patients who could not use nitroglycerin due to headache or fainting, or in cases when it was not at hand. As already noted, often patients report that after eructation they often noted the disappearance of pain.

    As it seems paradoxical at first glance, another facilitation factor in some cases is the continuation or renewal of the load. One of the interesting variants of angina is known in the United States as "angina of the first effort", and in England as "angina of the second breath".The usual anamnesis is as follows: unpleasant sensations or pain in the chest at the patient appear at the first pit of the golf course and later do not repeat even on steep hills. Although the nature of pain is indicative of angina, this form of angina should be borne in mind until the doctor confirms the diagnosis. Similarly, some patients can continue walking and even seek the disappearance of pain - the so-called "passing" angina. This creates the possibility of confusion: some patients do not "have time to achieve" angina due to the development or progression of intermittent claudication. Every patient who undergoes MI hopes that angina pectoris, which bothered him before a heart attack, will not resume when he again starts his usual activity. Significant improvement in the condition is observed in patients treated with their p-blockers and some other drugs. One of the main problems in assessing the efficacy of these drugs is the placebo effect, which is particularly important in this area. In recent years, the use of coronary bypass surgery has improved the condition of many patients, this improvement may remain in some patients even after transplant thrombosis. Concomitant symptoms of

    In a patient with angina pectoris, dyspnea becomes noticeable when walking with him, but he rarely complains about it, since the most important sensation for the patient is anginal pain. Allan Burns noted: "Difficulty breathing a patient for the person next to him seems. .. the most pronounced symptom."For many years it is known that at the time of the onset of spontaneous attacks of angina, the end diastolic pressure in the left ventricle( CVDL) increases. It is curious that with angina pectoris provoked by the stimulation of the pacemaker, CPDL falls at the moment of impact on the pacemaker, and then rises above the initial level. Despite the fact that angina attacks are often accompanied by a significant tachycardia, patients almost never complain of a heartbeat. Probably, this is due to the fact that angina itself, like shortness of breath, dominates the sensations of the patient.

    With angina pectoris may accompany anxiety. The quiet, motionless, somewhat abstract behavior of the patient at the time of the attack is often better than any words that testifies to the suffering that he is experiencing. This behavior is a sharp contrast to the replaying of an inexperienced actor or patient, trying for any personal reasons to simulate "pain in the heart."In the most extreme case, anxiety can prevail: the so-called angor animi( Fear of death) Nowadays, the most terrible attacks for a patient occur, probably at night, if it is left alone, and there is no supply of nitroglycerin.

    Some patients during an attack can feel a sharp weakness or even lose consciousness. However, of the 5 patients he described, 3 had aortic stenosis, in which there was a tendency to fainting; in the fourth patient, syncope was associated with hard work, especially after eating, and was preceded by a feeling of heaviness in the epigastric region that was not associated with exercise,and the last angina did not exist, but atrial flutter and blockade 4: 1 were noted. Therefore, the statement that the first description of fainting with angina belongs to him seems somewhat questionable.

    We note a clear relationship between coronary heart disease and peripheral arterial disease. A common factor in many cases may be smoking. Therefore, it is necessary to question the patient carefully, whether he suffers from intermittent claudication, since this fact is of great importance, especially if surgery on coronary vessels is expected.

    There are cases when in the physical examination of a patient the doctor fixes his attention on pathological signs, proceeding from "prestigious" considerations, rather demonstrating his erudition than contributing to the clarification of the true diagnosis. Here are some examples: immediately after hearing a loud aortic "machine" noise in the patient, the doctor nevertheless examines his pulse for detecting a dicrotic pulsation;careful examination of the nail bed to detect a capillary pulse in the patient, while the head is shaken as a result of aortic insufficiency;or the doctor tries to find out "a symptom of a coin" from a patient who has an obvious tympanic percussion sound, no breath, and on the roentgenogram of the chest - a significant pneumothorax. In a certain respect, this also applies to objective signs of angina, when listening to the elusive III or IV heart tone for a practical doctor seems more like a "cardiac super-art" than a useful diagnostic sign. The identification of such signs is undoubtedly of interest, even if their contribution to the diagnosis is not great enough.

    In addition to examining the patient at the time of the attack, the main goal of the clinical study is to identify factors that cause or enhance angina, and to search for known clinical conditions similar to coronary disease. In this respect, it is necessary to bear in mind the following defeats. AD) Aortic stenosis. It is likely that he especially often is either the cause of angina pectoris, or strengthens it, but in the elderly it is often not diagnosed. Systolic murmur on the aorta is common in elderly people, and its presence is not enough to make a diagnosis. In this case, the slow rise of the pulse wave, the clinical and electrocardiographic signs of left ventricular hypertrophy, and the calcification of aortic valves, as determined by the X-ray diffraction data, can help in this case.

    B) Insufficiency of aortic valves. Among the various causes of this lesion, syphilis is particularly important, since occlusion of the coronary arteries is often detected. The recognition of the disease is assisted by data on the presence of calcification of the descending aorta, radiographic indications of the presence of bismuth in the muscles of the buttocks in the elderly, and positive serological responses. Syphilis is often not diagnosed, as it is rare in our day.

    This lesion is diagnosed more and more often, it should be sought in young people with late systolic noise at the apex or unclear electrocardiographic data indicating hypertrophy of the left ventricle. Although the cause of angina pectoris may often be other forms of cardiomyopathy, some authors consider them rare.

    3. Mitral stenosis

    Amongst 400 patients with mitral stenosis, angina detected in 8.5% of cases and referred to Nothnagel, who more than 60 years ago drew attention to this relationship. More than half of the patients examined by Stuckey had significant signs of pulmonary hypertension. Wood( 1962) considered that more than 10% of patients with mitral stenosis who need surgical treatment experience pain in the chest, indistinguishable from pain in angina pectoris. They could be the result of either self-induced coronary heart disease, or severe pulmonary hypertension.

    4. Hypertension

    Angina is more common in patients with hypertension than in people with normal blood pressure.

