IHD is an acute or chronic pathological process in the myocardium, caused by inadequate blood supply due to atherosclerosis of the coronary arteries, coronary spasm of intact arteries, or a combination thereof.
Etiology:
1. The main etiological factor of IHD is atherosclerotic narrowing of the coronary arteries(in 97% of patients) does not allow increasing coronary blood flow and oxygen demand during physical activity, and then ensuring adequate blood flow at rest. The coronary arteries must be narrowed by at least 50–75% for clinical signs of myocardial ischemia to appear. Insufficiency of collateral circulation plays a certain role.
2. Spasm of sclerotically unchanged coronary arteries, occurring spontaneously, at rest, as a result of disruption of regulatory neurohumoral mechanisms, or under the influence of overproduction of catecholamines under stress. Coronary spasm can also occur against the background of atherosclerosis of the coronary arteries.
3. Formation of platelet aggregates in the blood when there is an imbalance between prostacyclin, produced in the vascular intima and having antiplatelet and coronary dilating activity, and thromboxane, produced by platelets and which is a powerful vasoconstrictor and stimulator of platelet aggregation. This situation can arise when ulceration and destruction of an atherosclerotic plaque, as well as when the rheological properties of the blood are disrupted, for example, when the SAS is activated.
4. Hyperproduction of catecholamines under stress, it causes direct damage to the myocardium - lipid peroxidation is activated, lipases, phospholipases are activated, and sarcolemmas are damaged. Under the influence of SAS, the blood coagulation system is activated and fibrinolytic activity is inhibited. The work of the heart and the myocardium’s need for oxygen increases. Coronary spasm develops, ectopic foci of excitation appear.
Pathogenesis:
1. As a result of inadequate blood flow, myocardial ischemia occurs. The subendocardial layers are primarily affected.
2. Changes in biochemical and electrical processes occur in the heart muscle. In the absence of a sufficient amount of oxygen, cells switch to an anaerobic type of oxidation - the energy reserve in cardiomyocytes is depleted.
3. Disorders of heart rhythm and conduction occur. The contractile function of the myocardium is impaired.
4.Depending on the duration of ischemia, changes can be reversible and irreversible (angina pectoris - myocardial infarction).
Pathanatomy:
Ischemic, necrotic and fibrotic changes in the myocardium develop. The most dangerous localization of atherosclerosis is the main trunk of the left coronary artery.
WHO classification of coronary heart disease (1979) with changes from the All-Russian Scientific Center of the Academy of Medical Sciences of the SSR (1984) and modern additions:
1.Sudden coronary death (primary cardiac arrest) - non-violent death in the presence of witnesses, occurring instantly or within 6 hours from the onset of a heart attack, if resuscitation measures were not carried out or were ineffective. Currently, it is proposed that the time interval from the first symptoms of the disease to death be considered no more than 1 hour.
The most common cause of sudden coronary death is ventricular fibrillation or, less commonly, cardiac asystole, resulting from acute myocardial ischemia and electrical instability of the myocardium. Death that occurs in the early stages of myocardial infarction with its complications of cardiogenic shock or pulmonary edema, myocardial rupture is considered as death from myocardial infarction.
Sudden death is provoked by physical and psycho-emotional stress and alcohol intake. Adrenaline and norepinephrine under stress cause the appearance of ectopic foci of excitation in the ventricles.
Risk factors for sudden death– a sharp decrease in exercise tolerance, ST depression, ventricular extrasystoles during exercise. The history often reveals ischemic heart disease. In some patients, sudden death may be the first and last sign of coronary artery disease, but is it really that sudden? In 1/2 of the patients, when questioning relatives, signs of unstable angina were noted. In other individuals, there may have been silent myocardial ischemia, which was not clinically manifested, but could be detected during instrumental examination.
Symptoms of sudden death: loss of consciousness, respiratory arrest, absence of pulse, heart sounds, dilated pupils, pale gray skin tone.
2. Angina pectoris– “angina pectoris” (described by Heberden in 1768) for 140 years was the only definition of coronary artery disease until the clinical description of myocardial infarction was described in 1908. A classic attack of angina occurs when exposed to factors that increase the myocardial oxygen demand (physical activity, increased blood pressure, food intake, heartbeat, stress). Without sufficient blood supply through the narrowed coronary arteries, myocardial ischemia occurs. The following symptoms are characteristic of angina:
· Compressive or pressing nature of pain, but there may be pain such as burning or shortness of breath.
· Localization behind the sternum– “fist” symptom. The patient shows the place of pain not with his finger, but with his palm.
· Attacks of pain.
· Irradiation to the left arm, shoulder, shoulder blade, neck, jaw.
· Provoke seizures physical or emotional stress or other factors that increase oxygen demand. (Emotions - due to activation of the sympathoadrenal system, leading to an increase in heart rate and blood pressure).
Reduction or cessation of pain after taking nitroglycerin in 2-3 minutes.
· Duration of pain 1–15 minutes, if more than 30 minutes, you need to think about the development of myocardial infarction.
· Feeling of fear– the patients freeze.
The attack is stopped more quickly in a standing or sitting position, since in the lying position the venous return to the heart increases, which leads to an increase in blood supply to the left ventricle and an increase in the myocardial oxygen demand.
As angina progresses, attacks occur at very low loads, and then at rest.
Angina pectoris characterized by transient attacks of chest pain caused by physical or emotional stress, or other factors leading to an increase in the metabolic needs of the myocardium (increased blood pressure, heart rate). As a rule, the pain quickly disappears with rest or when taking nitroglycerin.
Distinguish:
New-onset angina pectoris– lasting up to 1 month from the moment of appearance. It can regress, turn into stable or progressive angina, end in myocardial infarction or even sudden coronary death. Patients with new-onset angina are subject to hospitalization, as its consequences are unpredictable.
Stable exertional angina– lasting more than 1 month. Characterized by a stable flow. Indicate the functional class depending on the ability to perform physical activity (Canadian classification):
I class– Patients tolerate normal physical activity well. Attacks occur during high-intensity exercise (walking for a long time and at a fast pace). High tolerance to VEM test.
II class– Slight limitation of usual physical activity (activity). Seizures occur when walking normally over a distance of more than 500 m on level ground or when climbing more than 1 floor. The likelihood of angina increases in cold weather, emotional excitement, and in the first hours after waking up.
III class– Marked limitation of usual physical activity. Seizures occur when walking on level ground at a distance of 100–500 m, or when climbing one floor.
IV class– Angina occurs with light physical exertion, walking a distance of less than 100 m. Characteristic attacks of angina at rest are caused by increased metabolic needs of the myocardium (increased blood pressure, heart rate, increased venous blood flow to the heart when moving to a horizontal position, during dreams).
Progressive angina pectoris– a sudden increase in the frequency, severity and duration of angina attacks in response to the usual load for a given patient, an increase in the daily number of nitroglycerin tablets, reflecting the transition of angina to a new FC or MI. According to old classifications, this was considered a “pre-infarction condition.”