    5. Primary pulmonary hypertension

    Primary pulmonary hypertension may be the cause of angina pectoris. This disease, which occurs mainly in women 20-30 years old, is easy to diagnose( wave "a" of the venous pulse, right ventricular IV tone, right ventricular hypertrophy, dilated pulmonary artery and signs of right ventricular hypertrophy on the ECG).Shortness of breath and fainting with exercise are frequent symptoms of this disease, but sometimes angina also occurs.

    6. Pulmonary artery stenosis

    Systolic pulsation on the pulmonary artery and the noise, expansion of the main pulmonary artery and signs of right ventricular hypertrophy facilitate the diagnosis of this disease, but it is rarely the cause of angina pectoris.

    7. Shunt from left to right

    Unoperated patients with non-intersaturation, interventricular septum or botanic duct rarely survive to the age at which angina pectoris may occur;at the same time, the correction of the shunt can lead to the disappearance of angina pectoris.

    8. Hyperthyroidism

    9. Obesity

    10. Anemia

    If angina occurs under certain circumstances that are difficult to interpret, it is useful to observe the patient when these circumstances recur. This is applicable to a patient with shortness of breath, which appears when the load is applied, when there is doubt about its intensity, and which is observed when climbing the ladder;this refers to a patient with possible dysphagia, which is observed at the time of swallowing. You should also carefully monitor the patient with angina pectoris when walking on a ladder or on a "treadmill."The patient at the time of angina attack, regardless of whether he appeared spontaneously or was provoked, prefers to stop or sit down. Very characteristic signs are immobility and absent or anxious expression of the face, while the patient is often pale, only with an intense attack there is a grayish shade of the face or even sweating. Often observed shortness of breath, may erupt.

    The heart rate is usually increased, and blood pressure is usually higher than before the attack. It is often reported that the product of the indices of systolic blood pressure and heart rate during an attack of angina remains remarkably constant regardless of the way they are defined. Sometimes a bradycardia occurs during an attack. Alternating pulse is the physical sign, which is found the more often, the more often it is searched, especially when registering blood pressure curves. It can then arise, then disappear, as was noted by the author in a patient who, after a Valsalva trial, had pulsus alternans for several minutes. To identify this sign, the authors palpated the radial artery, but it is likely that this sign can be detected more often if you use the auscultatory method of measuring blood pressure at the time of pressure drop in the cuff, or even better when registering the blood pressure curves.

    Regardless of the presence of an attack, one can observe a pathological pulsation of the left ventricular aneurysm;Sometimes there is a region of dyskinesia, but it can be seen only at the time of the attack. Low-frequency IV heart tone is easier to palpate than to listen;this tone is widely recognized as a frequent sign of coronary disease. It reflects the final diastolic pressure of the left ventricle and may appear during an attack and disappear after taking nitroglycerin. Horwitz( 1974) found that he is found 7 times more likely in people with chest pain and angiographic signs of coronary disease than those who have coronary angiograms in the presence of chest pains."The appearance of the gallop rhythm during pain in the chest is an important evidence of coronary disease."Banks and Shugoll revealed an IV heart tone in 11 of 12 patients with angina outside the attack, and one patient showed up at the time of pain. However, IV tone is by no means pathognomonic for coronary disease. It occurs with hypertrophy of the left atrium as a consequence of hypertension or aortic stenosis, if concomitant mitral stenosis does not interfere with rapid evacuation of the left atrium. The presence of IV tone also depends on the heart rate, and it is possible that the latter often causes the appearance of such a tone at the time of the attack, at which tachycardia may appear. There are also reports of a paradoxical splitting of the tone during an attack of angina.

    The appearance of systolic murmur of mitral regurgitation at the apex at the time of the attack that was observed in the patient during smoking Oram, Sowton( 1963) is the most revealing pathological physical sign indicating either an increase in the diastolic volume of the left ventricle or a weakening of the papillary muscles that leadsto mitral insufficiency.

    Coping painful attacks by squeezing the carotid sinus has already been considered. Of 12 patients examined at the time of angina attack, seven of the squeezing of the carotid sinus relieved pain.

    In substantiating the diagnosis, it is necessary to take into account two principal problems. The first is the presence of numerous factors that make it difficult to recognize angina in patients, the second problem is related to the fact that there is no reliable test to confirm this diagnosis. Vaisrub( 1974) described the diagnostic triad of clinical, electrophysiological and angiographic signs of angina pectoris, but indicated that none of them is a clear evidence of this disease.

    A simple question is often enough: "Do you have any unpleasant sensations in the chest when climbing a mountain or a ladder?" To reveal angina in a patient. Indeed, it has been shown that the answer to this question included in the questionnaire can, from a diagnostic point of view, be successfully compared with anamnesis data obtained in the usual way. Even cardiologists can give different conclusions about whether the patient suffers from angina pectoris. It turned out that if one doctor diagnosed angina, the other two confirmed his diagnosis only in 55% of cases. The results obtained with the questionnaire corresponded to the diagnosis in 26 cases, when all the doctors unanimously denied the presence of angina, and in all cases except three, when they diagnosed this disease. On the basis of this, Rose concluded: "It seems that the slight advantage achieved by the method of medical questioning was obtained due to the fact that doctors spent 15 times more time and each of them applied his method of questioning."

    But even with the use of questionnaires there are still difficulties, because among those who answered positively the question: "Do you have unpleasant sensations in the chest when climbing a mountain or a ladder?", A significant number of people have been identified who responded negatively tothe previous question: "Have you ever had unpleasant sensations in the chest?".The latter question is often used as a rapid screening test for the detection of angina pectoris. However, if we focus only on one question, then the obtained data will be unreliable. Many doctors have more than once heard a typical history of angina pectoris from those patients who have responded negatively to this question. From this it follows that not only the nature of the questions is important, but also the order in which they are asked. The diagnosis often becomes clearer if you ask the patient what time is more preferable for him to be examined by a doctor at the time of angina attack.