Spontaneous angina– vasospastic, in which attacks occur without any visible connection with factors leading to an increase in the metabolic needs of the myocardium – at rest, more often at night or early in the morning. An anginal attack is longer and more intense than with angina pectoris, and is more difficult to stop with nitroglycerin. It is not preceded by increased blood pressure or tachycardia. A cold test or a test with ergometrine is positive. Its cause is a regional spasm of unchanged or sclerotic large coronary arteries. Spontaneous angina can be combined with exertional angina.
Spontaneous angina, accompanied by transient rises in the ST segment from 2 to 20 mm for 5–10 minutes in the absence of changes in QRS and enzyme activity characteristic of myocardial infarction, is classified as variant angina or Prinzmetal's angina. During coronary angiography, in 10% of patients with spontaneous angina, coronary arteries unaffected by atherosclerosis are found; such patients tolerate physical activity well (a construction worker climbs the 10th floor without pain and on the same day experiences pain when walking slowly in the cold).
Any changes in angina attacks in a patient - progressive, new-onset, spontaneous - are combined with the term “unstable” angina. Patients with unstable angina are subject to hospitalization due to the high risk of sudden death. The most dangerous is the progression of angina pectoris - myocardial infarction develops in 10–20% of patients with progressive angina pectoris.
3. Myocardial infarction– based on the clinical picture, ECG changes and enzyme activity in the blood serum, the following are distinguished:
Large focal (with Q wave);
Finely focal (probable, without Q wave).
4. Post-infarction cardiosclerosis is established no earlier than 2 months after the onset of MI. The diagnosis indicates the presence of a chronic cardiac aneurysm, internal myocardial ruptures, conduction disorders, arrhythmias, and stages of heart failure. The diagnosis can be made on the basis of medical documentation, that is, retrospectively using an ECG.
5. Violations heart rhythm- indicating the form.
6. Heart failure – indicating the form and stage.
The 5th and 6th forms of IHD are based on post-infarction and atherosclerotic cardiosclerosis, leading to the replacement of muscle fibers with connective ones and dysfunction of the heart muscle.
Diagnostics:
1. Anamnesis allows you to make the correct diagnosis of IHD during a classic attack of pain in 90% of cases.
2. Electrocardiography – the diagnosis is reliable when identifying acute focal, ischemic and cicatricial changes in the myocardium. But with angina pectoris there can be a normal ECG. Myocardial ischemia is manifested by depression of the terminal part of the ventricular complex – ST is shifted by 1 mm or more, horizontally, convexly, obliquely ascending. The T wave may be reduced and flattened. With spontaneous angina, at the time of the attack there may be ST elevations to the form of an infarction “roof”.
3. Holter monitoring An ECG is carried out during the day in the conditions of the patient’s daily life, usually in leads V 2-5. The ECG is interpreted using a computer. The method is informative for identifying spontaneous angina. The patient keeps an hourly diary about his activities, which is then compared with ECG data.
If there are no changes in the ECG at rest, exercise tests and pharmacological tests are used.
4. Bicycle ergometer test (VEM) carried out according to the method of step-by-step continuously increasing loads. Indications for VEM:
atypical pain syndrome,
· ECG changes uncharacteristic of myocardial ischemia in middle-aged and elderly people, as well as in young men with a preliminary diagnosis of coronary artery disease,
· no changes on the ECG if CHD is suspected.
Start with a load of 150 kgm/min. and continue for 3 – 4 minutes at each stage until the test stops. They are guided by submaximal heart rate, which should be equal to 75% of the maximum heart rate for age.
Contraindications to VEM:
Myocardial infarction earlier than 3 weeks;
· unstable angina;
· cerebrovascular accidents;
thrombophlebitis and thromboembolic complications;
· CHF – PB – W st.;
· valvular stenosis of the aortic mouth;
· Blood pressure more than 230/130 mm Hg. Art.;
· aneurysm of the aorta, heart;
· severe rhythm disturbances;
Complete block of the left bundle branch.
Indications for stopping the test:
· attack of angina pectoris;
· blood pressure drop by 25%;
· blood pressure rise to 220/130 mm Hg;
· brain symptoms.
If the patient achieves a submaximal heart rate without clinical and ECG signs of ischemia, the test is negative. It is positive if, at the time of exercise, an attack of angina appears, blood pressure decreases, and a decrease or rise in ST by 1 mm or more is observed.
5. If it is impossible to carry out VEM, it is carried out transesophageal electrical stimulation of the atria (TEES)) using a pacemaker and an esophageal bipolar electrode. A rhythm of 100 pulses per minute or more is imposed until signs of ischemia appear.
6. Test with bicycle ergometrine– 0.05 mg of the drug is administered intravenously, and after 5 – 6 minutes more 0.1 – 0,15– 0.2 mg. The test is considered positive if, at the time of the test, an attack of angina occurs with an ST shift of more than 1 mm
7. Cold test– after 15 – After 20 minutes of horizontal position, the patient lowers his hand into a bath of cold water with ice up to the middle of the forearm. After 5 minutes an ECG is taken. The last two tests are used to diagnose Prinzmetal's angina.
8.Test with chimes is based on inducing steal syndrome - after intravenous administration of the drug an attack of angina appears.
9.X-ray contrast coronary angiography is usually performed not to diagnose ischemic heart disease, but to select a treatment method – conservative or surgical (coronary artery bypass grafting or balloon angioplasty). The catheter is inserted through the femoral or brachial artery.
10.Echocardiography can establish a local violation of contractility (hypokinesis) at the time of an attack, but it is difficult to detect this, so an echo CG is performed with a load - stress echo CG (with the introduction of dopamine into a vein, etc.).
11.Scintigraphy(radioisotope scan of the heart with a waist) in case of coronary artery disease reveals defects in the filling of areas of the myocardium with reduced blood supply; a “cold spot” can appear only during exercise.
12Radionuclide ventriculography used to detect cardiac aneurysms.
13. Positron emission tomography defines “dormant myocardium”
Differential diagnosis is carried out:
· with angina pectoris as a syndrome in aortic heart defects;
· with systemic diseases (periarteritis nodosa);
· with myocarditis (coronaryitis);
· with dissecting aortic aneurysm;
· with osteochondrosis;
· with cardiomyopathies.
Lecture7
ISCHEMICDISEASEHEARTS. CEREBROVASCULARDISEASES
Coronary heart disease and cerebrovascular disease are widespread throughout the world, especially in economically developed countries. They are the main causes of death in people with cardiovascular pathology.
Coronary heart disease(CHD) is a group of diseases caused by absolute or relative insufficiency of coronary circulation. In the vast majority of cases, IHD develops due to atherosclerosis of the coronary arteries, so there is a synonym for the name - coronary disease.
IHD was identified by WHO as an independent group of diseases in 1965 due to its great social significance. Until 1965, all cases of ischemic heart disease were described as a cardiac form of atherosclerosis or hypertension. The classification of IHD into an independent group was dictated by the epidemic increase in morbidity and mortality from its complications and the need to urgently develop measures to combat them.
Changes in the myocardium similar to ischemic heart disease develop much less frequently without atherosclerosis of the coronary arteries of the heart and are caused by other diseases leading to relative or absolute insufficiency of coronary circulation: congenital anomalies of the coronary arteries, arteritis, thromboembolism of the coronary arteries with thromendocarditis, impaired blood oxygenation with severe “cyanotic” defects heart disease, anemia, poisoning with carbon monoxide (II) CO, pulmonary failure, etc. Changes in the myocardium in the listed diseases do not relate to coronary artery disease, but are considered as complications of these diseases.
Epidemiology. IHD is the leading cause of death in many economically developed countries of the world. In the USA, for example, 5.4 million new cases of illness are registered every year, ] / 2 of which 550,000 are disabled and die. Since the late 60s, incidence rates of coronary artery disease among the working-age male population began to increase sharply, which led to talk of an epidemic of coronary artery disease. In recent years, in many countries there has been a tendency towards stabilization of morbidity and mortality rates from coronary artery disease, which is due to many reasons: smoking ban, reduction of cholesterol in food, correction of high blood pressure, surgical treatment, etc.
Etiology and pathogenesis. IHD has common etiological and pathogenetic factors with atherosclerosis and hypertension, which is not accidental, since IHD is actually a cardiac form of atherosclerosis and hypertension.
Pathogenetic factors of IHD are also called risk factors, since they determine the likelihood of developing the disease. According to the degree of significance, they are divided into first- and second-order factors. The most important first-order risk factors include: hyperlipidemia, tobacco smoking, arterial hypertension, decreased physical activity, obesity, nutritional factor (cholesterol diet), stress, decreased
glucose tolerance, male gender, alcohol consumption. Among the second-order risk factors are disturbances in the content of microelements (zinc), increased water hardness, increased levels of calcium and fibrinogen in the blood, hyperuric acid.
Hyperlipidemia. Hypercholesterolemia and hypertriglyceridemia are the most important pathogenetic factors in the development of atherosclerosis of the coronary arteries of the heart. A direct relationship has been established between blood cholesterol levels and mortality due to coronary artery disease. People with cholesterol concentrations less than 150 mg/L and relatively low levels of low-density lipoprotein (LDL) develop CHD relatively rarely. The independent significance of hypertriglyceridemia is controversial, but a correlation has been shown between an increase in their concentration in the blood in parallel with LDL. The frequent development of ischemic heart disease in patients with diabetes mellitus becomes clear.
Tobacco smoking, IHD develops 2.14 times more often in smokers than in non-smokers. The main effect of smoking is due to stimulation of the sympathetic part of the autonomic nervous system, accumulation of carbon monoxide (11) in the blood, immune damage to the vascular wall and activation of platelet aggregation. People who smoke more than 25 cigarettes per day have decreased levels of high-density lipoprotein (HDL) and increased levels of very low-density lipoprotein (VLDL). The risk of developing CHD increases with the number of
cigarettes smoked.
Arterial hypertension. It aggravates the course of atherosclerosis, promotes the development of hyalinosis of arterioles and causes hypertrophy of the left ventricular myocardium. All these factors together increase ischemic damage in the myocardium
The role of atherosclerosis of the coronary arteries. More than 90% of patients with coronary artery disease have stenotic atherosclerosis of the coronary arteries with stenosis of 75% of at least one main artery. The results of experimental and clinical observations show that 75% of coronary artery stenosis cannot meet the oxygen needs of the heart muscle even with a light load Immediate reasons ischemic damage to the myocardium in coronary artery disease are thrombosis of the coronary arteries, thromboembolism, prolonged spasm, functional overstrain of the myocardium in conditions of stenosing atherosclerosis of the coronary arteries and insufficient collateral circulation. Thrombosis of the coronary arteries is found in 90% of cases of transmural myocardial infarction - one of the most severe forms of coronary artery disease. The thrombus is usually localized in the ulcerated area
atherosclerotic plaque. The genesis of a thrombus is associated with platelet aggregation at the site of plaque ulceration, where the subendothelial layer is exposed and tissue thromboplastin is released. In turn, platelet aggregation leads to the release of agents that cause vasospasm - thromboxane A2, serotonin, histamine, etc. Aspirin reduces the synthesis of thromboxane A2 and inhibits platelet aggregation and vasospasm.
Thromboembolism in the coronary arteries usually occurs when thrombotic masses are separated from their proximal sections, as well as from the cavity of the left ventricle.
Prolonged spasm of the coronary arteries was proven by angiographic data. Spasm develops in the main trunks of the coronary arteries affected by atherosclerosis. The mechanism of vasospasm is complex, caused by the local release of vasoactive substances formed during platelet aggregation on the surface of atherosclerotic plaques. After resolution of prolonged vasospasm, blood circulation in the myocardium is restored, but this often leads to additional damage associated with reperfusion - reperfusion injury. Vasospasm can also result in coronary artery thrombosis. The mechanism of thrombosis may be due to damage to the atherosclerotic plaque during spasm, which especially often occurs with atherocalcinosis.
Functional overstrain in conditions of insufficiency of collateral circulation in atherosclerosis of the coronary arteries can also lead to ischemic damage to the myocardium. At the same time, the importance of the degree of stenosis and the prevalence of atherosclerosis has been proven. Stenosis of more than 75% of at least one main trunk of the coronary artery is considered significant.
Morphogenesis. In IHD, ischemic myocardial damage and regeneration processes develop in stages.
The mechanism of ischemic myocardial damage is complex and is caused by the cessation of oxygen supply to myocardiocytes, impaired oxidative phosphorylation and, consequently, the occurrence of ATP deficiency. As a result, the functioning of ion pumps is disrupted, and excess amounts of sodium and water enter the cells, while at the same time the cells lose potassium. All this leads to edema and swelling of mitochondria and the cells themselves. An excess amount of calcium also enters the cell, causing activation of Ca 2+ -dependent proteases
calpains, dissociation of actin microfilaments. activation of phospholipase A 2. In myocardiocytes, anaerobic glycolysis increases, glycogen reserves are broken down, which leads to thyroidosis. Under conditions of oxygen deficiency, reactive oxygen species and lipid peroxides are formed. Then comes destruction
When membrane structures, primarily mitochondrial ones, become damaged, irreversible damage occurs.
Typically, ischemic myocardial damage follows the path of coagulation and apoptosis. In this case, immediately reacting genes are activated, primarily c-fos, and the program of “programmed death” - apoptosis - is activated. Calcium mechanisms of damage are of great importance. During apoptosis, calcium endonucleases are activated with DNA hydrolysis into single-stranded fragments.