    Some patients with angina pectoris, which was identified using questionnaires, answered the same questions a year later negatively. This circumstance, according to Rose, confirms the widely held belief that once a patient has a typical anamnesis of angina, he does not necessarily get it later. Perhaps this fact is partly due to the nature of the patient and the various nuances of the survey, as well as the heterogeneity of the conclusions of even qualified doctors.

    It should not be assumed that only other physicians are unable to detect a "true history" of angina pectoris, and it is easier to understand especially those doctors who themselves took part in the Rose tests described, the purpose of which was to discern discrepancies in the results obtained by individual surveyors.

    If we take into account that both the patient and the examiner can make mistakes and the results may be different, it would be good to have such an objective and reliable test that could unconditionally confirm the diagnosis of angina pectoris. Unfortunately, such a test does not exist. For 300 autopsies of American soldiers killed in Korea, 77.3% of the cases revealed significant changes in coronary vessels with an average age of death of about 22 years( in the first 100 cases, the age was not recorded, so the average age is calculated for the remaining 200).The most frequent lesion was noted in the medial lobe of the left coronary artery. White and co-workers.(1950) calculated the number of cases of coronary atherosclerosis in pathoanatomical studies in the age-old decades from 30 to 80 years. They found that after 49 years, the average American has, by the time of his death, significant coronary atherosclerosis of both left and right coronary arteries. Maximum.such cases occur at the age of 55 years, after which their frequency decreases, probably as a result of coronary death at an earlier age.

    The difficulty of normal coronary blood flow usually causes the development of intercoroscopic anastomoses. They develop especially intensively, if occlusion occurs gradually. By the time of angina pectoris, the lumen of the entire coronary tree can be blocked by 80%.In pathoanatomical studies, more pronounced lesions of the coronary arteries are usually detected than it is found in angiography. Currently, there are many indications that in a few patients with a typical angina picture, coronary arteries can be unchanged in angiographic and even pathoanatomical studies, although other causes of angina pectoris, such as aortic valve damage, obstructive cardiomyopathy, thyroid disease and hypertension,were excluded. In some of these cases, the cause of angina pectoris appears to be the "spasm" of the coronary vessels.

    Horwitz( 1974) noted that many patients with atypical pain patterns had obstructive lesions of the coronary vessels, while patients with a typical manifestation of angina did not have angiographic damage to the coronary arteries. When Horwitz wrote that "this observation raises the question of whether the descriptions of angina based on cases diagnosed only on clinical data are sufficiently accurate," he, like many others, meant that the error was due only to clinical interpretation. However, coronaroangiography can not be considered the main method that allows the diagnosis of angina pectoris to be reliably established, since angiographic changes characteristic of angina pectoris are common, although on average and less pronounced, findings in elderly people who have never suffered from angina pectoris, at least in Western countries. If a diagnosis of angina is made and the coronary angiogram is interpreted as normal, then various explanations are possible. The arteriogram can be technically inadequate or misinterpreted. Perhaps, an error was made while clarifying the anamnesis, and a detailed interview with the patient may reveal some other cause of angina pectoris. Two possibilities are particularly important in this respect: diseases of the esophagus and pericardium. During a physical examination, perhaps, one of the other causes of angina pectoris was examined. Disturbances of microcirculation are noted in Friedrich ataxia, Marfan syndrome, coronary embolism, rheumatism, rheumatoid arthritis, diabetes mellitus or scleroderma. Earlier, there was a "spasm" of the coronary vessels. Finally, the patient can "take over" complaints from another patient, consciously or subconsciously, as an expression of depression or for some purpose.

    If morphological signs and coronaroangiography coincide to some extent in patients with and without angina pectoris, it can hardly be expected that any indirect test will help differentiate these two groups of individuals."Now, in every village, big or small, there is always one( electrocardiograph) or even a few, and therefore people whose peace and happiness can be disturbed by an erroneous diagnosis due to a misinterpretation of the electrocardiogram is no less than those who are at riskbe killed or wounded in an atomic explosion. "

    It used to be that the ECG taken off at the load will help in differentiating the diagnosis.

    Other authors prefer to examine venous coronary blood to determine the concentration of lactates as an indicator of myocardial ischemia. Using this method, the same response to heart rate stimulation and the same concentration of lactate in coronary venous blood as in patients with coronary artery disease was found in the patient of the control group;in the subsequent authors managed to reveal in his anamnesis stenocardia. If it is impossible to recognize the separation of "pathological" indicators from "normal" in angina pectoris, then special care should be taken when using invasive methods that, as it is commonly believed, can be valuable in this case. An example of such an extreme is the combination of excitation of the pacemaker driver l taking blood samples from the coronary sinus using three venous and three arterial catheters simultaneously. Friedberg( 1972) considered that invasive methods have no practical significance for the clinical diagnosis of angina pectoris. He made the following general conclusion: "One of the difficulties in interpreting the various messages about electrocardiographic data after exercise is that researchers tend to apply tests whose value is still sub judice in deciding whether the patient suffers from coronary insufficiency or not. The load and other tests can serve only as a supplement to the data of the anamnesis and can not be a decisive factor in the diagnosis of angina pectoris. "

    Analyzing the type of pain sensations, studying their relationship to the effects of loads and cold, emotional stress, occurrence at night, it is revealed that these factors do not have a differential value. After eating, the pain occurred most often in individuals with altered coronary angiograms. As already noted, pain at rest was observed somewhat more often in patients with normal angiograms. Pain in the chest was typical for both groups, irradiation of it in the hands and neck was much more common in the group of patients with pathological coronary angiogram, and the spread of pain in the epigastric region and back in the group with unchanged angiograms. The nature of the pain does not help diagnosis, although the word "acute"( probably in the sense of intense, rather than stitching) was more often used by persons with normal coronary angiograms. Of the concomitant complaints, "weakness" was 2 times more common in patients without coronary disease, but was also noted in 41% of patients suffering from it. Lack of air, nausea and heart beat were not of differential significance.

    IV heart tone is particularly characteristic, it was found in 92% of patients with coronary disease and in 30% of patients without radiologic signs of coronary artery disease. The incidence of hypertension in both groups did not differ significantly. Attenuation of the pulse,

    III heart tone, extrasystoles and cardiomegaly were observed only in persons with coronary artery disease, but were rare and did not represent diagnostic value.