In peripheral areas, ischemic injury usually ends in liquefaction necrosis with cellular edema and myocytolysis, which is especially typical for reperfusion injuries.
Ischemic myocardial damage can be reversible or irreversible.
Reversible ischemic damage develop in the first 20-30 minutes of ischemia and, if the influence of the factor causing them ceases, completely disappear. Morphological changes are detected mainly by electron microscopy (EM) and histochemical studies. EM makes it possible to detect swelling of mitochondria, deformation of their cristae, and relaxation of myofibrils. Histochemically, a decrease in the activity of dehydrogenases and phosphorylases, a decrease in glycogen reserves, intracellular potassium and an increase in the concentration of intracellular sodium and calcium are detected. Some authors note that light microscopy reveals wavy muscle fibers at the periphery of the ischemic zone.
Irreversible ischemic damage cardiomyocytes begin after ischemia lasting more than 20-30 minutes. In the first 18 hours, morphological changes are recorded only using EM, histochemical and luminescent methods. EM reveals ruptures of the sarcolemma, deposits of amorphous material (calcium) in mitochondria, destruction of their cristae, chromatin condensation and the appearance of heterochromatin. In the stroma - edema, plethora, diapedesis of erythrocytes, marginal standing of polymorphonuclear leukocytes, which can also be observed with light microscopy.
After 18-24 hours of ischemia, a necrosis zone is formed, visible micro- and macroscopically, i.e. myocardial infarction is formed. During myocardial infarction, three types of necrosis develop:
- coagulation - localized in the central zone, cardiomyocytes are elongated, characterized by karyopyknosis and calcium accumulation. Coagulative necrosis is actually a manifestation of apoptosis; necrotic masses are removed by phagocytosis by macrophages;
Coagulation followed by myocytolysis - necrosis of muscle bundles with the phenomena of overcontraction and coagulation necrosis, as well as the accumulation of calcium in the cells, but with subsequent lysis of necrotic masses. This necrosis is located in the peripheral parts of the infarction and is caused by the action of ischemia and reperfusion;
- myocytolysis - liquefaction necrosis - swelling and destruction of mitochondria, accumulation of sodium and water in the cell, development of hydropic dystrophy. Necrotic masses are eliminated by lysis and phagocytosis.
Around the zone of necrosis, a zone of demarcation inflammation is formed, represented in the first days by full-blooded vessels with diapedesis of erythrocytes and leukocyte infiltration. Subsequently, a change in cellular cooperation occurs, and macrophages and fibroblasts, as well as newly formed vessels, begin to predominate in the inflammation zone. By the 6th week, the necrosis zone is replaced by young connective tissue. After a myocardial infarction, a focus of sclerosis forms at the site of former necrosis. A patient who has suffered an acute catastrophe is left with chronic heart disease in the form of post-infarction cardiosclerosis and stenosing atherosclerosis of the coronary arteries.
Classification. IHD flows in waves, accompanied by coronary crises, i.e. with episodes of acute (absolute) and/or chronic (relative) coronary insufficiency. In this regard, acute ischemic heart disease and chronic ischemic heart disease are distinguished. Acute IHD is characterized by the development of acute ischemic damage in the myocardium, chronic IHD is characterized by cardiosclerosis as a result of ischemic damage.
ClassificationIHD
ACUTE IHD
Sudden cardiac death
Acute focal ischemic dystrophy of the myocardium
Myocardial infarction
CHRONIC IHD
Large focal cardiosclerosis
Small focal cardiosclerosis
Acute ischemic heart disease is divided into three forms: sudden cardiac death, acute focal ischemic myocardial dystrophy and myocardial infarction.
Chronic ischemic heart disease is represented by post-infarction large-focal and diffuse small-focal cardiosclerosis.
Sudden cardiac death. In the literature, sudden cardiac death is defined as death that develops
instantly or within minutes, several hours after the onset of symptoms of heart damage. In most cases (up to 80%), it occurs in patients with coronary artery disease with atherosclerosis of the coronary arteries. However, it should be remembered that sudden cardiac death can also develop in other diseases.
Sudden cardiac death in acute ischemic heart disease is considered death in the first 6 hours of acute myocardial ischemia. During this period, 74-80% of patients show changes in teeth Q, G, S-T interval, lethal arrhythmias (ventricular fibrillation, asystole) on the ECG, but blood enzymes do not yet change during this time interval.
Morphological changes may correspond to the early stages of ischemic damage against the background of unchanged myocardium, but more often - against the background of cardiosclerosis or previously developed myocardial infarction. In this case, damage is often localized in the area of the conduction system, which is what causes the development of arrhythmias. In the foci of acute ischemic injuries that caused sudden death, macroscopic changes are not detected. Microscopically, wave-like changes in muscle fibers and initial manifestations of coagulation necrosis in the peripheral parts can be detected. EM reveals damage to mitochondria, calcium deposits in them, ruptures of the sarcolemma, chromatin margination, histochemically - a decrease in the activity of dehydrogenases, and the disappearance of glycogen.
Acute occlusion of the coronary arteries by a thrombus or thromboembolism is found only in 40-50% of autopsies of people who died from sudden cardiac death. The relative low incidence of thrombosis can be explained by developing fibrinolysis as well as the possible role of vasospasm and functional overstrain of the myocardium under conditions of coronary circulation deficiency in the genesis of sudden cardiac death.
Thanatogenesis (mechanism of dying) in sudden cardiac death is caused by the development of lethal arrhythmias.
Acute focal ischemic dystrophy of the myocardium. A form of acute ischemic heart disease that develops in the first 6-18 hours after the onset of acute myocardial ischemia. Characteristic changes are recorded on the ECG. An increase in the content of enzymes coming from the damaged myocardium - muscle-type creatinine kinase and glutamate noxaloacetate transaminase - may be detected in the blood. With EM and with the help of histochemical reactions, the same changes are recorded as with sudden cardiac death, corresponding to early ischemic damage, but more pronounced. In addition, with EM, one can observe the phenomena of apoptosis and marginal necrosis in areas of overcontraction of muscle fibers.
At the section table, early ischemic injuries are diagnosed using potassium tellurite and tetrazolium salts, which do not stain the ischemic zone due to the lack of oxygen in it and a decrease in the activity of dehydrogenases.
Myocardial infarction. A form of acute ischemic heart disease, characterized by the development of ischemic myocardial necrosis. It develops 18 hours after the onset of ischemia, when the necrosis zone becomes visible micro- and macroscopically. In addition to ECG changes, it is characterized by fermentemia.
Macroscopically, the infarction is irregular in shape, white with a hemorrhagic rim. Microscopically, a zone of necrosis is determined, surrounded by a zone of demarcation inflammation, separating the first from the intact myocardial tissue. In the necrosis zone, coagulation necrosis in the center, coagulation myocytolysis and liquefaction necrosis along the periphery are determined.