    Pain relief within 3 min after taking nitroglycerin was noted in 72% of cases of coronary disease, confirmed angiographically. In 14% of patients, the pain disappeared later than 3 min, but earlier than 10 min, and in 6 patients the drug was ineffective. All patients with delayed response to nitroglycerin intake or its absence revealed lesions of two or three coronary arteries, as well as violations of the dementia of ventricular myocardium. Only 2 patients with normal angiograms had pain disappearance less than 3 min after taking the drug, in 10patients had a delayed response, and 5 had none at all.

    Differential diagnosis of angina pectoris first of all comes from the need to establish the nature of the disease, respectively the etiology, leading symptoms and signs:

    Next, it is necessary to conduct differential diagnosis of angina and diseases with a similar clinical picture:

    With the simultaneous occurrence of angina and other pathological conditions during whichanginal pain occurs in the left part of the chest, or before coronary insufficiency occurs,and to what extent each of them is the cause of coronary insufficiency.

    In clinical practice, it is not uncommon for differential diagnosis to overlook the possibility of the parallel existence of angina pectoris( based on coronary atherosclerosis) and other cardiac and non-cardiac diseases. Therefore, it is extremely important to establish the type and degree of participation of each individual disease, or pathological condition, in the appearance of pain in the left half of the chest or coronary insufficiency. Experience shows that, for example, at first, angina pectoris may occur with esophagitis, and then join the first attacks of angina pectoris. When both diseases are combined, certain difficulties arise in differential diagnosis.

    However, today's level of modern diagnostic methods and knowledge makes it possible to minimize hyper-and hypodiagnosis of angina pectoris.

    Because cardiovascular diseases, and especially CHD, are the most common cause of disability and mortality, their accurate and timely diagnosis, as well as early recognition of clinical variants of the disease( different prognosis), are of vital importance for the patient.

    In clinical practice very often there are difficulties in the recognition and differential diagnosis of different clinical forms of IHD, especially when one clinical form is transferred to another( usually from mild to more severe, for example, from angina to myocardial infarction).

    As is known, the term "ischemic heart disease" combines various clinical forms of coronary insufficiency, which in 90% of cases is caused by coronary artery atherosclerosis. Therefore, one should not use this term when the cause of the disease is not atherosclerosis, but various coronary arteries.

    The National Heart, Blood and Lung Institute( USA) in 1978 simplified the classification of IHD for etiology, a clinical picture based on ECG data, laboratory and other characteristics, taking into account primarily anginal pain, which greatly facilitated differential diagnosis and recognitionappropriate forms of the disease.

    The classification of clinical forms of ischemic heart disease is as follows:

    Stable angina is characterized by a prolonged course( usually at least 2 months) and classic features:

    If, during a stress test on a veloergometer at a load of 120-150 W for 14 min, anginal pain does not appear in the subject(and also equivalent symptoms and specific ECG signs of ischemia), then it is possible to exclude angina with good reason. In cases where doubts remain, it is necessary to resort to coronarography. Negative coronary angiography excludes angina pectoris.

    Unlike all other types of chest pain, angina pectoris as a characteristic pain syndrome is established on the basis of a detailed study of the subjective feelings of the patient( the character of anginal pain), which provoke various influences, primarily mental and physical stress. Pain with angina rapidly disappears after stopping the load or taking nitroglycerin( usually already for 1 minute).However, it must be borne in mind that anginal pain sometimes appears atypically.

    To atypical manifestations of stenocardia is primarily the atypical irradiation of anginal pain: the right shoulder, jaw, tip of the nose, the tip of the tongue, the hard palate and throat, eyebrows, the back of the head.

    It should also be remembered that the equivalent of typical anginal pain may be shortness of breath of varying severity.

    When conducting differential diagnostics, the following are especially helpful: detailed inquiry, positive dynamics of specific ECG changes( ischemia), positive test with nitroglycerin( with simultaneous clinical observation and ECG recording).

    If there is no positive dynamics of the ECG, the pains of a protracted character in the left half of the chest indicate either a severe form of ischemic heart disease( IHD) or a lack of their connection with IHD.

    Angina is usually indicated by positive ECG data in the form of depression( or elevation) of the ST segment more than 2 mm below or above the isoelectric line. Many authors are of the opinion that the appearance of a negative T wave during the loading test is of similar importance.

    A physical sample should not be performed in case of positive ECG data at rest, preferably after taking nitroglycerin, repeat the loading test.

    Deterioration of the subjective state of the patient and the dynamics of ECG changes, indicating a severe degree of ischemia, indicate an exacerbation of angina pectoris, which in turn requires special measures. To this end, it is necessary to urgently appoint adequate therapy and bed rest to prevent the development of unstable angina or myocardial infarction.

    Unstable angina is a transitional clinical form between stable angina and myocardial infarction. It represents an extremely inhomogeneous group of states. Synonyms for unstable angina are: intermittent coronary syndrome, pre-infarction angina, acute coronary insufficiency, threatening myocardial infarction, prolonged acute angina, microinfarction.

    According to the latest classification, unstable angina is referred to;the first arising angina;progressive stable angina, with frequent and severe attacks, appearing and at rest;severe and protracted attacks of angina( lasting 12-30 min), not stopping nitroglycerin and eliminating the load, but which do not lead to myocardial infarction.

    Along with the angina pain of the above character, unstable angina is also evidenced by typical ECG data( depression and ST-segment elevation and T-wave inversion), as well as an increase in CK in serum.

    Unstable angina has a more uncertain prognosis than stable angina and represents a transitional form of IHD that can disappear, go into a stable form or develop myocardial infarction.

    Therefore, differential diagnosis, respectively, accurate recognition of this form of CHD and timely treatment have an extremely important preventive value in improving the reliability of the prognosis of this disease.