The zone of demarcation inflammation in the first days of a heart attack is represented by a leukocyte shaft and full-blooded vessels with diapedesis, and from the 7-10th day - by young connective tissue, gradually replacing the necrosis zone and maturing. Scarring of the infarction occurs by the 6th week.
During a heart attack, two stages are distinguished: necrosis and scarring.
Classificationheart attackmyocardium
I. By time of occurrence
Primary (first appeared)
Recurrent (developing within 6 weeks after the previous one)
Repeated (developed more than 6 weeks after the previous one)
II. By localization
Anterior wall of the left ventricle and anterior sections of the interventricular septum
Posterior wall of the left ventricle
Lateral wall of the left ventricle
Interventricular septum
Extensive heart attack
III. By prevalence
Subendocardial
Intramural
Subendocardial
Transmural
Depending on time of occurrence There are primary infarctions (which occurred for the first time), recurrent (developed within 6 weeks after the previous one), and repeated (developed after 6 weeks after the previous one). For recurrent
infarction, foci of scarring infarction and fresh foci of necrosis are detected. If repeated, there are old post-infarction scars and foci of necrosis.
By localization isolated infarction of the anterior wall of the left ventricle, the apex and anterior sections of the interventricular septum - 40-50% of cases, develops with obstruction, stenosis of the left descending artery; posterior wall of the left ventricle - 30-40% of cases, with obstruction, stenosis of the right coronary artery; lateral wall of the left ventricle - 15-20% of cases, with obstruction, stenosis of the circumflex branch of the left coronary artery. An isolated infarction of the interventricular septum develops less frequently - 7-17% of cases, as well as an extensive infarction - with obstruction of the main trunk of the left coronary artery.
By prevalence subendocardial, intramural, subepicardial and transmural infarctions are distinguished. ECG diagnostics allows to differentiate subendocardial and transmural infarction. It is believed that transmural infarction always begins with damage to the subepicardial sections due to the characteristics of their blood supply. Subendocardial infarction is often not accompanied by coronary thrombosis. It is believed that in such cases it develops as a result of vasospasm induced by local humoral factors. On the contrary, with transmural infarction, thrombosis of the coronary arteries of the heart is found in 90% of cases. Transmural infarction is accompanied by the development of parietal thrombosis and pericarditis.
Complications of a heart attack: cardiogenic shock, ventricular fibrillation, asystole, acute heart failure, myomalacia and cardiac rupture, acute aneurysm, parietal thrombosis with thromboembolic complications, pericarditis.
The mortality rate for myocardial infarction is 35 % and develops most often in the early, preclinical period of the disease from lethal arrhythmias, cardiogenic shock and acute heart failure. In a later period - from thromboembolism and cardiac rupture, often in the area of acute aneurysm with tamponade of the pericardial cavity.
Large-focal (post-infarction) cardiosclerosis. It develops as a result of a heart attack and is represented by fibrous tissue. The preserved myocardium undergoes regenerative hypertrophy. If large-focal cardiosclerosis occurs after a transmural myocardial infarction, a complication may develop - a chronic cardiac aneurysm. Death occurs from chronic heart failure or thromboembolic complications.
Diffuse small-focal cardiosclerosis. As a form of chronic ischemic heart disease, diffuse small-focal cardiosclerosis develops as a result of relative coronary insufficiency with the development of small foci of ischemia. May be accompanied by atrophy and lipofuscinosis of cardiomyocytes. Cerebrovascular diseases(allocated into a separate group - WHO in 1977) are characterized by acute disorders of cerebral circulation, the background for the development of which is atherosclerosis and hypertension. Patients with cerebrovascular diseases make up more than 50% of patients in neurological hospitals.
Classificationcerebrovasculardiseases
I. Brain diseases with ischemic damage
Ischemic encephalopathy
Ischemic cerebral infarction
Hemorrhagic cerebral infarction
II. Intracranial hemorrhages
Intracerebral
Subarachnoid
Mixed
III. Hypertensive cerebrovascular diseases
Lacunar changes
Subcortical leukoencephalopathy
Hypertensive encephalopathy
The following main groups of diseases are distinguished: 1) brain diseases associated with ischemic damage - ischemic encephalopathy, ischemic and hemorrhagic cerebral infarction; 2) intracranial hemorrhages; 3) hypertensive cerebrovascular diseases - lacunar changes, subcortical leukoencephalopathy, hypertensive encephalopathy.
The clinic uses the term stroke (from the Latin in-sultare - to jump), or brain stroke. Stroke can be represented by a variety of pathological processes: - hemorrhagic stroke - hematoma, hemorrhagic impregnation, subarachnoid hemorrhage; - ischemic stroke - ischemic and hemorrhagic infarction.
Brain diseases caused by ischemicdamage. Ischemic encephalopathy. Stenosing atherosclerosis of the cerebral arteries is accompanied by disturbances in maintaining a constant level of blood pressure in the vessels of the brain. Chronic ischemia occurs
Mia. The most sensitive to ischemia are neurons, primarily pyramidal cells of the cerebral cortex and piriform neurons (Purkinje cells) of the cerebellum, as well as neurons of the Zimmer zone of the hippocampus. Calcium damage with the development of coagulative necrosis is recorded in these cells And apoptosis. The mechanism may be due to the production of neurotransmitters (glutamate, aspartate) by these cells, which can cause acidosis and opening of ion channels. Ischemia also causes activation of c-fos genes in these cells, leading to apoptosis.
Morphologically, ischemic changes in neurons are characteristic - coagulation and eosinophilia of the cytoplasm, pyknosis of the nuclei. Gliosis develops in place of dead cells. The process does not affect all cells. When small groups of pyramidal cells of the cerebral cortex die, they speak of laminar necrosis. Most often, ischemic encephalopathy develops at the border of the anterior and middle cerebral arteries, where, due to the peculiarities of angioarchitectonics, there are favorable conditions for hypoxia - weak anastomosis of vessels. Foci of coagulative necrosis, also called dehydrated infarcts, are sometimes found here. With the long-term existence of ischemic encephalopathy, atrophy of the cerebral cortex occurs. A coma with loss of cortical functions may develop.
Cerebral infarctions. The causes of cerebral infarction are similar to those of ischemic heart disease, but in some cases, ischemia can be caused by compression of the vessel by outgrowths of the dura mater during brain dislocation, as well as a drop in systemic blood pressure.
Ischemic cerebral infarction is characterized by the development of liquefaction necrosis of irregular shape ("focus of softening") - Macroscopically determined only after 6-12 hours. After 48-72 hours, a zone of demarcation inflammation is formed, and then resorption of necrotic masses occurs And a cyst forms. In rare cases, a glial scar develops at the site of small necrosis.
Hemorrhagic cerebral infarction is often the result of embolism of the cerebral arteries and has a cortical localization. The hemorrhagic component develops due to diapedesis in the demarcation zone and is especially pronounced during anticoagulant therapy.