    Myocardial infarction is the most severe form of IHD.In the classic clinical picture, among the characteristic signs, acute anginal pain predominates, lasting 15 minutes, or a protracted anginal condition lasting for hours and days, which is stopped only by narcotic drugs. It is characterized by classical ECG changes that develop in accordance with morphological changes( ischemia, damage, necrosis), and laboratory data( acceleration of ESR, hyperglycemia, leukocytosis, elevated ACT, ALT, CKF, etc.) and body temperature. These biochemical and ECG signs indicate necrosis of the myocardium in acute myocardial infarction.

    In the differential diagnosis of anginal pain and the definition of the clinical form of IHD in favor of angina, a good general condition is better than with myocardial infarction, clinical analyzes, absence of tachycardia, dyspnea, hypertension, biochemical disorders, MI-specific ECG data( pathological Q,elevation of the ST segment and elevated body temperature).

    In contrast, MI, even in the absence of anginal pain, is indicated by the sudden appearance( without apparent other causes) of heart failure and collapse. However, a more detailed study of the anamnesis suggests the existence of a patient with IHD.The establishment of a definitive diagnosis indicating MI is assisted by specific ECG changes and relevant biochemical data.

    An anginal attack can be triggered( in addition to the physical and mental stresses already mentioned) in both coronary artery disease and in the absence of coronary artery atherosclerosis: tachycardia( any cause), bradycardia( especially in the atrioventricular block), high body temperature, metabolic disordersthyrotoxicosis, severe anemia and hypoglycemia), intoxication with nicotine, a sharp change in climatic conditions( cold, hot or humid air) and the environment( stay in high-altitude areas), hopesUse by large doses of alcohol.

    Decreased perfusion coronary blood flow with concomitant syndrome of coronary insufficiency reduces the shock volume of the heart, which is especially significant: pronounced bradycardia, arterial hypotension, heart failure.

    Differential diagnosis between angina and other cardiovascular diseases is carried out primarily with those diseases in which coronary insufficiency occurs.

    These include:

    When conducting differential diagnosis it is important to remember that there are great therapeutic options for correcting coronary insufficiency in the above diseases, primarily by treating the underlying disease.

    Among the congenital and acquired heart defects, the following diseases are of particular importance in differential diagnosis:

    In patients with intermittent mitral valve prolapse, anginal pains arise spontaneously at rest, often accompanied by fainting, shortness of breath and ECG changes indicative of ischemia and rhythm disturbances.

    According to numerous studies, including those conducted in Yugoslavia, a favorable therapeutic effect in the treatment of this disease is achieved with the help of calcium antagonists.

    Acquired and congenital heart defects, most often leading to an increase in the requirements for coronary blood flow, or relative( secondary) coronary insufficiency, are as follows:

    For various types of acquired heart defects, pains of an anginal character occur with different frequencies:

    The greater the severity of heart failure,the more often there is anginal pain.

    The use of the coronary angiography method really makes it possible to detect stenosing arteriosclerosis of the coronary arteries with different heart defects. In this way it was found that it is equally represented in patients with aortic( 17%) and mitral( 20%) heart defects. The main role in the pathogenesis of coronary syndrome with acquired heart defects is hemodynamic insufficiency, and not the degree of atherosclerotic changes in the coronary vessels.

    In aortic insufficiency, the appearance of anginal pain in the chest is caused by low diastolic pressure and a "suction" effect on the coronary arteries of the reverse blood flow in the hypertrophied myocardium of the left ventricle of the heart.

    In aortic stenosis, including subaortic stenosis, anginal pain is more pronounced as a result of a decrease in systolic and minute blood volume in conditions of increased demand for hypertrophied left ventricular myocardium, which causes a decrease in coronary blood flow.

    With mitral malignancy, anginal pains are caused by blood stasis in the coronary sinus as a result of increased pressure in the right atrium, as well as a reduced stroke volume and its inadequate increase in physical activity.

    Pericarditis( acute and chronic) can be accompanied by pain in the left half of the chest, which simulates angina.

    The sharp onset and persistent intense pain of atypical localization in the chest with acute pericarditis can simulate angina, especially since ECG signs indicate this( ST segment elevation and negative T wave, even the appearance of Q wave in some cases).

    In differential diagnosis, difficulty represents not only pain syndrome, but also the acceleration of ESR, an increase in the number of leukocytes, which is typical of severe forms of coronary heart disease, myocardial infarction and pericarditis. However, a clear clinical definition of pericarditis, especially the corresponding angiographic data( silhouette of the heart in the form of a trapezoid) and the above ECG changes that do not reflect the dynamics, help the differential diagnosis of acute pericarditis.

    Chronic pericarditis accompanied by partial atresia or lime deposition may also resemble angina due to:

    In the differential diagnosis, along with the characteristics given in favor of this type of pericarditis, the corresponding results of angiography( the presence of adhesion and lime deposits) also testify.

    Embolism of the coronary arteries( fat, air, tumor cells) leads to coronary insufficiency. Therefore, in differential diagnosis, it is necessary to remember the etiological factors that lead to a similar embolism of the coronary arteries.

    Pain in the left side of the chest

    Pain in the left side of the chest, in addition to angina, can be caused by many other cardiac and noncardiac diseases, accompanied by coronary insufficiency or without it:

    In the so-called cardio-phobic syndrome, which is most often manifested in people with neurastheniaand hysteria, in the left half of the chest can arise pain simulating angina. These pains are localized in the region of the apex of the heart, rarely given to the left shoulder and left arm, last for hours, and often days;Do not stop nitroglycerin, strengthen with a deep breath, and disappear after physical exertion. Differential diagnosis is facilitated by the characteristic stigmatization of neurasthenia and hysteria, and hyperventilation and dystonia of the blood vessels are especially noticeable, accompanied by an unstable blood pressure( hypo- or hypertension).However, in elderly people with a pronounced neurasthenic syndrome, care must be taken in the findings, since this syndrome can be combined with angina at the same time. Pay special attention to all the characteristics of pain in the left side of the chest. However, difficulties in differential diagnosis occur even if there is no direct relationship between the degree of coronary artery atherosclerosis and the clinical picture of angina pectoris. This is evidenced by the analysis of positive coronarography results and pathoanatomical data in patients with coronary artery disease who did not have anginal symptoms during life, as well as detection of atherosclerosis of coronary arteries established by autopsy in young American soldiers who died during the war in Korea who did not experience unpleasant anginalsensations. On the contrary, intravital severe angina pectoris with positive ECG data indicative of coronary artery disease, analysis of autopsy results in persons who died in a car crash during the life of those with severe angina syndrome with positive ECG data showed that they show slight changes indicating arteriosclerosis of the coronary arteries.

    Diseases of the nervous, muscular and other structures of the chest, spine, shoulder joints, which are most often subjected to inflammatory processes, can be accompanied by pain in the left half of the chest, which simulates angina. To this group of pathological conditions are neuromyositis, neuritis, osteochondritis, bursitis.

    In the clinical picture of cervical and thoracic( less often) osteochondrosis in combination with radiculitis, pain in the left side of the chest and, respectively, angina pectoris.

    With cervical osteochondrosis, often found in practice, pain in the left half of the chest can be prolonged, bearing the character of compression and pressure. It increases with certain movements( for example, a sharp movement of the left arm back) or positions( lying on the back), as in forced situations( prolonged sitting).Palpation can establish pain points along the near-vertebral line. The pain disappears after taking an analgesic and physiotherapy procedures.

    Although a small decrease in the T wave in a number of leads is recorded on the ECG, the results of radiography of the spine help in differential diagnosis.

    Intercostal chondritis can also be accompanied by pain in the left half of the chest, which is most pronounced at the junction of the cartilage with the sternum at the level of the III-IV rib. The pains often radiate along the costal arches in the direction of the scapula and neck, increasing with the load. A detailed anamnesis reveals previous long-term microtrauma of the chest, resulting from severe physical exertion or due to prolonged cough associated with chronic respiratory diseases.

    The rib and shoulder syndrome and the extra rib are often accompanied by pain in the left half of the chest that can simulate angina pectoris. However, if you conduct a detailed study, you can find the characteristic clinical signs: a weakening of the pulse, cyanosis, swelling( less often), as a result of compression of the arteries and veins.

    Diseases of the respiratory and mediastinal organs can be accompanied by pain in the chest, especially with pleurisy, pneumothorax, mediastinitis.

    Differential diagnosis of these diseases does not present difficulties due to known clinical and roentgenological features.

    Pain in the left side of the chest that simulates angina and manifests itself as a result of coronary insufficiency can manifest itself in a number of diseases of the gastrointestinal tract, especially in cardiopasmia( achalasia) of the esophagus, bile colic, hernia of the esophagus, diaphragm, esophagitis, gastritis,duodenal ulcers, diseases of the diaphragm.

    With cardiopasmia( achalasia) of the esophagus, pain is usually localized in the lower third of the sternum, does not have a typical irradiation, often disappears after taking nitroglycerin. However, a detailed study of the history of anamnesis helps to establish that the clinical picture is dominated by difficulty swallowing, heartburn, a feeling of "stuck" food in the esophagus and the urge to vomit. Pain increases with errors in the diet or due to neuropsychic stress, especially exaltation. In determining the diagnosis, radiographic detection of esophagospasm is crucial.

    In case of biliary colic( due to stones or inflammatory process in the biliary tract), visceral-visceral reflexes can cause chest pain simulating angina pectoris and can provoke real coronary insufficiency. Clear clinical signs of this disease and positive radiographic evidence for the presence of gall bladder stones help with differential diagnosis.

    Hernia of the esophageal opening of the diaphragm can be accompanied by a prolonged pain syndrome in 1/6 cases or manifested in the form of short attacks.

    It should be remembered that with a hernia of the diaphragm these pains appear or intensify due to food intake, with a transition from vertical to horizontal position, as well as increased intra-abdominal pressure( flexion of the trunk during training).The final diagnosis determines the fluoroscopy of the patient in the knee-elbow position( Trendelenburg position).

    In most gastrointestinal disorders, pain in the chest appears in the position of the patient lying down. With duodenal ulcer, pain in the chest is characterized by a certain seasonality and often occur at night, especially before sunrise, resembling angina.

    Diseases of the endocrine system, especially hyperthyroidism and hypofunction of the thyroid gland, adrenal diseases( Cushing's syndrome) can be accompanied not only by anginal sensations, but also by real coronary insufficiency.

    Given the typical clinical picture of the aforementioned endocrine diseases, it is not difficult to make a differential diagnosis of angina pectoris, which is mainly based on coronary artery atherosclerosis. However, it is necessary to bear in mind the possibility of coronary insufficiency in these diseases, requiring a different therapeutic approach.

    Anemia and hypoxia can also cause anginal sensations, and therefore this variant of coronary insufficiency due to qualitative changes in blood composition should be considered. Differential diagnosis provides a clear clinical picture of blood diseases, therapeutic correlation simultaneously improves the clinical picture of coronary insufficiency.

    Today, there is practically no such period of a person's life that would have spared cardiovascular diseases. On the contrary, every period of life is accompanied by the corresponding heart disease.

    The maternal period and, above all, the very appearance of a child in the world are marked by certain cardiovascular diseases, such as congenital heart disease. Some of them( especially complex and combined) are incompatible with life;others have hidden and weakly expressed signs, and therefore can be identified only as a result of persistent and thorough research;the third appear immediately at birth or somewhat later, when the child becomes physically more active as it develops;the fourth congenital heart disease manifests only in adulthood, are found accidentally due to their complications or death.

    In early childhood and at school age, cardiovascular diseases have their own characteristics. During this period of life, acute rheumatism and, as a consequence, acquired heart disease, inflammatory heart diseases( primary and secondary) can occur as a result of various infections or complications of other diseases, damage to the heart and blood vessels. It becomes possible the emergence of IHD and especially angina, but primarily as a consequence of congenital anomalies of the coronary arteries and some disorders of connective tissue. Often there is also an arterial hypertension, first of all secondary symptomatic, arising as a result of nephroparenchymal, nephrovascular and urological diseases, endocrine gland diseases, CNS, which contribute to the appearance of coronary insufficiency.