Intracranial hemorrhages. They are divided into intracerebral (hypertensive), subarachnoid (aneurysmal), mixed (parenchymal and subarachnoid - arteriovenous defects).
Intracerebral hemorrhages. They develop when microaneurysms rupture at the sites of intracerebral bifurcations.
arteries in patients with hypertension (hematoma), as well as as a result of diapedesis (petechial hemorrhages, hemorrhagic impregnation). Hemorrhages are most often localized in the subcortical ganglia of the brain and the cerebellum. As a result, a cyst with rusty walls is formed due to hemosiderin deposits.
Subarachnoid hemorrhages. They arise due to the rupture of aneurysms of large cerebral vessels, not only of atherosclerotic, but also of inflammatory, congenital and traumatic origin.
Hypertensive cerebrovascular diseases. Develops in people suffering from hypertension.
Lacunar changes. They are represented by many small rusty cysts in the area of the subcortical nuclei.
Subcortical leukoencephalopathy. Accompanied by subcortical axonal loss and the development of demyelination with gliosis and arteriolohyalinosis.
Hypertensive encephalopathy. Arises at patients with a malignant form of hypertension and is accompanied by the development of fibrinoid necrosis of the vascular walls, petechial hemorrhages and edema.
Complications of strokes. Paralysis, cerebral edema, dislocation of the brain with herniations, breakthrough of blood in the cavities of the ventricles of the brain, leading to death.
Pathological anatomy: lecture notes Marina Aleksandrovna Kolesnikova
7. Coronary heart disease
7. Coronary heart disease
Coronary heart disease is a group of diseases caused by absolute or relative insufficiency of coronary blood flow.
The immediate causes are prolonged spasm, thrombosis, atherosclerotic occlusion, as well as psycho-emotional stress.
The pathogenetic factors of coronary disease are the same as in atherosclerosis and hypertension. The course is wavy with short crises, against the background of chronic coronary circulatory failure.
Myocardial infarction is ischemic necrosis of the heart muscle.
Classification
By time of occurrence: acute (first hours), acute (2–3 weeks), subacute (3–8 weeks) and scarring stage.
By localization: in the basin of the anterior interventricular branch of the left coronary artery, in the basin of the circumflex branch of the left coronary artery and the main trunk of the left coronary artery.
According to the localization of the necrosis zone: anteroseptal, anteropical, anterolateral, high anterior, widespread anterior, posterodiaphragmatic, posterobasal, posterolateral and widespread posterior.
By prevalence: small-focal, large-focal and transmural.
Downstream: necrotic stage and scarring stage. In the necrotic stage (histologically), the infarction is a zone of necrosis, in which islands of preserved myocardium are preserved perivascularly. The necrosis zone is delimited from healthy tissue by a demarcation line (leukocyte infiltration).
The stage of scarring is spoken of when macrophages and young fibroplastic cells take the place of leukocytes. Newly formed connective tissue is initially loose, then it matures and turns into coarse fibrous tissue. Thus, when a heart attack occurs, a dense scar forms in its place.
This text is an introductory fragment. From the book Pathological Anatomy: Lecture Notes author Marina Aleksandrovna Kolesnikova From the book Practical Homeopathy author Victor Iosifovich Varshavsky From the book Paramedic's Handbook author Galina Yurievna Lazareva From the book Breathing gymnastics by A.N. Strelnikova author Mikhail Nikolaevich Shchetinin From the book Home Directory of Diseases author Y. V. Vasilyeva (comp.) From the book Healthy Heart and Vessels author Galina Vasilievna Ulesova From the book Diabetes author S. Trofimov (ed.) From the book Golden Recipes: Herbal Medicine from the Middle Ages to the Present Day author Elena Vitalievna Svitko From the book Complete Medical Diagnostics Guide by P. Vyatkin From the book Everything that heals the heart and blood vessels. The best folk recipes, healing nutrition and diet, gymnastics, yoga, meditation author Irina Stanislavovna PigulevskayaProfessor E.D. Cherstvyi, Associate Professor D.G. Grigoriev
Coronary heart disease (CHD) is a disease caused by relative or absolute insufficiency of coronary blood supply. It includes cases of coronary circulation disorders as a result of changes in the functional state of the coronary arteries (spasm), atherosclerotic occlusion and violations of the rheological properties of blood (thrombosis, thromboembolism).
In most cases, IHD is a cardiac form of atherosclerosis and/or hypertension.
At the same time, ischemic conditions of the myocardium caused by damage to the coronary arteries of another origin (rheumatism, vasculitis, systemic lupus erythematosus, septic endocarditis, cardiomyopathies) or hemodynamic disorders (aortic stenosis, aortic valve insufficiency, etc.) are not classified as ischemic heart disease, but are considered as complications of corresponding diseases.
IHD classification:
1. Angina pectoris.
1.1. Stable angina.
1.2. Unstable angina.
1.3. Spontaneous angina. Prinzmetal's angina.
2. Sudden coronary death.
3. Myocardial infarction.
3.1. Large focal myocardial infarction.
3.2. Small focal myocardial infarction.
4. Post-infarction cardiosclerosis.
5. Atherosclerotic cardiosclerosis.
All forms of IHD can be divided into acute (sudden coronary death, myocardial infarction) and chronic (angina pectoris, cardiosclerosis). However, it should be noted that in most cases, IHD has a long-term wave-like course with episodes of exacerbation in the form of acute (absolute) coronary insufficiency that occurs against the background of chronic (relative) coronary circulatory insufficiency. Thus, in fact, we are talking about forms-stages that replace and complement each other (for example: angina pectoris - myocardial infarction - angina pectoris and post-infarction cardiosclerosis).
Angina pectoris is a form of coronary artery disease characterized by attacks of chest pain. There are three types of this pathology, differing in the conditions of occurrence, duration of attacks and prognosis: stable, unstable and spontaneous angina.
Stable angina (syn.: stable, typical, exertional angina) is the most common form that develops during functional stress on the heart (physical activity, emotional arousal). It is based on a decrease in coronary myocardial perfusion to a critical level due to stenosing atherosclerosis. At the time of the attack, spasm of the coronary arteries develops and, as a consequence, reversible ischemic dystrophy of the myocardium (see section VCS) mainly in the subendocardial zone of the left ventricle. Attacks of this angina usually disappear with rest or after taking nitroglycerin.
Spontaneous angina (syn.: special angina, rest angina, Prinzmetal angina) - manifests itself in the form of heart attacks at rest, rest, sleep. The attacks are caused by spasm of the coronary arteries with the development of reversible ischemic dystrophy of the myocardium mainly in the subendocardial zone of the left ventricle. Stenosing coronary atherosclerosis is noted, but in 15% of patients the coronary arteries are not changed. Attacks of this angina are often well relieved with nitroglycerin.