    In adulthood, people are also accompanied by cardiovascular diseases such as congenital heart disease, various nonspecific and specific diseases of endocardium, myocardium and pericardium, hypertension. IHD is associated with various precursors, respectively risk factors, secondary cardiovascular diseases caused by violations of the endocrine, genitourinary, hematopoietic systems and shifts in the metabolism of water, salts and vitamins.

    In the reproductive period, there are also diseases of the cardiovascular system. In women during pregnancy and in the postpartum period, there are cardiovascular disorders that have reappeared or existed before the onset of pregnancy( myocardiopathy of pregnant women, arterial hypertension).In this period of life, women are protected more than men by hormones from the occurrence of IHD, especially angina pectoris, which is much less common among women than men of the same age.

    Cardiovascular diseases in older people have certain characteristics. In this period, primarily degenerative diseases of the heart and blood vessels are found, especially atherosclerosis and its complications, which are more pronounced than with a large number of risk factors are associated. At the same time, atherosclerosis of the coronary arteries, arterial hypertension and ischemic heart disease dominate the cardiovascular pathology of this period. In the elderly, long-term consequences of previously transmitted specific infections( syphilis, tuberculosis) also manifest themselves, and diseases acquired at a younger age are aggravated. In general, the spectrum of cardiovascular diseases is very wide. First of all, degenerative changes due to IHD and arterial hypertension are presented, as the duration of the risk factors increases with age. In this period, namely the sixth decade of human life. IHD, especially angina pectoris, reaches its peak.

    Although atherosclerosis and its clinical manifestations are most often noted in the so-called third period of life, it must be remembered that it begins as early as childhood, and therefore its prevention, and at the same time prevention of coronary heart disease, is most effective if it starts from early years.

    At any age, congenital heart and vascular defects through relative coronary insufficiency can lead to the development of IHD.Similarly, IHD can appear again as a result of such different conditions as anemia, hypoxia, endocrine( primarily hyperthyroidism) and metabolic disturbances and restoration of viscero-visceral reflexes beginning in different organs.

    The current level of development of preventive cardiology makes it possible to provide active cardiological protection, namely: to determine the severity of the disease, to study the history of the disease and to prescribe complex therapy that influences the course of the disease, its complications and prognosis.

    The number of potential diseases from which it is necessary to differentiate angina is generally inversely related to the thoroughness of the patient's questioning. It has become customary to include relatively trivial concepts when considering this issue, and Tietze's syndrome may serve as an example of such "diligence": it is rarely found in cardiac practice and manifests itself in pain in the anterior part of the chest, which increases with movement and breathing, often accompanied by redness, swelling andtension over the affected rib-cartilage joint. It is necessary to have a truly remarkable flair to include this disease in such an unlike and separate group as angina pectoris.

    Practically there are extremely few diseases that mimic angina pectoris. Sometimes the pain with pericarditis, which is aggravated by inhalation, can also be aggravated by increased breathing due to exercise. Difficulties in diagnosis arise only in cases where patients have no pain at rest. Typically, pain is associated with a change in the patient's position, and the presence of pericardial friction noise or changes in ECG, characteristic of pericarditis, make it possible to distinguish these diseases. At times, the ulcer of the stomach or duodenum is manifested by pains in the lower part of the chest connected with the load. In such cases, the duration of pain is greater than with angina pectoris, sometimes up to 1 hour. Patients waiting for surgery on the stomach, and who have determined the vital capacity of the lungs, often complained of the occurrence of pain in deep breathing. This observation can provide a clue to the disclosure of the mechanism of the onset of pain in patients with peptic ulcer disease. The author cites the case when a man of 20 years of age, spontaneous pneumothorax caused unpleasant sensations in the middle of the thorax, associated only with the load. The bronchial asthma caused by the load sometimes imitates angina: the patient can complain of heaviness in the chest. Usually this sensation lasts longer than with angina pectoris, it is often accompanied audible at a distance by dry rales and can be provoked by a blockage of bronchi caused by the load.

    more difficult differential diagnosis between spontaneous episodes of angina and recurring pain in the lower chest or upper abdominal region caused by other reasons. Confidence in the diagnosis of angina can give typical ischemic changes on the ECG at the time of a pain attack, but there are reports of the presence of small changes on the electrocardiogram in some extracardiac diseases, it is necessary to bear in mind. Vaginal pain, similar to angina pectoris, at times quite intense, is observed in disorders of peristalsis of the esophagus or spasms of it;at the same time there is no feeling of burning behind the sternum typical for esophagitis. It is necessary to differentiate the asymptomatic narrowing of the esophagus, often found in elderly people, also called twisted, corkscrew gullet, from diffuse spasm of the lower part of the esophagus. The latter can cause severe pain, occurs with nervous or emotional stress and also disappears under the influence of taking nitroglycerin. Cold and hot food can cause both pain and esophageal obstruction symptoms. The descriptions of these sensations show that pain can be caused by a stressful situation, but the interval between stress and pain is sometimes 1-2 days;sensations can be accompanied by pricking in the fingers, pain in the elbows, shoulders, neck and ears, and eructation at times brings relief. Thus, spasm of the esophagus, accompanied by similar manifestations, can be considered a potentially determined twin of angina pectoris. Therefore, when dealing with a long incomprehensible pain that occurs at rest, it is useful to find out whether the patient's difficulty in swallowing, and if so, ask for it during the next attack to drink a sip of water and observe the result. Often, a sip of water relieves the pain associated with a violation of peristalsis in the lower third of the esophagus. This is well traced by roentgenology when using barium. The diagnosis can be confirmed by detecting changes in pressure in the esophagus, but such changes are often found in the absence of pain, especially in the elderly. Esophagoscopy usually gives a normal picture. The pain can be repeated and be quite intense;In some patients, sensations disappear after removal of the esophageal myoma.

    Pain associated with the reflux oesophagitis can be adopted for dekubitalnuyu angina, but in the former case it is usually a feeling described as heartburn;swallowing hot food causes the appearance of pain, often there is a reflux of the contents of the stomach in the mouth, and the torso of the body or the horizontal position of the body are the usual provoking factors. A pain attack can be stopped if the patient rises, sits down or drinks fluids, especially milk or alkaline water.

    Nevertheless, many doctors know from experience that sometimes sending angina patients on surgery for his existing hiatal hernia and display some of its symptoms, they found that he returns after surgery to get rid of angina. To find an explanation for this fact, it is necessary to know whether preoperative treatment of anemia has been carried out, and also to bear in mind that the arrest of angina may have been preceded by a rest period. This may be related to the placebo effect of the surgical operation performed. Julian( 1953) reported an interesting case of over-the phrenic diverticulum of the esophagus when a patient after taking solid food for a few minutes, pain in the chest and arms;In the future, the same pain was provoked by a load and was accompanied by changes in the ECG.Esophagoscopic aspiration of the contents of the diverticulum and subsequent excision of it led to the disappearance of changes on the ECG even after the load.

    A frequent cause of night pain in the lower part of the chest is duodenal ulcer, which can be mistaken for decubital angina. However, differentiate these two diseases by the presence of other signs of peptic ulcer. Patients with exacerbation of cholelithiasis often fall into the cardiology departments because many doctors incorrectly believe that biliary colic has the same time dependence as the intestinal colic. As in cases of kidney pain, the word "colic" is not applied correctly, as usually pain in biliary colic develops gradually, lasts 1 or 2 hours and then subsides;less symptomatic of her remitting pain. Sometimes the pain in biliary colic can be irradiated to the left arm. Attack of biliary colic in its duration does not allow to confuse it with angina, as such attacks are usually too long to be taken for angina pectoris. Nevertheless, sometimes this is the reason for the erroneous hospitalization of such patients in cardiology departments.

    An anxiety condition may be associated with pain localized to the left in the apex of the heart. This kind of pain often appears for the first time when the patient has the impression that the doctor discovered a heart disease. For angina, this localization is atypical, and sensations appear rather with fatigue than after a load. The gestures used by the patients are not the same as those described by Martin. In such cases, diagnostic errors are unlikely to occur. It is believed that people with hyperventilation syndrome can also have heart pain;However, if they are observed during an attack, then it is easy to diagnose. In this condition, the sensations of discomfort in the upper limbs are stitching, and in severe cases the hand can take the form of "midwifery hand".An important evidence in favor of such an anamnesis is a simultaneous tingling around the mouth and in the soles of the feet. It is also necessary to take into account the fact that hyperventilation can cause changes on the ECG.

    It has long been known that MI is often preceded by angina, which appears either suddenly or rapidly progresses. In 2/3 of the patients hospitalized for myocardial infarction, it was precisely these symptoms that appeared 1-2 months before the infarction. Later it became clear that not all patients with such symptoms preceded the development of myocardial infarction, so attempts were made to find a suitable term that would indicate the need for progression of symptoms up to the infarction. To refer to "cases that can not be called proper angina pectoris or myocardial infarction, but something intermediate," we settled on the expression "acute coronary insufficiency."Among other terms, you can answer the following: "coronary insufficiency", "intermediate coronary syndrome", "easy coronary attack", "prodromal syndrome", "acute and subacute coronary insufficiency".

    The confusion caused by the abundance of names required the introduction of a generally accepted term that would be sufficiently informative, but would not imply a pre-known outcome of the disease. For this purpose, the term "unstable angina" has become widely used. Unfortunately, its introduction turned out to be in some way self-destruction - one name is used to refer to a whole range of diseases that differ significantly from one another in symptoms, morphological features and prognosis.

    Symptoms described under the general heading of "unstable angina" include everything from a sudden onset of angina in a patient who has not previously experienced it, up to resting uninterrupted prolonged pain attacks that are not stopped by ingestion of nitroglycerin or other drugs. Some authors believe that to make such a diagnosis it is necessary to have changes on the ECG at the time of the attack. Other researchers believe that there is no need to register an ECG in such cases or an ECG can be normal. Some reports indicate that the elevation of the level of cardiac enzymes in the serum is quite acceptable, while in other works only cases with normal levels of these enzymes are reported. Some authors refer to this category only those patients in whom coronary angiography exhibits severe vascular lesions;other authors of similar studies did not conduct.

    Various designations that are part of the concept of "unstable angina" are listed at the end of the chapter in the appendix.

    It is likely that in many cases, the cause of the occurrence of unstable forms of angina is the spread of the lesion of the coronary vessels with the development of a critical degree of their narrowing, either in connection with progressive atherosclerosis, or joined coronary thrombosis, or subintimal hemorrhages. In other cases, the provoking factors may be anemia, hypotension, asphyxia, various arrhythmias, embolism of the pulmonary artery branches, hypertensive and hyperthyroid crises. In some patients, the cause of the disease is spasm of the coronary arteries, in others, seizures can result from an increase in the release of catecholamines under the influence of stressful situations. Moreover, in some cases, the characteristic symptoms develop as a result of MI, although it is so small that it does not cause changes on the ECG and serum enzymes.

    As is commonly believed, unstable angina is not a lethal disease, although its complications leading to death may develop. From this it is clear that morphological changes can be established only when a patient suffering from angina pierces from another cause. Such a catastrophe is possible as a result of coronary angiography or coronary bypass surgery.

    In patients with angina pectoris developed as a result of CBC, with appropriate therapeutic treatment, there has been a significant improvement.

    Solving the problem for each patient requires an individual approach. The external absence of the effect of treatment does not mean the actual absence of a favorable effect of therapeutic effects, but rather is the result of an ill-considered attempt to use their capabilities( see the scheme below).

    Proper use of nitroglycerin and beta-blockers improves the condition of patients. Apparently, these drugs have some effect on the prognosis.

    Therapeutic treatment does not negate surgical treatment, but rather complements it. The current possibilities and their results indicate that therapeutic treatment satisfactorily affects many patients at least for the time being.