Unstable angina (syn.: unstable, rapidly increasing angina) is characterized by attacks, the frequency and duration of which progressively increases.
In most patients, the cause of the development of this angina is the destruction and ulceration of the atherosclerotic plaque of the coronary artery with mural thrombosis, possible thromboembolism and/or vasospasm. As a result, irreversible ischemic dystrophy of the left ventricular myocardium may develop, leading to sudden coronary death or developing into myocardial infarction. Therefore, the unstable form is also called pre-infarction angina or acute coronary insufficiency (ACF).
Sudden coronary death (SCD, synonym: primary cardiac arrest) is death that occurs instantly or within 6 hours from the onset of a heart attack. However, the time of death with VCS can be longer – up to 24 hours. From a pathomorphological point of view, this diagnosis corresponds to all cases of death of patients with OKN before the development of ischemic myocardial necrosis. In this case, characteristic ECG changes are clinically noted (the so-called “ischemic stage of myocardial infarction”), but there is no fermentemia (increased activity of transaminases, lactate dehydrogenase, etc. - markers of cardiomyocyte necrosis).
The structural basis for the development of acute contractile myocardial failure in VCS is ischemic myocardial dystrophy (IDM), which develops as a result of the direct damaging effect of ischemia on muscle fibers during coronary circulatory disorders. As a result, acute general circulatory disorders with multiple organ pathologies arise, the nature of which depends on the immediate causes of death.
The main pathological processes developing in the coronary arteries during VCS are prolonged spasm, plasma saturation of the arterial wall, atherosclerosis and thrombosis. Plasma impregnation and signs of spasm are determined in both extra- and intramural arteries. In the presence of atherosclerotic changes, hemorrhages into the thickness of the fibrous plaque, atheromatous changes and tears in its “cover” may occur with the subsequent development of thrombosis. Thrombosis is secondary in nature, developing as a result of damage to the endothelium during arterial spasm and exacerbation of the atherosclerotic process. The significance of thrombosis is very great, since it is it that determines the irreversibility of the pathological process.
In case of death from VCS, only the diversity of its individual sections is macroscopically determined from the myocardium, associated with focal circulatory disorders, aggravated by postmortem hypostases. These changes can be observed against the background of cardiosclerosis. Macroscopic diagnosis of IDM is possible using tetrazolium and potassium tellurite salts, because in the ischemic zone, the activity of redox enzymes is sharply reduced and grains of formazan and reduced tellurium do not fall out. In this case, the IDM area looks light against the dark background of the unchanged myocardium.
Several techniques are used for microscopic diagnosis of IDM. Among them, the most informative are polarization microscopy, staining using the Lee (GOPP) and MSB (OKG) methods. These methods make it possible to visualize the contractile apparatus of cardiomyocytes and determine their various changes, including the earliest ones.
IDM represents pre-necrotic changes in cardiomyocyte myofibrils (contractural damage, clumpy disintegration and myocytolysis) that occur in the myocardium immediately after the onset of ischemia.
The contracture type of damage to cardiomyocyte myofibrils is a persistent pathological total or focal overcontraction of myofibrils with temporary or final loss of the ability to contract muscle fibers. This prenecrotic pathological process occurs as a result of exposure to various damaging factors, including ischemia. Polarizing microscopy reveals a decrease in the height of isotropic disks and an increase in the height of anisotropic disks (Fig. 1). Contractures differ from physiological contractions in their resistance to the action of fixing solutions and pronounced anisotropy of the A-disks of myofibrils, which is not characteristic of normal contraction. This type of damage is reversible in most cases.
Lumpy disintegration of cardiomyocyte myofibrils is a pathological mosaic recontraction of groups of sarcomeres and lysis of non-contracted sections of myofibrils. This irreversible pathological process occurs primarily as a result of ischemia and in all cases ends in coagulative necrosis. In polarized light, cardiomyocytes with clumpy disintegration of myofibrils are identified by the disappearance of regular transverse striations, instead of which multiple clumps of a brightly luminous anisotropic substance are visible, alternating with isotropic foci (Fig. 2).
Intracellular myocytolysis is a focal lysis of myofibrils with the appearance of zones of disappearance of anisotropy in cardiomyocytes (Fig. 3). This special type of damage to cardiomyocytes appears to develop as a result of impaired intracellular respiration with the accumulation of acidic products and activation of hydrolytic enzymes. The process is reversible if the damaging effect was short-term.
In IDM, all of the above types of pre-necrotic changes in cardiomyocytes occur, but the characteristic feature is the clumpy disintegration of myofibrils. The following dynamics of pathomorphological changes in the myocardium in acute insufficiency are noted.
During the first 2-4 hours of the development of OKN in the zone of myocardial ischemia, multiple small foci of damage to muscle fibers are detected in the form of contractures, intracellular myocytolysis and clumpy disintegration of myofibrils. In the muscle fibers of the ischemic zone, there is a gradual disappearance of glycogen and a decrease in the activity of redox enzymes. A peri-infarction zone is formed, in which contractural damage to cardiomyocytes and clumpy disintegration of their myofibrils are detected.
In the period from 2-4 to 8 hours, the foci of muscle fiber damage gradually merge with each other and predominantly clumpy disintegration of myofibrils is found in them. With a significantly reduced activity of redox enzymes in the cardiomyocytes of the ischemic zone, a sharply positive PAS reaction is detected due to increasing plasma impregnation of the muscle fibers.
In the period from 8 to 12 hours after the onset of an acute violation of the coronary circulation, the ischemic zone is well defined when stained with hematoxylin and eosin due to pronounced hemodynamic disorders (venous congestion, interstitial edema, stasis in the capillaries, diapedetic perivascular hemorrhages) with signs of dystrophy and necrobiosis of muscle fibers ( eosinophilia and lumpy sarcoplasm, pyknosis of cardiomyocyte nuclei). There is a fusion of individual foci with contracture damage and clumpy disintegration of myofibrils. Cardiomyocytes are strongly PAS-positive.
Starting from 12 hours, muscle fibers lose their cross-striations and karyolysis is detected in them. In this case, individual cardiomyocytes are weakly stained with eosin and become basophilic. Basophilia of sarcoplasm coincides in time with pyknosis and karyolysis of nuclei. Cellular infiltrates consisting of polymorphonuclear leukocytes appear in the interstitium. These changes progress up to 24 hours and are accompanied by a gradual fusion of foci of ischemic dystrophy with its transition to myocardial infarction.
It should be noted that the presented histological picture of the dynamics of pathomorphological changes in acute disorders of the coronary circulation can change significantly when thrombosis occurs. In these cases, in the central areas of the ischemic zone of the myocardium, cytolysis of cardiomyocytes is observed, determined in polarized light in the form of “overstretching” of myofibrils with expansion of isotropic discs. This is the most severe and irreversible alterative process, quickly leading to myocardial necrosis. In cases of primary blockage of large trunks of coronary arteries due to hemorrhage into an atherosclerotic plaque or its atheromatous ulceration with thrombosis, extensive foci of necrosis appear within the first 2-3 hours.
The immediate causes of death in VCS can be acute heart failure, ventricular fibrillation, cardiogenic shock and asystole. The nature of general circulatory disorders depends on these causes.
In acute heart failure, dilation of the heart cavities and acute general venous congestion develops with edema and hemorrhages of the lungs, dystrophic and necrotic changes in the epithelium of the kidney tubules, centrilobular necrosis and hemorrhages in the liver.
With fibrillation of the ventricles of the heart, subsegmental contractures of myofibrils are determined in 2-5 rows of muscle fibers adjacent to the epicardium and endocardium, in the papillary muscles; acute general venous congestion.
Cardiogenic shock is pathomorphologically characterized by pronounced dilatation of the cavities of the heart; congestion and pulmonary edema; congestion of the central parts of the liver lobules with necrosis and hemorrhages; plethora and hemorrhages in the spleen; shunting blood flow in the kidneys; hemorrhages in the pancreas; necrosis and hemorrhages in the gastric mucosa; small focal diapedetic hemorrhages in the brain.
Asystole pathomorphologically has no specific signs; destructive changes are noted in the area of the conduction system of the heart: vacuolar degeneration and necrosis of fibers, sometimes hemorrhages in the His bundle; general acute venous congestion of internal organs.
Myocardial infarction is ischemic necrosis of the heart muscle, formed on the basis of previous IDM. As a rule, it looks like a white infarction with a hemorrhagic rim, but if thrombolytic therapy was used, it looks red (due to hemorrhagic impregnation).
Myocardial infarction (MI) is classified according to the following criteria:
1) by time of occurrence - primary (acute) MI, developing over about 8 weeks; repeated MI occurring 8 weeks after the initial one; recurrent myocardial infarction – within 8 weeks of the primary one;
2) by localization in a specific part of the myocardium. In this case, the areas of the apex, anterior and lateral walls of the left ventricle are more often affected, corresponding to the basin of the anterior interventricular branch of the left coronary artery, which is more strongly affected by atherosclerosis than others;
3) by prevalence - small focal MI (subendocardial, subepicardial and intramural - in the thickness of the myocardium) and large focal MI (transmural - affecting the entire thickness of the heart muscle).
In its development, MI goes through two stages - necrotic and scarring. In the necrotic stage, the zone of myocardial damage has unclear boundaries and may include islands of unchanged myocardium, resulting from heterogeneous sensitivity to ischemia of cardiomyocytes. The area of necrosis is delimited by a zone of plethora and leukocyte infiltration - demarcation inflammation. Perifocal to MI, secondary circulatory disorders with IDM and small focal necrosis develop in the heart muscle.
At the stage of scarring, the MI is replaced by connective tissue (organization) due to the activation of fibroblasts from the demarcation zone and areas of preserved myocardium within the area of necrosis. This process follows phagocytosis of detritus by macrophages, which are replaced by polymorphonuclear leukocytes. First, granulation and then coarse fibrous connective tissue is formed with regenerative hypertrophy of the surrounding myocardium. The entire scarring process is completed 7-8 weeks after the onset of MI. However, these periods may vary depending on the size of the lesion and the reactivity of the patient’s body.
Coronary heart disease (CHD)- a group of diseases resulting from myocardial ischemia caused by relative or absolute insufficiency of coronary circulation. IHD is essentially a cardiac form of atherosclerosis and hypertension (which serve as underlying diseases). The course of IHD is chronic with episodes of acute coronary insufficiency, and therefore pathogenetically closely related acute and chronic forms of the disease are distinguished.
Acute coronary heart disease
It includes angina pectoris, sudden coronary death and myocardial infarction. The cause of all these diseases can be prolonged spasm, thrombosis, embolism and functional overstrain of the myocardium with stenotic atherosclerosis of the coronary arteries of the heart and insufficient collateral circulation.Myocardial infarction
Myocardial infarction- vascular necrosis of the heart muscle - in the vast majority of cases develops in the left ventricle. This is the most severe variant of acute ischemic heart disease, ending in death in almost every third case. There are infarctions of the anterior, posterior and lateral walls of the left ventricle, interventricular septum, apex of the heart, as well as extensive infarction. In relation to the layer of the heart muscle, transmural (most common), subendocardial, intramural and rare subepicardial myocardial infarction are distinguished. Depending on the temporal characteristics of the occurrence, primary (acute) myocardial infarction is distinguished, occurring for the first time, repeated, developing within 4 weeks after the primary infarction, and recurrent, observed within 4 weeks after the primary or repeated infarction.In its development, myocardial infarction goes through 2 stages. The necrotic stage is characterized by the presence in the myocardium of a focus of irregular shape, yellowish-white color, flabby consistency, surrounded by a dark red rim. Microscopic examination of the heart muscle reveals three zones: necrotic, demarcation and preserved myocardium. Glycogen disappears from cardiomyocytes in the necrosis zone. The necrosis zone is represented by cardiomyocytes with the phenomena of karyolysis, plasmolysis and plasmorexis, surrounded by demarcation inflammation, in the zone of which, in addition to numerous hyperemic vessels, there is a large number of polymorphonuclear leukocytes (leukocyte shaft). Edema phenomena are observed in the intact myocardium.
Organization stage
From the 3rd day, the disintegration of dead muscle cells begins, and individual fibroblasts appear. By the 7th day, granulation tissue with a large number of fibroblasts and macrophages forms at the edges of the necrosis zone, gradually replacing the affected area. As a result, a scar is formed (post-infarction cardiosclerosis).Complications and causes of death
Most often, patients die from acute cardiovascular failure, cardiogenic shock, ventricular fibrillation, and asystole. As a result of softening of the heart muscle in the area of the infarction (myomalacia), the development of an acute cardiac aneurysm with its subsequent rupture is possible. In this case, death occurs from tamponade of the pericardial cavity.Chronic ischemic disease heart disease includes post-infarction (large-focal) cardiosclerosis, diffuse small-focal (atherosclerotic) cardiosclerosis and chronic cardiac aneurysm.
Post-infarction cardiosclerosis is represented by a scar that occurs as a result of the organization of a heart attack. It has the appearance of a whitish focus of dense consistency, irregular shape and is surrounded by compensatory hypertrophied myocardium.
With diffuse small-focal cardiosclerosis, multiple small, up to 1-2 mm in diameter, foci of whitish connective tissue are observed in the myocardium. In this case, fibrous plaques narrowing the lumen are found in the coronary arteries of the heart.
Chronic cardiac aneurysm is formed from an unruptured acute aneurysm or as a result of the protrusion of post-infarction scar tissue under blood pressure. The heart is enlarged in size with a protruding wall of the left ventricle, thinned in the area of the aneurysm, formed by fibrous tissue. In the area of the aneurysm, mural thrombi are often found.
